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:

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:

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

1. (nosaka2025jshpracticalguidelines pages 1-3): Kisato Nosaka and Takuya Fukushima. Jsh practical guidelines for hematological malignancies, 2023: ii. lymphoma 9—adult t-cell leukemia–lymphoma (atl). International Journal of Hematology, 122:177-189, Jun 2025. URL: https://doi.org/10.1007/s12185-025-04011-2, doi:10.1007/s12185-025-04011-2. This article has 3 citations and is from a peer-reviewed journal.

2. (tsukasaki2020diagnosticapproachesand pages 1-2): Kunihiro Tsukasaki, Ambroise Marçais, Rihab Nasr, Koji Kato, Takahiro Fukuda, Olivier Hermine, and Ali Bazarbachi. Diagnostic approaches and established treatments for adult t cell leukemia lymphoma. Frontiers in Microbiology, Jun 2020. URL: https://doi.org/10.3389/fmicb.2020.01207, doi:10.3389/fmicb.2020.01207. This article has 63 citations and is from a peer-reviewed journal.

3. (altieri2025htlv1andatll pages 7-9): Adrian Altieri, Sean Patrick Reilly, Abu Mansalay, Alan Soo-Beng Khoo, Nettie Johnson, Zafar K. Khan, Amy Leader, Pooja Jain, and Pierluigi Porcu. Htlv-1 and atll: epidemiology, oncogenesis, and opportunities for community-informed research in the united states. Viruses, 17:1333, Sep 2025. URL: https://doi.org/10.3390/v17101333, doi:10.3390/v17101333. This article has 6 citations.

4. (nakahata2023understandingtheimmunopathology pages 1-2): Shingo Nakahata, Daniel Enriquez-Vera, M. Ishrat Jahan, Kenji Sugata, and Yorifumi Satou. Understanding the immunopathology of htlv-1-associated adult t-cell leukemia/lymphoma: a comprehensive review. Biomolecules, 13:1543, Oct 2023. URL: https://doi.org/10.3390/biom13101543, doi:10.3390/biom13101543. This article has 35 citations.

5. (o’donnell2023integratedmolecularand pages 3-4): Jake S O’Donnell, Stewart K Hunt, and Keith J Chappell. Integrated molecular and immunological features of human t-lymphotropic virus type 1 infection and disease progression to adult t-cell leukaemia or lymphoma. The Lancet Haematology, 10:e539-e548, Jul 2023. URL: https://doi.org/10.1016/s2352-3026(23)00087-x, doi:10.1016/s2352-3026(23)00087-x. This article has 23 citations and is from a highest quality peer-reviewed journal.

6. (nosaka2025jshpracticalguidelines media 8f3eac9b): Kisato Nosaka and Takuya Fukushima. Jsh practical guidelines for hematological malignancies, 2023: ii. lymphoma 9—adult t-cell leukemia–lymphoma (atl). International Journal of Hematology, 122:177-189, Jun 2025. URL: https://doi.org/10.1007/s12185-025-04011-2, doi:10.1007/s12185-025-04011-2. This article has 3 citations and is from a peer-reviewed journal.

7. (iordan2024clinicalfeaturesand pages 1-2): Iuliana Iordan, Ana-Maria Vlădăreanu, Cristina Mambet, Minodora Onisâi, Diana Cîșleanu, and Horia Bumbea. 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. Medicina, 60:872, May 2024. URL: https://doi.org/10.3390/medicina60060872, doi:10.3390/medicina60060872. This article has 1 citations.

8. (o’donnell2023integratedmolecularand pages 2-3): Jake S O’Donnell, Stewart K Hunt, and Keith J Chappell. Integrated molecular and immunological features of human t-lymphotropic virus type 1 infection and disease progression to adult t-cell leukaemia or lymphoma. The Lancet Haematology, 10:e539-e548, Jul 2023. URL: https://doi.org/10.1016/s2352-3026(23)00087-x, doi:10.1016/s2352-3026(23)00087-x. This article has 23 citations and is from a highest quality peer-reviewed journal.

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10. (o’donnell2023integratedmolecularand pages 5-6): Jake S O’Donnell, Stewart K Hunt, and Keith J Chappell. Integrated molecular and immunological features of human t-lymphotropic virus type 1 infection and disease progression to adult t-cell leukaemia or lymphoma. The Lancet Haematology, 10:e539-e548, Jul 2023. URL: https://doi.org/10.1016/s2352-3026(23)00087-x, doi:10.1016/s2352-3026(23)00087-x. This article has 23 citations and is from a highest quality peer-reviewed journal.

11. (iordan2024clinicalfeaturesand pages 5-6): Iuliana Iordan, Ana-Maria Vlădăreanu, Cristina Mambet, Minodora Onisâi, Diana Cîșleanu, and Horia Bumbea. 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. Medicina, 60:872, May 2024. URL: https://doi.org/10.3390/medicina60060872, doi:10.3390/medicina60060872. This article has 1 citations.

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