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0
Mappings
0
Definitions
0
Inheritance
5
Pathophysiology
1
Histopathology
7
Phenotypes
5
Pathograph
4
Genes
4
Treatments
4
Subtypes
0
Differentials
0
Datasets
0
Trials
0
Models
11
References
1
Deep Research
🏷

Classifications

Harrison's Chapter
cancer hematologic malignancy
ICD-O Morphology
Lymphoma

Subtypes

4
Acute ATLL
Most aggressive form with leukemic presentation, hypercalcemia, organ infiltration, and opportunistic infections. Median survival is 6-10 months despite treatment. Characterized by high tumor burden and poor response to chemotherapy.
Show evidence (1 reference)
PMID:1751370 PARTIAL
"MST was 6.2 months for acute type"
Shimoyama classification study confirms acute ATLL has median survival of 6.2 months, supporting the poor prognosis described.
Lymphoma Type ATLL
Presents with lymphadenopathy without significant blood involvement. May have better prognosis than acute form if responsive to chemotherapy. Less frequently associated with hypercalcemia.
Show evidence (1 reference)
PMID:1751370 PARTIAL
"Lymphoma type, no lymphocytosis, 1% or less abnormal T-lymphocytes, and histologically-proven lymphadenopathy with or without extranodal lesions."
Shimoyama classification defines lymphoma type by lymphadenopathy without significant blood involvement.
Chronic ATLL
Indolent presentation with mild lymphocytosis and skin involvement. May remain stable for years before transforming to acute type. Better prognosis with median survival of several years.
Show evidence (1 reference)
PMID:1751370 PARTIAL
"24.3 months for chronic type"
Shimoyama study shows chronic type has median survival of 24.3 months, supporting the better prognosis described.
Smoldering ATLL
Most indolent form with at least 5% abnormal T lymphocytes in peripheral blood, normal total lymphocyte count, no hypercalcemia, and often skin-limited disease. May not require immediate treatment but requires monitoring for transformation to aggressive disease.
Show evidence (1 reference)
PMID:1751370 SUPPORT
"Smouldering type, 5% or more abnormal lymphocytes of T-cell nature in PB, normal lymphocyte level (less than 4 x 10(9)/l), no hypercalcaemia"
Shimoyama classification defines smoldering type by at least 5% abnormal T lymphocytes in peripheral blood, normal total lymphocyte count, and absence of hypercalcemia.

Pathophysiology

5
HTLV-1 Infection and Tax Oncoprotein Expression
HTLV-1 preferentially infects CD4+ T cells and integrates into the host genome. The viral Tax protein is the primary driver of transformation, functioning as a transcriptional activator that hijacks multiple cellular pathways. Tax activates NF-kappaB, CREB/ATF, and AP-1 transcription factors, driving T-cell proliferation and survival.
T cell link
viral transcription link
Show evidence (2 references)
PMID:15129647 PARTIAL
"HTLV-1 causes 2 major diseases: adult T-cell leukemia/lymphoma (ATLL) and tropical spastic paraparesis/HTLV-1-associated myelopathy."
Abstract states HTLV-1 causes ATLL, supporting the infectious etiology.
PMID:15129647 PARTIAL
"Tax is a 40-kDa phosphoprotein that is encoded by the pX region of the virus."
Abstract identifies Tax as a viral protein, supporting Tax oncoprotein expression.
Tax-Mediated NF-kappaB Activation
Tax activates both canonical and non-canonical NF-kappaB pathways through direct interaction with IKK complex and NIK. Constitutive NF-kappaB activation drives expression of anti-apoptotic genes (BCL-XL, cIAP, survivin), cytokines (IL-2, IL-15), and cell cycle regulators, promoting T-cell survival and proliferation.
positive regulation of NF-kappaB transcription factor activity link ↑ INCREASED
Genomic Instability and Accumulation of Mutations
Tax impairs multiple DNA repair pathways including nucleotide excision repair, base excision repair, and double-strand break repair. This leads to accumulation of somatic mutations over the decades-long latency period. Tax also causes aneuploidy through centrosome amplification and mitotic checkpoint dysfunction.
DNA damage response link ↓ DECREASED
Apoptosis Resistance
Multiple mechanisms contribute to apoptosis resistance: NF-kappaB-mediated upregulation of BCL-XL and cIAP, Tax-mediated p53 inhibition, and HBZ-mediated enhancement of regulatory T-cell survival. This allows accumulation of cells with genomic abnormalities.
apoptotic process link ↓ DECREASED
Uncontrolled T-Cell Proliferation
Combined effects of constitutive NF-kappaB activation, accumulated mutations, and apoptosis resistance result in clonal expansion of HTLV-1-infected T cells. ATLL cells acquire a CD4+CD25+FOXP3+ regulatory T-cell phenotype with immunosuppressive properties.
T cell link
cell population proliferation link ↑ INCREASED

Histopathology

1
T-Cell Lymphoproliferative Neoplasm VERY_FREQUENT
Adult T-cell lymphoma/leukemia is a rare T-cell lymphoproliferative neoplasm.
Show evidence (1 reference)
PMID:28796966 SUPPORT
"Adult T-cell lymphoma/leukemia (ATL) is a rare T-cell lymphoproliferative"
Abstract characterizes ATL as a rare T-cell lymphoproliferative neoplasm.

Pathograph

Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.
Pathograph: causal mechanism network for Adult T-Cell Leukemia/Lymphoma Interactive directed graph showing how pathophysiology mechanisms, phenotypes, genetic factors and variants, experimental models, environmental triggers, and treatments relate through causal and linked edges.

Phenotypes

7
Blood 1
Leukocytosis VERY_FREQUENT Increased total leukocyte count (HP:0001974)
Cardiovascular 2
Lymphadenopathy VERY_FREQUENT Lymphadenopathy (HP:0002716)
Splenomegaly FREQUENT Splenomegaly (HP:0001744)
Digestive 1
Hepatomegaly FREQUENT Hepatomegaly (HP:0002240)
Immune 1
Opportunistic Infections FREQUENT Recurrent infections (HP:0002719)
Integument 1
Skin Lesions FREQUENT Abnormal skin morphology (HP:0011121)
Metabolism 1
Hypercalcemia FREQUENT Hypercalcemia (HP:0003072)
Show evidence (1 reference)
PMID:24714244 SUPPORT
"Hypercalcemia occurs in about 70% of patients with acute adult T cell leukemia."
Review abstract reports hypercalcemia frequency in acute adult T cell leukemia.
🧬

Genetic Associations

4
HTLV-1 Tax (Viral Oncogene)
HTLV-1 HBZ (Viral Oncogene)
TP53 (Somatic Mutation)
CCR4 (Gain of Function Mutation)
💊

Treatments

4
Chemotherapy
Action: chemotherapy MAXO:0000647
Intensive combination chemotherapy regimens including CHOP-like protocols or more intensive regimens (VCAP-AMP-VECP). Response rates are modest and duration is typically short in aggressive disease.
Show evidence (1 reference)
PMID:22042945 PARTIAL
"The overall response rate ranged from 49% with chemotherapy alone to 81% with combined first-line therapy (chemotherapy with concurrent/sequential ZDV/IFN-α)."
Study shows chemotherapy alone achieves 49% response rate in aggressive ATLL, supporting modest efficacy.
Mogamulizumab
Action: immunotherapy Ontology label: Immunotherapy NCIT:C15262
Agent: mogamulizumab
Anti-CCR4 monoclonal antibody approved for relapsed/refractory ATLL. CCR4 is highly expressed on ATLL cells. Provides activity in patients with CCR4 mutations who have particularly high expression.
Show evidence (1 reference)
PMID:30573506 PARTIAL
"mogamulizumab treatment resulted in 11% cORR, with a tolerable safety profile."
International phase II trial showed mogamulizumab demonstrated responses in relapsed/refractory ATLL where chemotherapy showed no activity.
Allogeneic Stem Cell Transplantation
Action: hematopoietic stem cell transplantation MAXO:0000747
Only potentially curative treatment for ATLL. Graft-versus-ATLL effect contributes to efficacy. Reserved for younger patients with aggressive disease who achieve remission. Long-term survival of 30-40% in selected patients.
Show evidence (1 reference)
PMID:30573506 PARTIAL
"Allogeneic stem cell transplantation (allo-SCT) can significantly prolong survival, but there are few appropriate candidates"
Study confirms allo-SCT prolongs survival but notes limited candidates due to age and prior treatment response requirements.
Interferon-alpha and Zidovudine
Action: immunotherapy Ontology label: Immunotherapy NCIT:C15262
Agent: zidovudine
Combination of interferon-alpha and zidovudine (AZT) shows activity, particularly in leukemic subtypes. May be combined with or followed by chemotherapy. Mechanism involves both antiviral and pro-apoptotic effects.
Show evidence (1 reference)
PMID:22042945 PARTIAL
"Use of ZDV/IFN-α at any time prolonged survival in acute (P < .001) and lymphoma ATLL (P < .001) and was the sole factor associated with reduction in risk of death in aggressive ATLL"
UK study demonstrated ZDV/IFN-α significantly prolonged survival in both acute and lymphoma ATLL subtypes.
🔬

Biochemical Markers

3
HTLV-1 Antibodies
HTLV-1 Proviral Load
Soluble IL-2 Receptor (sIL-2R)
{ }

Source YAML

click to show
name: Adult T-Cell Leukemia/Lymphoma
creation_date: '2026-01-26T02:55:13Z'
updated_date: '2026-05-08T16:21:17Z'
description: >-
  Adult T-cell leukemia/lymphoma (ATLL) is an aggressive peripheral T-cell neoplasm
  caused by Human T-lymphotropic Virus type 1 (HTLV-1) infection. The disease develops
  in approximately 2-5% of HTLV-1 carriers after a prolonged latency of decades.
  ATLL is endemic in southwestern Japan, the Caribbean, parts of South America,
  and sub-Saharan Africa. The HTLV-1 Tax oncoprotein is the primary driver of
  transformation, activating NF-kappaB and CREB pathways, inducing genomic instability,
  and impairing DNA repair. ATLL cells characteristically display a CD4+CD25+ regulatory
  T-cell phenotype with flower-shaped nuclear morphology.
categories:
- Hematologic Malignancy
- T-Cell Lymphoma
- Virus-Associated Cancer
parents:
- T-cell leukemia
- T-cell lymphoma
has_subtypes:
- name: Acute ATLL
  description: >-
    Most aggressive form with leukemic presentation, hypercalcemia, organ
    infiltration, and opportunistic infections. Median survival is 6-10 months
    despite treatment. Characterized by high tumor burden and poor response
    to chemotherapy.
  evidence:
  - reference: PMID:1751370
    reference_title: "Diagnostic criteria and classification of clinical subtypes of adult T-cell leukaemia-lymphoma. A report from the Lymphoma Study Group (1984-87)."
    supports: PARTIAL
    snippet: >-
      MST was 6.2 months for acute type
    explanation: >-
      Shimoyama classification study confirms acute ATLL has median survival
      of 6.2 months, supporting the poor prognosis described.
- name: Lymphoma Type ATLL
  description: >-
    Presents with lymphadenopathy without significant blood involvement.
    May have better prognosis than acute form if responsive to chemotherapy.
    Less frequently associated with hypercalcemia.
  evidence:
  - reference: PMID:1751370
    reference_title: "Diagnostic criteria and classification of clinical subtypes of adult T-cell leukaemia-lymphoma. A report from the Lymphoma Study Group (1984-87)."
    supports: PARTIAL
    snippet: >-
      Lymphoma type, no lymphocytosis, 1% or less abnormal T-lymphocytes, and
      histologically-proven lymphadenopathy with or without extranodal lesions.
    explanation: >-
      Shimoyama classification defines lymphoma type by lymphadenopathy without
      significant blood involvement.
- name: Chronic ATLL
  description: >-
    Indolent presentation with mild lymphocytosis and skin involvement.
    May remain stable for years before transforming to acute type.
    Better prognosis with median survival of several years.
  evidence:
  - reference: PMID:1751370
    reference_title: "Diagnostic criteria and classification of clinical subtypes of adult T-cell leukaemia-lymphoma. A report from the Lymphoma Study Group (1984-87)."
    supports: PARTIAL
    snippet: >-
      24.3 months for chronic type
    explanation: >-
      Shimoyama study shows chronic type has median survival of 24.3 months,
      supporting the better prognosis described.
- name: Smoldering ATLL
  description: >-
    Most indolent form with at least 5% abnormal T lymphocytes in peripheral
    blood, normal total lymphocyte count, no hypercalcemia, and often
    skin-limited disease. May not require immediate treatment but requires
    monitoring for transformation to aggressive disease.
  evidence:
  - reference: PMID:1751370
    reference_title: "Diagnostic criteria and classification of clinical subtypes of adult T-cell leukaemia-lymphoma. A report from the Lymphoma Study Group (1984-87)."
    supports: SUPPORT
    snippet: >-
      Smouldering type, 5% or more abnormal lymphocytes of T-cell nature in PB,
      normal lymphocyte level (less than 4 x 10(9)/l), no hypercalcaemia
    explanation: >-
      Shimoyama classification defines smoldering type by at least 5% abnormal
      T lymphocytes in peripheral blood, normal total lymphocyte count, and
      absence of hypercalcemia.
infectious_agent:
- name: Human T-Lymphotropic Virus Type 1 (HTLV-1)
  infectious_agent_term:
    preferred_term: Human T-cell leukemia virus type I
    term:
      id: NCBITaxon:11908
      label: Human T-cell leukemia virus type I
  description: >-
    HTLV-1 is a deltaretrovirus that infects CD4+ T cells. Transmission occurs
    through breastfeeding, sexual contact, blood transfusion, and injection drug
    use. After infection, HTLV-1 integrates into the host genome and establishes
    lifelong persistent infection. The viral Tax protein is the major transforming
    factor, activating NF-kappaB, inducing genomic instability, and promoting
    T-cell proliferation. HBZ (HTLV-1 basic leucine zipper factor) expressed from
    the antisense strand also contributes to leukemogenesis.
  evidence:
  - reference: PMID:41553980
    reference_title: "CXCR3/CXCL10 Axis-Mediated T Cell Infiltration in the Lungs of Patients With HTLV-1-Associated Diseases: Implications for Subclinical Pulmonary Involvement."
    supports: PARTIAL
    snippet: "HTLV-1 is a retrovirus associated with adult T cell leukemia/lymphoma (ATL) and inflammatory diseases, including HTLV-1-associated myelopathy (HAM) and HTLV-1-associated bronchopneumonopathy (HAB)."
    explanation: This abstract explicitly links HTLV-1 to adult T-cell leukemia/lymphoma, supporting the infectious etiology.
pathophysiology:
- name: HTLV-1 Infection and Tax Oncoprotein Expression
  description: >-
    HTLV-1 preferentially infects CD4+ T cells and integrates into the host genome.
    The viral Tax protein is the primary driver of transformation, functioning as
    a transcriptional activator that hijacks multiple cellular pathways. Tax activates
    NF-kappaB, CREB/ATF, and AP-1 transcription factors, driving T-cell proliferation
    and survival.
  evidence:
  - reference: PMID:15129647
    reference_title: "HTLV-1 and associated adult T-cell leukemia/lymphoma."
    supports: PARTIAL
    snippet: "HTLV-1 causes 2 major diseases: adult T-cell leukemia/lymphoma (ATLL) and tropical spastic paraparesis/HTLV-1-associated myelopathy."
    explanation: "Abstract states HTLV-1 causes ATLL, supporting the infectious etiology."
  - reference: PMID:15129647
    reference_title: "HTLV-1 and associated adult T-cell leukemia/lymphoma."
    supports: PARTIAL
    snippet: "Tax is a 40-kDa phosphoprotein that is encoded by the pX region of the virus."
    explanation: "Abstract identifies Tax as a viral protein, supporting Tax oncoprotein expression."
  cell_types:
  - preferred_term: T cell
    term:
      id: CL:0000084
      label: T cell
  biological_processes:
  - preferred_term: viral transcription
    term:
      id: GO:0019083
      label: viral transcription
  downstream:
  - target: Tax-Mediated NF-kappaB Activation
    description: Tax constitutively activates NF-kappaB signaling
  - target: Genomic Instability and Accumulation of Mutations
    description: Tax impairs DNA repair and induces genomic instability
- name: Tax-Mediated NF-kappaB Activation
  description: >-
    Tax activates both canonical and non-canonical NF-kappaB pathways through
    direct interaction with IKK complex and NIK. Constitutive NF-kappaB activation
    drives expression of anti-apoptotic genes (BCL-XL, cIAP, survivin), cytokines
    (IL-2, IL-15), and cell cycle regulators, promoting T-cell survival and
    proliferation.
  biological_processes:
  - preferred_term: positive regulation of NF-kappaB transcription factor activity
    modifier: INCREASED
    term:
      id: GO:0043123
      label: positive regulation of canonical NF-kappaB signal transduction
  downstream:
  - target: Apoptosis Resistance
    description: NF-kappaB activates anti-apoptotic gene expression
  - target: Uncontrolled T-Cell Proliferation
    description: NF-kappaB and cytokine signaling drive proliferation
- name: Genomic Instability and Accumulation of Mutations
  description: >-
    Tax impairs multiple DNA repair pathways including nucleotide excision repair,
    base excision repair, and double-strand break repair. This leads to accumulation
    of somatic mutations over the decades-long latency period. Tax also causes
    aneuploidy through centrosome amplification and mitotic checkpoint dysfunction.
  biological_processes:
  - preferred_term: DNA damage response
    modifier: DECREASED
    term:
      id: GO:0006974
      label: DNA damage response
  downstream:
  - target: Uncontrolled T-Cell Proliferation
    description: Accumulated mutations in growth regulatory genes promote transformation
- name: Apoptosis Resistance
  description: >-
    Multiple mechanisms contribute to apoptosis resistance: NF-kappaB-mediated
    upregulation of BCL-XL and cIAP, Tax-mediated p53 inhibition, and HBZ-mediated
    enhancement of regulatory T-cell survival. This allows accumulation of cells
    with genomic abnormalities.
  biological_processes:
  - preferred_term: apoptotic process
    modifier: DECREASED
    term:
      id: GO:0006915
      label: apoptotic process
- name: Uncontrolled T-Cell Proliferation
  description: >-
    Combined effects of constitutive NF-kappaB activation, accumulated mutations,
    and apoptosis resistance result in clonal expansion of HTLV-1-infected T cells.
    ATLL cells acquire a CD4+CD25+FOXP3+ regulatory T-cell phenotype with
    immunosuppressive properties.
  cell_types:
  - preferred_term: T cell
    term:
      id: CL:0000084
      label: T cell
  biological_processes:
  - preferred_term: cell population proliferation
    modifier: INCREASED
    term:
      id: GO:0008283
      label: cell population proliferation
histopathology:
- name: T-Cell Lymphoproliferative Neoplasm
  finding_term:
    preferred_term: Adult T-Cell Leukemia/Lymphoma
    term:
      id: NCIT:C3184
      label: Adult T-Cell Leukemia/Lymphoma
  frequency: VERY_FREQUENT
  description: Adult T-cell lymphoma/leukemia is a rare T-cell lymphoproliferative neoplasm.
  evidence:
  - reference: PMID:28796966
    reference_title: "Adult T-Cell Leukemia/Lymphoma."
    supports: SUPPORT
    snippet: "Adult T-cell lymphoma/leukemia (ATL) is a rare T-cell lymphoproliferative"
    explanation: Abstract characterizes ATL as a rare T-cell lymphoproliferative neoplasm.

phenotypes:
- category: Hematologic
  name: Leukocytosis
  frequency: VERY_FREQUENT
  diagnostic: true
  description: >-
    Elevated white blood cell count with characteristic "flower cells" showing
    multilobated nuclei. Peripheral blood involvement is prominent in acute and
    chronic forms.
  phenotype_term:
    preferred_term: Increased total leukocyte count
    term:
      id: HP:0001974
      label: Increased total leukocyte count
- category: Lymphatic
  name: Lymphadenopathy
  frequency: VERY_FREQUENT
  description: >-
    Generalized lymphadenopathy is common, particularly prominent in
    lymphoma-type ATLL.
  phenotype_term:
    preferred_term: Lymphadenopathy
    term:
      id: HP:0002716
      label: Lymphadenopathy
- category: Metabolic
  name: Hypercalcemia
  frequency: FREQUENT
  diagnostic: true
  description: >-
    Hypercalcemia occurs in up to 70% of acute ATLL cases due to ATLL cell
    production of PTHrP (parathyroid hormone-related protein) and osteoclast-
    activating cytokines. Can be severe and life-threatening.
  evidence:
  - reference: PMID:24714244
    reference_title: "Hypercalcemic crisis due to adult T cell leukemia: a rare cause of paralytic ileus."
    supports: SUPPORT
    snippet: "Hypercalcemia occurs in about 70% of patients with acute adult T cell leukemia."
    explanation: "Review abstract reports hypercalcemia frequency in acute adult T cell leukemia."
  phenotype_term:
    preferred_term: Hypercalcemia
    term:
      id: HP:0003072
      label: Hypercalcemia
- category: Dermatologic
  name: Skin Lesions
  frequency: FREQUENT
  description: >-
    Skin involvement with erythematous papules, nodules, plaques, or
    erythroderma. Prominent in smoldering and chronic forms. May resemble
    mycosis fungoides.
  phenotype_term:
    preferred_term: Abnormal skin morphology
    term:
      id: HP:0011121
      label: Abnormal skin morphology
- category: Abdominal
  name: Hepatomegaly
  frequency: FREQUENT
  description: >-
    Liver enlargement from leukemic infiltration, common in acute ATLL.
  phenotype_term:
    preferred_term: Hepatomegaly
    term:
      id: HP:0002240
      label: Hepatomegaly
- category: Abdominal
  name: Splenomegaly
  frequency: FREQUENT
  description: >-
    Splenic enlargement from leukemic infiltration.
  phenotype_term:
    preferred_term: Splenomegaly
    term:
      id: HP:0001744
      label: Splenomegaly
- category: Infectious
  name: Opportunistic Infections
  frequency: FREQUENT
  description: >-
    ATLL cells have regulatory T-cell properties causing profound
    immunosuppression. Opportunistic infections including Pneumocystis,
    Strongyloides, and fungal infections are common and major causes of death.
  phenotype_term:
    preferred_term: Recurrent infections
    term:
      id: HP:0002719
      label: Recurrent infections
biochemical:
- name: HTLV-1 Antibodies
  notes: >-
    Seropositivity for HTLV-1 antibodies is required for diagnosis. ELISA
    screening followed by Western blot confirmation.
- name: HTLV-1 Proviral Load
  notes: >-
    Quantification of HTLV-1 proviral DNA by PCR. High proviral load is
    associated with increased risk of ATLL development.
- name: Soluble IL-2 Receptor (sIL-2R)
  notes: >-
    Markedly elevated sIL-2R reflects high tumor burden and T-cell activation.
    Useful for monitoring disease activity.
genetic:
- name: HTLV-1 Tax
  association: Viral Oncogene
  notes: >-
    Tax is the major HTLV-1 transforming protein. Activates NF-kappaB, CREB,
    and AP-1 pathways; induces genomic instability; inhibits DNA repair;
    and dysregulates cell cycle. Tax expression is often lost in established
    ATLL due to promoter methylation, suggesting its role is primarily in
    early transformation.
- name: HTLV-1 HBZ
  association: Viral Oncogene
  notes: >-
    HBZ (HTLV-1 basic leucine zipper factor) is expressed from the antisense
    strand and maintained in all ATLL cells. Promotes T-cell proliferation
    and regulatory T-cell phenotype. Contributes to transformation
    independently of Tax.
- name: TP53
  association: Somatic Mutation
  notes: >-
    TP53 mutations occur in approximately 20-40% of aggressive ATLL and
    are associated with poor prognosis. More common in acute than
    indolent forms.
- name: CCR4
  association: Gain of Function Mutation
  notes: >-
    CCR4 mutations occur in approximately 25% of cases and result in
    receptor stabilization and enhanced signaling. Target of mogamulizumab
    therapy.
treatments:
- name: Chemotherapy
  description: >-
    Intensive combination chemotherapy regimens including CHOP-like protocols
    or more intensive regimens (VCAP-AMP-VECP). Response rates are modest
    and duration is typically short in aggressive disease.
  evidence:
  - reference: PMID:22042945
    reference_title: "Use of zidovudine and interferon alfa with chemotherapy improves survival in both acute and lymphoma subtypes of adult T-cell leukemia/lymphoma."
    supports: PARTIAL
    snippet: >-
      The overall response rate ranged from 49% with chemotherapy alone to 81%
      with combined first-line therapy (chemotherapy with concurrent/sequential
      ZDV/IFN-α).
    explanation: >-
      Study shows chemotherapy alone achieves 49% response rate in aggressive
      ATLL, supporting modest efficacy.
  treatment_term:
    preferred_term: chemotherapy
    term:
      id: MAXO:0000647
      label: chemotherapy
- name: Mogamulizumab
  description: >-
    Anti-CCR4 monoclonal antibody approved for relapsed/refractory ATLL.
    CCR4 is highly expressed on ATLL cells. Provides activity in patients
    with CCR4 mutations who have particularly high expression.
  evidence:
  - reference: PMID:30573506
    reference_title: "Mogamulizumab versus investigator's choice of chemotherapy regimen in relapsed/refractory adult T-cell leukemia/lymphoma."
    supports: PARTIAL
    snippet: >-
      mogamulizumab treatment resulted in 11% cORR, with a tolerable safety
      profile.
    explanation: >-
      International phase II trial showed mogamulizumab demonstrated responses
      in relapsed/refractory ATLL where chemotherapy showed no activity.
  treatment_term:
    preferred_term: immunotherapy
    term:
      id: NCIT:C15262
      label: Immunotherapy
    therapeutic_agent:
    - preferred_term: mogamulizumab
      term:
        id: NCIT:C62510
        label: Mogamulizumab
- name: Allogeneic Stem Cell Transplantation
  description: >-
    Only potentially curative treatment for ATLL. Graft-versus-ATLL effect
    contributes to efficacy. Reserved for younger patients with aggressive
    disease who achieve remission. Long-term survival of 30-40% in selected
    patients.
  evidence:
  - reference: PMID:30573506
    reference_title: "Mogamulizumab versus investigator's choice of chemotherapy regimen in relapsed/refractory adult T-cell leukemia/lymphoma."
    supports: PARTIAL
    snippet: >-
      Allogeneic stem cell transplantation (allo-SCT) can significantly prolong
      survival, but there are few appropriate candidates
    explanation: >-
      Study confirms allo-SCT prolongs survival but notes limited candidates
      due to age and prior treatment response requirements.
  treatment_term:
    preferred_term: hematopoietic stem cell transplantation
    term:
      id: MAXO:0000747
      label: hematopoietic stem cell transplantation
- name: Interferon-alpha and Zidovudine
  description: >-
    Combination of interferon-alpha and zidovudine (AZT) shows activity,
    particularly in leukemic subtypes. May be combined with or followed
    by chemotherapy. Mechanism involves both antiviral and pro-apoptotic
    effects.
  evidence:
  - reference: PMID:22042945
    reference_title: "Use of zidovudine and interferon alfa with chemotherapy improves survival in both acute and lymphoma subtypes of adult T-cell leukemia/lymphoma."
    supports: PARTIAL
    snippet: >-
      Use of ZDV/IFN-α at any time prolonged survival in acute (P < .001) and
      lymphoma ATLL (P < .001) and was the sole factor associated with
      reduction in risk of death in aggressive ATLL
    explanation: >-
      UK study demonstrated ZDV/IFN-α significantly prolonged survival in both
      acute and lymphoma ATLL subtypes.
  treatment_term:
    preferred_term: immunotherapy
    term:
      id: NCIT:C15262
      label: Immunotherapy
    therapeutic_agent:
    - preferred_term: zidovudine
      term:
        id: CHEBI:10110
        label: zidovudine
disease_term:
  preferred_term: adult T-cell leukemia/lymphoma
  term:
    id: MONDO:0019471
    label: adult T-cell leukemia/lymphoma

classifications:
  icdo_morphology:
    classification_value: Lymphoma
  harrisons_chapter:
  - classification_value: cancer
  - classification_value: hematologic malignancy
references:
- reference: DOI:10.1111/bjh.13338
  title: 'Dose‐intensified chemotherapy alone or in combination with mogamulizumab in newly diagnosed aggressive adult T‐cell leukaemia‐lymphoma: a randomized phase <scp>II</scp> study'
  found_in:
  - Adult_T_Cell_Leukemia_Lymphoma-deep-research-falcon.md
  findings:
  - statement: 'Dose‐intensified chemotherapy alone or in combination with mogamulizumab in newly diagnosed aggressive adult T‐cell leukaemia‐lymphoma: a randomized phase <scp>II</scp> study'
    supporting_text: a dose‐intensified chemotherapy, further increases efficacy without compromising safety of patients with newly diagnosed aggressive adult T‐cell leukaemia‐lymphoma (
    evidence:
    - reference: DOI:10.1111/bjh.13338
      reference_title: 'Dose‐intensified chemotherapy alone or in combination with mogamulizumab in newly diagnosed aggressive adult T‐cell leukaemia‐lymphoma: a randomized phase <scp>II</scp> study'
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: a dose‐intensified chemotherapy, further increases efficacy without compromising safety of patients with newly diagnosed aggressive adult T‐cell leukaemia‐lymphoma (
      explanation: Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
- reference: DOI:10.1111/cas.13343
  title: 'Mogamulizumab for relapsed adult T‐cell leukemia–lymphoma: Updated follow‐up analysis of phase I and <scp>II</scp> studies'
  found_in:
  - Adult_T_Cell_Leukemia_Lymphoma-deep-research-falcon.md
  findings:
  - statement: The present study sought to elucidate the prognosis of adult T‐cell leukemia–lymphoma (ATL) patients receiving mogamulizumab, a defucosylated anti‐CCR4 monoclonal antibody.
    supporting_text: The present study sought to elucidate the prognosis of adult T‐cell leukemia–lymphoma (ATL) patients receiving mogamulizumab, a defucosylated anti‐CCR4 monoclonal antibody.
    evidence:
    - reference: DOI:10.1111/cas.13343
      reference_title: 'Mogamulizumab for relapsed adult T‐cell leukemia–lymphoma: Updated follow‐up analysis of phase I and <scp>II</scp> studies'
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: The present study sought to elucidate the prognosis of adult T‐cell leukemia–lymphoma (ATL) patients receiving mogamulizumab, a defucosylated anti‐CCR4 monoclonal antibody.
      explanation: Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
- reference: DOI:10.1111/ejh.12863
  title: Effects of mogamulizumab in adult T‐cell leukemia/lymphoma in clinical practice
  found_in:
  - Adult_T_Cell_Leukemia_Lymphoma-deep-research-falcon.md
  findings:
  - statement: The efficacy of mogamulizumab in adult T‐cell leukemia/lymphoma (ATLL) was reported in a previous phase 2 study.
    supporting_text: The efficacy of mogamulizumab in adult T‐cell leukemia/lymphoma (ATLL) was reported in a previous phase 2 study.
    evidence:
    - reference: DOI:10.1111/ejh.12863
      reference_title: Effects of mogamulizumab in adult T‐cell leukemia/lymphoma in clinical practice
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: The efficacy of mogamulizumab in adult T‐cell leukemia/lymphoma (ATLL) was reported in a previous phase 2 study.
      explanation: Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
- reference: DOI:10.1182/blood-2011-03-345702
  title: How I treat adult T-cell leukemia/lymphoma
  found_in:
  - Adult_T_Cell_Leukemia_Lymphoma-deep-research-falcon.md
  findings:
  - statement: Adult T-cell leukemia/lymphoma (ATL) is an aggressive malignancy of mature activated T cells caused by human T-cell lymphotropic virus type I.
    supporting_text: Adult T-cell leukemia/lymphoma (ATL) is an aggressive malignancy of mature activated T cells caused by human T-cell lymphotropic virus type I.
    evidence:
    - reference: DOI:10.1182/blood-2011-03-345702
      reference_title: How I treat adult T-cell leukemia/lymphoma
      supports: SUPPORT
      evidence_source: OTHER
      snippet: Adult T-cell leukemia/lymphoma (ATL) is an aggressive malignancy of mature activated T cells caused by human T-cell lymphotropic virus type I.
      explanation: Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
- reference: DOI:10.1182/bloodadvances.2020003053
  title: 'Mogamulizumab for adult T-cell leukemia-lymphoma: a multicenter prospective observational study'
  found_in:
  - Adult_T_Cell_Leukemia_Lymphoma-deep-research-falcon.md
  findings:
  - statement: 'Mogamulizumab for adult T-cell leukemia-lymphoma: a multicenter prospective observational study'
    supporting_text: Monitoring of Immune Responses Following Mogamulizumab-Containing Treatment in Patients with Adult T-Cell Leukemia-Lymphoma (ATL) (MIMOGA) is a multicenter prospective observational study to establish the most effective and safe treatment strategy using mogamulizumab for ATL patients (UMIN000008696).
    evidence:
    - reference: DOI:10.1182/bloodadvances.2020003053
      reference_title: 'Mogamulizumab for adult T-cell leukemia-lymphoma: a multicenter prospective observational study'
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: Monitoring of Immune Responses Following Mogamulizumab-Containing Treatment in Patients with Adult T-Cell Leukemia-Lymphoma (ATL) (MIMOGA) is a multicenter prospective observational study to establish the most effective and safe treatment strategy using mogamulizumab for ATL patients (UMIN000008696).
      explanation: Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
- reference: DOI:10.1186/s12985-023-02077-0
  title: 'Zidovudine and Interferon Alfa based regimens for the treatment of adult T-cell leukemia/lymphoma (ATLL): a systematic review and meta-analysis'
  found_in:
  - Adult_T_Cell_Leukemia_Lymphoma-deep-research-falcon.md
  findings:
  - statement: ATLL (Adult T-Cell Leukemia/Lymphoma) is an aggressive hematological malignancy.
    supporting_text: ATLL (Adult T-Cell Leukemia/Lymphoma) is an aggressive hematological malignancy.
    evidence:
    - reference: DOI:10.1186/s12985-023-02077-0
      reference_title: 'Zidovudine and Interferon Alfa based regimens for the treatment of adult T-cell leukemia/lymphoma (ATLL): a systematic review and meta-analysis'
      supports: SUPPORT
      evidence_source: OTHER
      snippet: ATLL (Adult T-Cell Leukemia/Lymphoma) is an aggressive hematological malignancy.
      explanation: Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
- reference: DOI:10.3390/biom13101543
  title: 'Understanding the Immunopathology of HTLV-1-Associated Adult T-Cell Leukemia/Lymphoma: A Comprehensive Review'
  found_in:
  - Adult_T_Cell_Leukemia_Lymphoma-deep-research-falcon.md
  findings:
  - statement: Human T-cell leukemia virus type-1 (HTLV-1) causes adult T-cell leukemia/lymphoma (ATL).
    supporting_text: Human T-cell leukemia virus type-1 (HTLV-1) causes adult T-cell leukemia/lymphoma (ATL).
    evidence:
    - reference: DOI:10.3390/biom13101543
      reference_title: 'Understanding the Immunopathology of HTLV-1-Associated Adult T-Cell Leukemia/Lymphoma: A Comprehensive Review'
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: Human T-cell leukemia virus type-1 (HTLV-1) causes adult T-cell leukemia/lymphoma (ATL).
      explanation: Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
- reference: DOI:10.3390/medicina60060872
  title: 'Clinical Features and Survival Outcome in Aggressive-Type Adult T-Cell Leukemia/Lymphoma Patients: Real-Life Experience of a Single Center from an HTLV-1 Endemic Country'
  found_in:
  - Adult_T_Cell_Leukemia_Lymphoma-deep-research-falcon.md
  findings:
  - statement: Adult T-cell leukemia/lymphoma (ATLL) is a highly aggressive T-cell lymphoproliferative disease associated with the human T-cell lymphotropic virus type I (HTLV-1).
    supporting_text: Adult T-cell leukemia/lymphoma (ATLL) is a highly aggressive T-cell lymphoproliferative disease associated with the human T-cell lymphotropic virus type I (HTLV-1).
    evidence:
    - reference: DOI:10.3390/medicina60060872
      reference_title: 'Clinical Features and Survival Outcome in Aggressive-Type Adult T-Cell Leukemia/Lymphoma Patients: Real-Life Experience of a Single Center from an HTLV-1 Endemic Country'
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: Adult T-cell leukemia/lymphoma (ATLL) is a highly aggressive T-cell lymphoproliferative disease associated with the human T-cell lymphotropic virus type I (HTLV-1).
      explanation: Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
- reference: DOI:10.3390/v16101616
  title: Current State of Therapeutics for HTLV-1
  found_in:
  - Adult_T_Cell_Leukemia_Lymphoma-deep-research-falcon.md
  findings:
  - statement: Human T cell leukaemia virus type-1 (HTLV-1) is an oncogenic retrovirus that causes lifelong infection in ~5–10 million individuals globally.
    supporting_text: Human T cell leukaemia virus type-1 (HTLV-1) is an oncogenic retrovirus that causes lifelong infection in ~5–10 million individuals globally.
    evidence:
    - reference: DOI:10.3390/v16101616
      reference_title: Current State of Therapeutics for HTLV-1
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: Human T cell leukaemia virus type-1 (HTLV-1) is an oncogenic retrovirus that causes lifelong infection in ~5–10 million individuals globally.
      explanation: Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
- reference: DOI:10.3390/v17050664
  title: 'Human T-Lymphotropic Virus (HTLV): Epidemiology, Genetic, Pathogenesis, and Future Challenges'
  found_in:
  - Adult_T_Cell_Leukemia_Lymphoma-deep-research-falcon.md
  findings:
  - statement: Human T-lymphotropic viruses (HTLVs) are deltaretroviruses infecting millions of individuals worldwide, with HTLV-1 and HTLV-2 being the most widespread and clinically relevant types.
    supporting_text: Human T-lymphotropic viruses (HTLVs) are deltaretroviruses infecting millions of individuals worldwide, with HTLV-1 and HTLV-2 being the most widespread and clinically relevant types.
    evidence:
    - reference: DOI:10.3390/v17050664
      reference_title: 'Human T-Lymphotropic Virus (HTLV): Epidemiology, Genetic, Pathogenesis, and Future Challenges'
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: Human T-lymphotropic viruses (HTLVs) are deltaretroviruses infecting millions of individuals worldwide, with HTLV-1 and HTLV-2 being the most widespread and clinically relevant types.
      explanation: Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
- reference: DOI:10.3390/v17101333
  title: 'HTLV-1 and ATLL: Epidemiology, Oncogenesis, and Opportunities for Community-Informed Research in the United States'
  found_in:
  - Adult_T_Cell_Leukemia_Lymphoma-deep-research-falcon.md
  findings:
  - statement: 'HTLV-1 and ATLL: Epidemiology, Oncogenesis, and Opportunities for Community-Informed Research in the United States'
    supporting_text: Human T-cell leukemia virus type 1 (HTLV-1), the first oncogenic human retrovirus, causes adult T-cell leukemia/lymphoma (ATLL), an aggressive neoplasm of mature CD4+ T-cells that is incurable in most patients and is associated with a median survival of less than 1 year.
    evidence:
    - reference: DOI:10.3390/v17101333
      reference_title: 'HTLV-1 and ATLL: Epidemiology, Oncogenesis, and Opportunities for Community-Informed Research in the United States'
      supports: SUPPORT
      evidence_source: OTHER
      snippet: Human T-cell leukemia virus type 1 (HTLV-1), the first oncogenic human retrovirus, causes adult T-cell leukemia/lymphoma (ATLL), an aggressive neoplasm of mature CD4+ T-cells that is incurable in most patients and is associated with a median survival of less than 1 year.
      explanation: Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
📚

References & Deep Research

References

11
Dose‐intensified chemotherapy alone or in combination with mogamulizumab in newly diagnosed aggressive adult T‐cell leukaemia‐lymphoma: a randomized phase <scp>II</scp> study
1 finding
Dose‐intensified chemotherapy alone or in combination with mogamulizumab in newly diagnosed aggressive adult T‐cell leukaemia‐lymphoma: a randomized phase <scp>II</scp> study
"a dose‐intensified chemotherapy, further increases efficacy without compromising safety of patients with newly diagnosed aggressive adult T‐cell leukaemia‐lymphoma ("
Show evidence (1 reference)
DOI:10.1111/bjh.13338 SUPPORT Human Clinical
"a dose‐intensified chemotherapy, further increases efficacy without compromising safety of patients with newly diagnosed aggressive adult T‐cell leukaemia‐lymphoma ("
Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
Mogamulizumab for relapsed adult T‐cell leukemia–lymphoma: Updated follow‐up analysis of phase I and <scp>II</scp> studies
1 finding
The present study sought to elucidate the prognosis of adult T‐cell leukemia–lymphoma (ATL) patients receiving mogamulizumab, a defucosylated anti‐CCR4 monoclonal antibody.
"The present study sought to elucidate the prognosis of adult T‐cell leukemia–lymphoma (ATL) patients receiving mogamulizumab, a defucosylated anti‐CCR4 monoclonal antibody."
Show evidence (1 reference)
DOI:10.1111/cas.13343 SUPPORT Human Clinical
"The present study sought to elucidate the prognosis of adult T‐cell leukemia–lymphoma (ATL) patients receiving mogamulizumab, a defucosylated anti‐CCR4 monoclonal antibody."
Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
Effects of mogamulizumab in adult T‐cell leukemia/lymphoma in clinical practice
1 finding
The efficacy of mogamulizumab in adult T‐cell leukemia/lymphoma (ATLL) was reported in a previous phase 2 study.
"The efficacy of mogamulizumab in adult T‐cell leukemia/lymphoma (ATLL) was reported in a previous phase 2 study."
Show evidence (1 reference)
DOI:10.1111/ejh.12863 SUPPORT Human Clinical
"The efficacy of mogamulizumab in adult T‐cell leukemia/lymphoma (ATLL) was reported in a previous phase 2 study."
Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
How I treat adult T-cell leukemia/lymphoma
1 finding
Adult T-cell leukemia/lymphoma (ATL) is an aggressive malignancy of mature activated T cells caused by human T-cell lymphotropic virus type I.
"Adult T-cell leukemia/lymphoma (ATL) is an aggressive malignancy of mature activated T cells caused by human T-cell lymphotropic virus type I."
Show evidence (1 reference)
"Adult T-cell leukemia/lymphoma (ATL) is an aggressive malignancy of mature activated T cells caused by human T-cell lymphotropic virus type I."
Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
Mogamulizumab for adult T-cell leukemia-lymphoma: a multicenter prospective observational study
1 finding
Mogamulizumab for adult T-cell leukemia-lymphoma: a multicenter prospective observational study
"Monitoring of Immune Responses Following Mogamulizumab-Containing Treatment in Patients with Adult T-Cell Leukemia-Lymphoma (ATL) (MIMOGA) is a multicenter prospective observational study to establish the most effective and safe treatment strategy using mogamulizumab for ATL patients (UMIN000008696)."
Show evidence (1 reference)
DOI:10.1182/bloodadvances.2020003053 SUPPORT Human Clinical
"Monitoring of Immune Responses Following Mogamulizumab-Containing Treatment in Patients with Adult T-Cell Leukemia-Lymphoma (ATL) (MIMOGA) is a multicenter prospective observational study to establish the most effective and safe treatment strategy using mogamulizumab for ATL patients (UMIN000008696)."
Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
Zidovudine and Interferon Alfa based regimens for the treatment of adult T-cell leukemia/lymphoma (ATLL): a systematic review and meta-analysis
1 finding
ATLL (Adult T-Cell Leukemia/Lymphoma) is an aggressive hematological malignancy.
"ATLL (Adult T-Cell Leukemia/Lymphoma) is an aggressive hematological malignancy."
Show evidence (1 reference)
"ATLL (Adult T-Cell Leukemia/Lymphoma) is an aggressive hematological malignancy."
Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
Understanding the Immunopathology of HTLV-1-Associated Adult T-Cell Leukemia/Lymphoma: A Comprehensive Review
1 finding
Human T-cell leukemia virus type-1 (HTLV-1) causes adult T-cell leukemia/lymphoma (ATL).
"Human T-cell leukemia virus type-1 (HTLV-1) causes adult T-cell leukemia/lymphoma (ATL)."
Show evidence (1 reference)
DOI:10.3390/biom13101543 SUPPORT Human Clinical
"Human T-cell leukemia virus type-1 (HTLV-1) causes adult T-cell leukemia/lymphoma (ATL)."
Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
Clinical Features and Survival Outcome in Aggressive-Type Adult T-Cell Leukemia/Lymphoma Patients: Real-Life Experience of a Single Center from an HTLV-1 Endemic Country
1 finding
Adult T-cell leukemia/lymphoma (ATLL) is a highly aggressive T-cell lymphoproliferative disease associated with the human T-cell lymphotropic virus type I (HTLV-1).
"Adult T-cell leukemia/lymphoma (ATLL) is a highly aggressive T-cell lymphoproliferative disease associated with the human T-cell lymphotropic virus type I (HTLV-1)."
Show evidence (1 reference)
DOI:10.3390/medicina60060872 SUPPORT Human Clinical
"Adult T-cell leukemia/lymphoma (ATLL) is a highly aggressive T-cell lymphoproliferative disease associated with the human T-cell lymphotropic virus type I (HTLV-1)."
Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
Current State of Therapeutics for HTLV-1
1 finding
Human T cell leukaemia virus type-1 (HTLV-1) is an oncogenic retrovirus that causes lifelong infection in ~5–10 million individuals globally.
"Human T cell leukaemia virus type-1 (HTLV-1) is an oncogenic retrovirus that causes lifelong infection in ~5–10 million individuals globally."
Show evidence (1 reference)
DOI:10.3390/v16101616 SUPPORT Human Clinical
"Human T cell leukaemia virus type-1 (HTLV-1) is an oncogenic retrovirus that causes lifelong infection in ~5–10 million individuals globally."
Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
Human T-Lymphotropic Virus (HTLV): Epidemiology, Genetic, Pathogenesis, and Future Challenges
1 finding
Human T-lymphotropic viruses (HTLVs) are deltaretroviruses infecting millions of individuals worldwide, with HTLV-1 and HTLV-2 being the most widespread and clinically relevant types.
"Human T-lymphotropic viruses (HTLVs) are deltaretroviruses infecting millions of individuals worldwide, with HTLV-1 and HTLV-2 being the most widespread and clinically relevant types."
Show evidence (1 reference)
DOI:10.3390/v17050664 SUPPORT Human Clinical
"Human T-lymphotropic viruses (HTLVs) are deltaretroviruses infecting millions of individuals worldwide, with HTLV-1 and HTLV-2 being the most widespread and clinically relevant types."
Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.
HTLV-1 and ATLL: Epidemiology, Oncogenesis, and Opportunities for Community-Informed Research in the United States
1 finding
HTLV-1 and ATLL: Epidemiology, Oncogenesis, and Opportunities for Community-Informed Research in the United States
"Human T-cell leukemia virus type 1 (HTLV-1), the first oncogenic human retrovirus, causes adult T-cell leukemia/lymphoma (ATLL), an aggressive neoplasm of mature CD4+ T-cells that is incurable in most patients and is associated with a median survival of less than 1 year."
Show evidence (1 reference)
DOI:10.3390/v17101333 SUPPORT Other
"Human T-cell leukemia virus type 1 (HTLV-1), the first oncogenic human retrovirus, causes adult T-cell leukemia/lymphoma (ATLL), an aggressive neoplasm of mature CD4+ T-cells that is incurable in most patients and is associated with a median survival of less than 1 year."
Deep research cited this publication as relevant literature for Adult T Cell Leukemia Lymphoma.

Deep Research

1
Falcon
Adult T-Cell Leukemia/Lymphoma (ATLL/ATL) — Disease Characteristics Research Report
Edison Scientific Literature 57 citations 2026-05-08T08:22:10.434085

Adult T-Cell Leukemia/Lymphoma (ATLL/ATL) — Disease Characteristics Research Report

Target Disease

  • Disease name: Adult T-cell leukemia/lymphoma (ATL/ATLL) (nosaka2025jshpracticalguidelines pages 1-3, tsukasaki2020diagnosticapproachesand pages 1-2)
  • MONDO ID: Not retrieved in this run
  • Category: Mature T-cell neoplasm / peripheral T-cell lymphoma-leukemia, HTLV-1–associated (nosaka2025jshpracticalguidelines pages 1-3, tsukasaki2020diagnosticapproachesand pages 1-2)

1. Disease Information

1.1 Concise overview

Adult T-cell leukemia/lymphoma (ATLL; also written ATL) is a distinct mature/peripheral T-cell malignancy etiologically caused by human T-cell leukemia/lymphotropic virus type 1 (HTLV-1) (nosaka2025jshpracticalguidelines pages 1-3, tsukasaki2020diagnosticapproachesand pages 1-2). It typically develops after a long latency (≈20–30 years) in a minority of HTLV-1 carriers and is characterized by aggressive clinical behavior in acute and lymphoma subtypes, with frequent immunosuppression and opportunistic infections (altieri2025htlv1andatll pages 7-9).

Abstract quote (etiology/risk): “Human T-cell leukemia virus type-1 (HTLV-1) causes adult T-cell leukemia/lymphoma (ATL). … 5–10% of carriers lose this balance and develop ATL.” (Nakahata et al., Biomolecules, 2023-10; (nakahata2023understandingtheimmunopathology pages 1-2)).

1.2 Key identifiers and synonyms

Key naming and identifier fields available from retrieved evidence are summarized here:

Field Value Evidence / notes ICD-10 ICD-11 MeSH MONDO Orphanet OMIM
Preferred disease name Adult T-cell leukemia/lymphoma Distinct mature/peripheral T-cell malignancy caused by HTLV-1; often abbreviated ATL or ATLL (tsukasaki2020diagnosticapproachesand pages 1-2, nosaka2025jshpracticalguidelines pages 1-3) Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run
Concise disease overview Aggressive mature T-cell neoplasm arising after long-latency HTLV-1 infection, with leukemic and/or lymphomatous presentations Reviews/guidelines describe ATL as HTLV-1-caused, typically after decades of latency; median survival for aggressive disease remains poor (altieri2025htlv1andatll pages 7-9, nakahata2023understandingtheimmunopathology pages 1-2) Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run
Common abbreviations ATL; ATLL Both forms are used in recent literature and guidelines (nosaka2025jshpracticalguidelines pages 1-3, tsukasaki2020diagnosticapproachesand pages 1-2) Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run
Key synonyms / alternative names Adult T-cell leukaemia-lymphoma; Adult T-cell leukemia-lymphoma; HTLV-1-associated adult T-cell leukemia/lymphoma British and American spellings both appear; disease is frequently described as HTLV-1-associated ATL/ATLL (o’donnell2023integratedmolecularand pages 3-4, tsukasaki2020diagnosticapproachesand pages 1-2) Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run
Causative agent Human T-cell leukemia/lymphotropic virus type 1 (HTLV-1) Causal viral etiology is consistently stated across guideline and reviews (nosaka2025jshpracticalguidelines pages 1-3, tsukasaki2020diagnosticapproachesand pages 1-2, nakahata2023understandingtheimmunopathology pages 1-2) Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run
Typical target cell / lineage Mature CD4+ T-cell neoplasm; commonly CD3+, CD4+, CD25+, often CCR4+ Immunophenotypic description from overview/review sources (altieri2025htlv1andatll pages 7-9, tsukasaki2020diagnosticapproachesand pages 1-2) Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run
Canonical clinical classification Four Shimoyama subtypes: acute, lymphoma, chronic, smoldering Current guideline retains Shimoyama clinical subtyping; acute/lymphoma and unfavorable chronic are aggressive, favorable chronic and smoldering are indolent (nosaka2025jshpracticalguidelines pages 1-3, altieri2025htlv1andatll pages 7-9, nosaka2025jshpracticalguidelines media 8f3eac9b) Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run
Aggressive vs indolent grouping Aggressive: acute, lymphoma, chronic with unfavorable factors; Indolent: chronic without unfavorable factors, smoldering Unfavorable chronic defined by abnormal BUN, LDH, or low albumin in guideline summary (nosaka2025jshpracticalguidelines pages 1-3) Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run
Latency / temporal development Usually develops after long latency, about 20-30 years after HTLV-1 infection; many carriers remain asymptomatic for decades Long latency emphasized in recent reviews; only a minority of carriers progress to ATL/ATLL (altieri2025htlv1andatll pages 7-9, o’donnell2023integratedmolecularand pages 3-4, nakahata2023understandingtheimmunopathology pages 1-2) Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run
Mode of knowledge represented here Aggregated disease-level literature and guidelines, not individual-patient EHR data Information in this summary comes from reviews, consensus/guideline documents, and cohort studies (nosaka2025jshpracticalguidelines pages 1-3, tsukasaki2020diagnosticapproachesand pages 1-2, iordan2024clinicalfeaturesand pages 1-2) Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run Not retrieved in this run

Table: This table summarizes the core disease naming, etiology, subtype classification, and latency concepts for adult T-cell leukemia/lymphoma. Identifier fields are included for ontology/database curation and marked as not retrieved where this evidence run did not supply them.

Note: ICD-10/ICD-11/MeSH/MONDO/Orphanet/OMIM codes were not directly retrieved from the full text evidence in this tool run; they should be added via targeted ontology/registry queries.

1.3 Evidence sources represented in this report

This report is derived from aggregated disease-level resources: reviews, guidelines/consensus documents, clinical trials, and cohort studies (nosaka2025jshpracticalguidelines pages 1-3, tsukasaki2020diagnosticapproachesand pages 1-2, iordan2024clinicalfeaturesand pages 1-2). It does not include individual EHR-derived patient records.

2. Etiology

2.1 Primary causes

ATLL is causally linked to HTLV-1 infection, a deltaretrovirus that persists via proviral integration and clonal expansion of infected T cells (nosaka2025jshpracticalguidelines pages 1-3, o’donnell2023integratedmolecularand pages 2-3). Viral proteins Tax and HBZ contribute to oncogenesis and immune dysregulation (o’donnell2023integratedmolecularand pages 3-4, nakahata2023understandingtheimmunopathology pages 1-2).

2.2 Risk factors

Infectious exposure and transmission routes: Major transmission routes include mother-to-child via breastfeeding, sexual contact, and exposure to infected blood products/transfusion (tsukasaki2020diagnosticapproachesand pages 1-2, branda2025humantlymphotropicvirus pages 10-12).

High proviral load: In a 2023 Lancet Haematology review, higher baseline proviral load strongly predicted ATLL risk; proviral load “>4 copies per 100 PBMCs” was associated with HR 3.57 (95% CI 2.25–5.68) for developing ATLL (o’donnell2023integratedmolecularand pages 3-4).

Coinfection/host immune state: Strongyloides coinfection is cited as promoting ATLL development, consistent with the concept that immune status influences progression (nakahata2023understandingtheimmunopathology pages 1-2).

2.3 Protective factors

Evidence in this run supports breastfeeding modification as protective against HTLV-1 transmission (see Prevention). Specific genetic protective variants were not retrieved as explicit “protective variants” in the excerpts, although host HLA influences transmission risk and immune control (o’donnell2023integratedmolecularand pages 2-3).

2.4 Gene–environment interactions

Host genetics (e.g., HLA concordance between mother and infant) influences HTLV-1 transmission risk, modifying how an environmental exposure (breastfeeding) translates into infection (o’donnell2023integratedmolecularand pages 2-3).

3. Phenotypes

3.1 Clinical subtypes and defining features (Shimoyama)

ATLL is classically divided into acute, lymphoma, chronic, and smoldering subtypes (nosaka2025jshpracticalguidelines pages 1-3, nosaka2025jshpracticalguidelines media 8f3eac9b). A 2023 Lancet Haematology review provides quantitative subtype proportions: smouldering (5–10%), chronic (10–20%), lymphoma (20–25%), with acute accounting for the remainder (o’donnell2023integratedmolecularand pages 5-6).

Smouldering ATL is defined by specific blood and laboratory thresholds: “presence of abnormal T cells with flower cell morphology in peripheral blood (≥5%)”, normal lymphocyte count (≤4×10^9/L), “no hypercalcaemia (corrected calcium concentration <2·74 mmol/L)”, and only mild LDH elevation (o’donnell2023integratedmolecularand pages 5-6).

3.2 Common symptoms/signs and lab abnormalities

Across guidelines and reviews, common features include: - Leukocytosis with abnormal “flower cells” (nosaka2025jshpracticalguidelines pages 1-3) - Lymphadenopathy, hepatosplenomegaly, skin rash/skin lesions (nosaka2025jshpracticalguidelines pages 1-3, altieri2025htlv1andatll pages 7-9) - Elevated LDH, hypercalcemia (nosaka2025jshpracticalguidelines pages 1-3, tsukasaki2020diagnosticapproachesand pages 1-2) - Opportunistic infections (e.g., Pneumocystis, aspergillosis, candidiasis, CMV; also Strongyloides) (altieri2025htlv1andatll pages 7-9, nosaka2025jshpracticalguidelines pages 1-3)

Real-world complications documented in a 2024 Romanian cohort included cytopenias and infections in all patients; pathogens included Candida albicans, C. difficile, bacterial infections, herpes zoster, SARS-CoV-2, CMV reactivation, and BK virus; symptomatic hypercalcemia was common (iordan2024clinicalfeaturesand pages 5-6).

3.3 Suggested HPO terms (examples)

(These are ontology suggestions; IDs should be verified against HPO.) - Hypercalcemia (HP:0003072) (nosaka2025jshpracticalguidelines pages 1-3, tsukasaki2020diagnosticapproachesand pages 1-2) - Lymphadenopathy (HP:0002716) (nosaka2025jshpracticalguidelines pages 1-3) - Hepatosplenomegaly (HP:0001433 / HP:0001744) (nosaka2025jshpracticalguidelines pages 1-3) - Skin rash / Cutaneous lesion (HP:0000988 / HP:0000951) (nosaka2025jshpracticalguidelines pages 1-3) - Elevated lactate dehydrogenase (HP:0003236) (nosaka2025jshpracticalguidelines pages 1-3) - Opportunistic infection (HP:0002719) (altieri2025htlv1andatll pages 7-9, nosaka2025jshpracticalguidelines pages 1-3) - Leukocytosis (HP:0001974) (nosaka2025jshpracticalguidelines pages 1-3)

3.4 Quality-of-life impact

Direct QoL instrument data (EQ-5D/SF-36/PROMIS) were not retrieved in this run; however, severe systemic symptoms, infections, and hypercalcemia complications in aggressive ATLL imply major functional and hospitalization burden (iordan2024clinicalfeaturesand pages 5-6).

4. Genetic/Molecular Information

4.1 Viral oncogenes and host alterations (core concepts)

Two viral gene products are repeatedly emphasized: - Tax: transiently expressed, highly immunogenic, drives proliferation/anti-apoptotic pathways and host gene dysregulation (o’donnell2023integratedmolecularand pages 3-4, nakahata2023understandingtheimmunopathology pages 1-2). - HBZ: persistently expressed antisense product with low immunogenicity; promotes clonal proliferation and immune evasion (o’donnell2023integratedmolecularand pages 3-4, o’donnell2023integratedmolecularand pages 2-3).

Abstract quote (Tax oncogenesis): “HTLV-1 encodes the viral transcription transactivator, Tax, in the pX region of its genome, which promotes oncogenesis.” (Nakahata et al., Biomolecules, 2023-10; (nakahata2023understandingtheimmunopathology pages 1-2)).

4.2 Somatic genomic/epigenetic alterations (host)

From a 2023 immunopathology review: - “~90% of ATL cases have activating TCR–NF-κB pathway mutations” (nakahata2023understandingtheimmunopathology pages 3-5). - “~40% show CpG island hypermethylation (CIMP)” (nakahata2023understandingtheimmunopathology pages 3-5). - HLA class I mutations/deletions and PD-L1 3′-UTR structural alterations that increase PD-L1 mRNA are enriched in ATL (nakahata2023understandingtheimmunopathology pages 3-5).

Single-cell features described include upregulation of immunosuppressive molecules (PD-L1, CD73, CD39) and activation markers (CD71, CD25, CD38) (nakahata2023understandingtheimmunopathology pages 3-5).

4.3 Suggested gene/protein targets for annotation

  • CCR4 (target of mogamulizumab) (ishida2017mogamulizumabforrelapsed pages 1-2)
  • PD-L1 (CD274) structural alterations and overexpression (nakahata2023understandingtheimmunopathology pages 3-5)
  • FOXP3 (Treg phenotype association) (nakahata2023understandingtheimmunopathology pages 3-5)

4.4 Suggested GO biological process terms (examples)

(IDs should be verified against GO.) - NF-κB signaling (nakahata2023understandingtheimmunopathology pages 3-5, o’donnell2023integratedmolecularand pages 3-4) - Regulation of T-cell activation / TCR signaling (nakahata2023understandingtheimmunopathology pages 3-5) - Immune evasion / negative regulation of immune response (nakahata2023understandingtheimmunopathology pages 3-5, o’donnell2023integratedmolecularand pages 3-4) - DNA methylation / epigenetic gene regulation (nakahata2023understandingtheimmunopathology pages 3-5)

4.5 Suggested CL (Cell Ontology) terms

  • CD4-positive, alpha-beta T cell (ATL cell of origin/target) (o’donnell2023integratedmolecularand pages 2-3)
  • Regulatory T cell (Treg-like phenotype; FOXP3-associated) (nakahata2023understandingtheimmunopathology pages 3-5, o’donnell2023integratedmolecularand pages 3-4)
  • Cytotoxic CD8-positive T cell (Tax-specific CTLs in immune control) (o’donnell2023integratedmolecularand pages 3-4)

5. Environmental Information

5.1 Infectious agent

HTLV-1 is the infectious agent underlying ATLL (nosaka2025jshpracticalguidelines pages 1-3, tsukasaki2020diagnosticapproachesand pages 1-2).

5.2 Lifestyle/environmental exposures

In this run, the key non-genetic exposures relate to transmission opportunities: breastfeeding, sexual exposure, contaminated blood/organ products, and injection-related exposures (altieri2025htlv1andatll pages 12-14, tsukasaki2020diagnosticapproachesand pages 1-2).

6. Mechanism / Pathophysiology

6.1 Causal chain (high-level)

1) HTLV-1 acquisition (breastfeeding/sexual/blood) → 2) proviral integration and clonal expansion of infected CD4+ T cells with generally quiescent transcription → 3) episodic Tax expression enables spread and promotes proliferative programs but drives immune recognition → 4) selection for immune escape with Tax silencing (e.g., 5′ LTR methylation/deletion) and persistence via HBZ-driven proliferation → 5) accumulation of host genetic and epigenetic lesions (e.g., TCR–NF-κB pathway mutations, CIMP, HLA/PD-L1 alterations) → 6) emergence of malignant clone with immune evasion and systemic immunodeficiency → clinical ATLL with hypercalcemia, organ infiltration, and opportunistic infections (o’donnell2023integratedmolecularand pages 3-4, nakahata2023understandingtheimmunopathology pages 3-5, nosaka2025jshpracticalguidelines pages 1-3).

6.2 Key mechanisms and pathways

  • Tax-driven activation of proliferative and anti-apoptotic pathways; selection for Tax-silenced clones due to immune pressure (o’donnell2023integratedmolecularand pages 3-4, nakahata2023understandingtheimmunopathology pages 1-2).
  • HBZ-driven clonal proliferation and immune evasion (low immunogenicity), with promotion of tolerogenic/Treg-like phenotypes (o’donnell2023integratedmolecularand pages 3-4, o’donnell2023integratedmolecularand pages 2-3).
  • TCR–NF-κB pathway mutations in most cases (nakahata2023understandingtheimmunopathology pages 3-5).
  • Immune checkpoint and antigen presentation alterations: PD-L1 structural alterations and HLA class I changes contribute to immune escape (nakahata2023understandingtheimmunopathology pages 3-5).

6.3 Molecular profiling (selected)

Single-cell transcriptomic observations include ATL cell upregulation of PD-L1, CD73, CD39, CD71, CD25, CD38, and dynamic HLA class II expression patterns during clonal expansion (nakahata2023understandingtheimmunopathology pages 3-5).

7. Anatomical Structures Affected

7.1 Organ-level involvement

  • Blood and bone marrow (leukemic manifestations in acute/chronic) (nosaka2025jshpracticalguidelines pages 1-3, tsukasaki2020diagnosticapproachesand pages 1-2)
  • Lymph nodes (lymphoma subtype and systemic disease) (nosaka2025jshpracticalguidelines pages 1-3)
  • Skin (skin lesions/rash; common) (nosaka2025jshpracticalguidelines pages 1-3, tsukasaki2020diagnosticapproachesand pages 1-2)
  • Liver/spleen (hepatosplenomegaly) (nosaka2025jshpracticalguidelines pages 1-3)
  • CNS/GI involvement can occur, particularly noted for acute subtype (tsukasaki2020diagnosticapproachesand pages 1-2)

7.2 Suggested UBERON terms (examples)

(IDs should be verified against UBERON.) - Peripheral blood; bone marrow; lymph node; skin; liver; spleen; central nervous system; gastrointestinal tract (tsukasaki2020diagnosticapproachesand pages 1-2, nosaka2025jshpracticalguidelines pages 1-3).

8. Temporal Development

ATLL typically develops after long latency from infection (20–30 years) (altieri2025htlv1andatll pages 7-9). Aggressive subtypes have a rapid course (months), while indolent subtypes have longer median survivals (years) (nosaka2025jshpracticalguidelines pages 1-3, o’donnell2023integratedmolecularand pages 5-6).

9. Inheritance and Population

9.1 Epidemiology and demographics

  • HTLV-1 carriers: estimated ~10–20 million worldwide; Japan ~1.08 million carriers (nosaka2025jshpracticalguidelines pages 1-3).
  • Lifetime risk of ATLL among carriers: ~2–5% (Japan guideline) (nosaka2025jshpracticalguidelines pages 1-3); another recent review states ATLL occurs in ~3–5% of HTLV-1 infections (altieri2025htlv1andatll pages 7-9).
  • Subtype frequencies in Japan (2012–2013): acute 51.9%, lymphoma 24.9%, chronic 12.5%, smoldering 10.7% (nosaka2025jshpracticalguidelines pages 1-3).

10. Diagnostics

10.1 Diagnostic criteria and subtype classification

Table 1 from the JSH guideline provides ATL diagnostic and subtype classification criteria and can be used as the primary structured reference for smoldering/chronic/lymphoma/acute definitions in routine practice (nosaka2025jshpracticalguidelines media 8f3eac9b).

10.2 Laboratory and pathology tests

HTLV-1 confirmation: The guideline states serology positive by particle agglutination, ELISA/Western blotting, or line immunoassay; confirmatory tests are recommended (nosaka2025jshpracticalguidelines pages 1-3). Where available, “Institutions capable of performing Southern blotting should do so to confirm integration of HTLV-1 provirus into ATL cells.” (nosaka2025jshpracticalguidelines pages 1-3).

Molecular assays: PCR/qPCR proviral testing and clonality analysis are referenced as diagnostic approaches (branda2025humantlymphotropicvirus pages 17-17, stUnknownyearprotocolforthe pages 5-10).

Immunophenotyping (flow cytometry): Recommended minimal panel includes CD3, CD4, CD7, CD8, CD25; typical tumor phenotype includes CD2/CD4/CD5/CD45RO/CD29/TCR with reduced CD3 and often negative for CD7, CD8, CD26 (bazarbachi2011howitreat pages 2-3).

Histology requirement at low blood tumor burden: When circulating abnormal lymphocytes are <5%, histological confirmation of neoplastic lesions is required for smoldering/chronic/acute ATL diagnosis (nosaka2025jshpracticalguidelines pages 1-3).

11. Outcome/Prognosis

11.1 Survival statistics (recent guideline + recent review)

From a nationwide Japan survey (2010–2011) summarized in the JSH guideline: - 4-year OS: acute 16.8%, lymphoma 19.6%, chronic unfavorable 26.6%, chronic favorable 62.1%, smoldering 59.8% (nosaka2025jshpracticalguidelines pages 1-3).

From a 2023 Lancet Haematology review (median OS): - Smouldering: median OS 55 months; 4-year OS 52% (o’donnell2023integratedmolecularand pages 5-6) - Chronic: median OS 31.5 months; 4-year OS 36% (o’donnell2023integratedmolecularand pages 5-6)

A Japanese cohort (2000–2009) reported median OS: acute 8.3 months; lymphoma 10.6 months; chronic 31.5 months; smoldering 55.0 months (munakata2018adulttcellleukemialymphoma. pages 12-14).

11.2 Real-world outcomes (2024)

A 2024 Romanian single-center cohort of aggressive ATLL reported median survival 6.37 months overall; lymphoma-type 8.16 months vs acute-type 3.60 months, with low response to chemotherapy (iordan2024clinicalfeaturesand pages 1-2).

12. Treatment

12.1 Established and emerging treatments (with quantitative outcomes)

A consolidated treatment evidence table from this run is provided here:

Treatment modality Setting Key efficacy statistics Safety / limitations Publication year URL / DOI Evidence
Zidovudine + interferon-α (AZT/IFN) Frontline, combination with chemotherapy, maintenance in selected subtypes 2023 meta-analysis of 15 studies/1,101 patients: overall response 67% (95% CI 0.50–0.80), CR 33% (95% CI 0.24–0.44), PR 31% (95% CI 0.24–0.39); better responses when used front-line and in indolent disease; aggressive subtype pooled CR 25%, indolent pooled CR 53%; one observational analysis reported HR for death 0.23 (95% CI 0.09–0.60) in aggressive ATLL; one report cited median PFS 48 months with AZT/IFN vs 11 months after chemotherapy in CR patients Evidence base is heterogeneous and largely non-randomized; interferon availability issues noted; some cohorts reported no significant survival difference vs chemotherapy; detailed pooled AE statistics not robustly available in retrieved evidence 2023 https://doi.org/10.1186/s12985-023-02077-0 (shafiee2023zidovudineandinterferon pages 1-2, shafiee2023zidovudineandinterferon pages 4-6, shafiee2023zidovudineandinterferon pages 8-9, shafiee2023zidovudineandinterferon pages 6-7, shafiee2023zidovudineandinterferon pages 7-8)
Intensive multiagent chemotherapy (e.g., VCAP-AMP-VECP, modified LSG15, CHOP/CHOP-like, hyper-CVAD) Frontline for aggressive acute/lymphoma ATL In randomized phase II study, adding mogamulizumab to mLSG15 increased CR to 52% vs 33% with mLSG15 alone and ORR to 86% vs 75%; Romanian real-world cohort using CHOP/CHOP-like, modified LSG15, or hyper-CVAD had only 6 responses among 20 patients and median survival 6.37 months overall (8.16 months lymphoma-type, 3.60 months acute-type) Conventional chemotherapy responses are often short; poor outcomes in aggressive disease; cytopenias/infections common in real-world practice 2015, 2024 https://doi.org/10.1111/bjh.13338 ; https://doi.org/10.3390/medicina60060872 (iordan2024clinicalfeaturesand pages 1-2, iordan2024clinicalfeaturesand pages 9-10, iordan2024clinicalfeaturesand pages 2-4)
Mogamulizumab monotherapy Relapsed/refractory aggressive ATL; also used prospectively in broader ATL population Phase II relapsed aggressive ATL: median PFS 5.2 months, 1-year PFS 26%, median OS 14.4 months, 3-year OS 23%; outcomes better with rash ≥grade 2: median PFS 11.7 months, median OS 25.6 months; multicenter observational study: ORR 65%, median PFS 7.4 months, median OS 16.0 months; retrospective real-world cohort: ORR 36%, CR 17%, median PFS 1.8 months, OS 4.0 months overall, better with ≥5 courses Rash is common and may correlate with response; fatal AEs reported; severe cutaneous reactions, HBV reactivation, infusion reactions reported; efficacy varies substantially by population and line of therapy 2017, 2020 https://doi.org/10.1111/cas.13343 ; https://doi.org/10.1182/bloodadvances.2020003053 ; https://doi.org/10.1111/ejh.12863 (ishida2017mogamulizumabforrelapsed pages 1-2, sekine2017effectsofmogamulizumab pages 14-18, sekine2017effectsofmogamulizumab pages 10-14, yonekura2020mogamulizumabforadult pages 12-12)
Mogamulizumab + intensive chemotherapy Frontline newly diagnosed aggressive ATL Randomized phase II: CR 52% (95% CI 33–71) and ORR 86% with mLSG15 + mogamulizumab vs CR 33% and ORR 75% with mLSG15 alone More grade ≥3 anemia, thrombocytopenia, lymphopenia, leukopenia, decreased appetite; CMV infection, interstitial lung disease, and skin disorders reported in combination arm 2015 https://doi.org/10.1111/bjh.13338 (wang2024currentstateof pages 12-14)
Mogamulizumab before allogeneic HSCT Pre-transplant exposure in transplant-eligible patients Not a benefit row: retrieved evidence emphasizes risk rather than efficacy Significantly increased risks of severe and steroid-refractory GVHD, non-relapse mortality, and overall mortality; 50-day washout before allo-HSCT recommended in 2024 review 2018, 2024 https://doi.org/10.1007/978-3-319-99716-2_7 ; https://doi.org/10.3390/v16101616 (wang2024currentstateof pages 34-35, wang2024currentstateof pages 12-14, munakata2018adulttcellleukemialymphoma. pages 16-17)
Allogeneic hematopoietic stem-cell transplantation (allo-HSCT) Consolidation/curative-intent for eligible aggressive ATL, typically early after remission/response Considered the only modality with curative potential in recent reviews/guidelines; exact pooled survival statistics not in retrieved 2023–2024 evidence here; Romanian cohort: only 2/20 patients underwent allo-HSCT Limited to fit/eligible patients; transplant morbidity/mortality substantial; timing complicated by prior mogamulizumab exposure 2023, 2024, 2025 https://doi.org/10.3390/biom13101543 ; https://doi.org/10.3390/v16101616 ; https://doi.org/10.3390/medicina60060872 ; https://doi.org/10.1007/s12185-025-04011-2 (nakahata2023understandingtheimmunopathology pages 2-3, nosaka2025jshpracticalguidelines pages 1-3, wang2024currentstateof pages 34-35, iordan2024clinicalfeaturesand pages 1-2, wang2024currentstateof pages 12-14)
Lenalidomide Relapsed/recurrent ATL; maintenance benefit discussed in review literature Mentioned as phase II ATLL-002 and case reports of maintenance benefit; no numeric ORR/PFS/OS values available in retrieved evidence Quantitative efficacy not in retrieved evidence; recognized as an approved/emerging option in reviews 2024 https://doi.org/10.3390/v16101616 (wang2024currentstateof pages 34-35)
Brentuximab vedotin Selected CD30-positive ATL; role discussed in reviews Not in retrieved evidence for quantitative efficacy statistics Mentioned as an approved/newer agent in review literature, but no trial outcome numbers captured in this run 2020 https://doi.org/10.3389/fmicb.2020.01207 (tsukasaki2020diagnosticapproachesand pages 1-2)
Valemetostat / EZH1/2-directed epigenetic therapy Relapsed/refractory ATL; investigational/early implementation Open-label single-arm phase II and preclinical activity mentioned; no numeric ORR/PFS/OS captured in retrieved evidence Early-phase/limited evidence in this run; quantitative outcomes not retrieved 2024 https://doi.org/10.3390/v16101616 (wang2024currentstateof pages 34-35)
Investigational CAR-T / gene-edited cell therapy (e.g., anti-CD7 CAR-T, CD70 allogeneic CRISPR-edited CAR-T) Relapsed/refractory T-cell malignancies including ATL in early-phase studies Trial programs identified: anti-CD7 CAR-T (NCT05620680; single-center phase 1, n=20) and CD70-directed allogeneic CRISPR-edited CTX131 (NCT06492304); efficacy statistics not in retrieved evidence Early-phase, small cohorts, relapsed/refractory setting; immune toxicity and translational challenges remain 2025 https://doi.org/10.1016/j.leukres.2025.107642 (epsteinpeterson2025newtreatmentsfor pages 15-15)
CRISPR/ZFN proviral excision / RNA-based or gene-therapy strategies Preclinical / future therapeutic modality No clinical efficacy statistics in retrieved evidence Delivery efficiency, off-target effects, and safety remain major challenges; promising concept rather than established therapy 2024, 2025 https://doi.org/10.3390/v16101616 ; https://doi.org/10.3390/v17050664 (branda2025humantlymphotropicvirus pages 23-25, wang2024currentstateof pages 1-2)

Table: This table summarizes key established and emerging treatment strategies for adult T-cell leukemia/lymphoma, including clinical setting, efficacy signals, and major safety limitations. It is useful for quickly comparing frontline, relapsed, transplant, and investigational approaches using only evidence retrieved in this run.

Key points: - AZT/IFN remains a widely used antiviral/immune-modulating regimen with pooled response estimates in a 2023 meta-analysis (OR 67%, CR 33%) and signals of greater benefit in indolent disease and in frontline combination use (shafiee2023zidovudineandinterferon pages 1-2, shafiee2023zidovudineandinterferon pages 4-6). - Mogamulizumab (anti-CCR4) shows clinically meaningful activity in relapsed aggressive ATL (phase II median OS 14.4 months; PFS 5.2 months) with rash as an immune-related AE correlated with improved outcomes (ishida2017mogamulizumabforrelapsed pages 1-2). Real-world results vary (e.g., ORR 36% and OS 4.0 months in one retrospective cohort) (sekine2017effectsofmogamulizumab pages 10-14). - Chemoimmunotherapy (mLSG15 + mogamulizumab) improved CR rates compared with chemotherapy alone, but with higher toxicity and opportunistic infections (wang2024currentstateof pages 12-14). - Allo-HSCT is emphasized as the only potentially curative approach in recent reviews and depends on eligibility and timing; pretransplant mogamulizumab exposure increases GVHD and mortality risk, motivating washout periods (wang2024currentstateof pages 34-35, wang2024currentstateof pages 12-14).

12.2 Suggested MAXO terms (examples)

(IDs should be verified against MAXO.) - Antiviral therapy (AZT/IFN) (shafiee2023zidovudineandinterferon pages 1-2) - Combination chemotherapy (iordan2024clinicalfeaturesand pages 1-2) - Monoclonal antibody therapy (mogamulizumab) (ishida2017mogamulizumabforrelapsed pages 1-2) - Hematopoietic stem cell transplantation (allo-HSCT) (nakahata2023understandingtheimmunopathology pages 2-3) - CAR T-cell therapy (investigational) (epsteinpeterson2025newtreatmentsfor pages 15-15)

13. Prevention

ATLL prevention is largely primary prevention of HTLV-1 acquisition, because disease typically follows long-term infection.

Breastfeeding modification: Early cessation of breastfeeding reduces transmission risk “from 14% to 4%” (o’donnell2023integratedmolecularand pages 2-3). A US-focused review states refraining from breastfeeding in HTLV-1-positive mothers can prevent 87% of early-life infections; short-term breastfeeding up to 3 months is proposed when formula is infeasible (altieri2025htlv1andatll pages 12-14).

Blood donor screening: Blood-donor screening is linked to a “significant reduction in transmission through blood transfusions” (branda2025humantlymphotropicvirus pages 10-12).

Organ donor screening: Receiving an organ from an HTLV-1-positive donor was described as having “100% risk of infection” (altieri2025htlv1andatll pages 4-5).

Sexual and injection-related transmission prevention: Safe-sex practices, partner testing/counseling, and harm-reduction needle exchange programs are recommended in public-health frameworks (altieri2025htlv1andatll pages 12-14).

14. Other Species / Natural Disease

This run retrieved animal-model discussions relevant to experimental systems (see Model Organisms) but did not retrieve evidence of naturally occurring ATLL in non-human species.

15. Model Organisms

A 2024 HTLV-1 therapeutics review summarizes multiple model systems: - Transgenic mice: Tax transgenic mice established Tax as an oncoprotein but often developed mesenchymal tumors rather than frank ATL-like disease; HBZ transgenic expression in CD4+ T cells induced leukemia/lymphoma after a long latency, aligning with HBZ constitutive expression in ATL (wang2024currentstateof pages 9-11, wang2024currentstateof pages 8-9). - Xenografts / patient-derived xenografts: NOD/SCID and NOG mice engrafted with ATL cells better recapitulate disease; the MET-1 NOD/SCID model demonstrated tumor inhibition and prolonged survival with daclizumab + depsipeptide (HDAC inhibitor) (wang2024currentstateof pages 8-9). - Humanized mice: Models (e.g., huNSG formats) allow HTLV-1 infection with rising proviral load, clonal CD25+CD4+ expansion, and ATL-like pathology; limitations include incomplete recapitulation of long-term persistence and immune context (wang2024currentstateof pages 9-11).

Limitations of this evidence run

  • Formal ICD/MeSH/MONDO/Orphanet/OMIM identifiers were not retrieved from the accessed full texts.
  • Several key sources are 2025 (still recent and authoritative), because some 2023 guideline documents were published later; core mechanistic sources prioritized include 2023–2024 reviews.
  • Some treatment modalities (lenalidomide, brentuximab, valemetostat) are mentioned but lacked extractable trial efficacy numbers in retrieved excerpts.

Key references (URLs/DOIs and publication dates)

  • O’Donnell et al. Lancet Haematology (2023-07). https://doi.org/10.1016/S2352-3026(23)00087-X (o’donnell2023integratedmolecularand pages 3-4)
  • Nakahata et al. Biomolecules (2023-10). https://doi.org/10.3390/biom13101543 (nakahata2023understandingtheimmunopathology pages 1-2)
  • Wang et al. Viruses (2024-10). https://doi.org/10.3390/v16101616 (wang2024currentstateof pages 1-2)
  • Shafiee et al. Virology Journal (2023-06). https://doi.org/10.1186/s12985-023-02077-0 (shafiee2023zidovudineandinterferon pages 1-2)
  • Ishida et al. Cancer Science (2017-08). https://doi.org/10.1111/cas.13343 (ishida2017mogamulizumabforrelapsed pages 1-2)
  • Iordan et al. Medicina (2024-05). https://doi.org/10.3390/medicina60060872 (iordan2024clinicalfeaturesand pages 1-2)
  • Nosaka & Fukushima International Journal of Hematology (2025-06; “JSH practical guidelines 2023”). https://doi.org/10.1007/s12185-025-04011-2 (nosaka2025jshpracticalguidelines pages 1-3)

References

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