3
Mappings
0
Definitions
0
Inheritance
8
Pathophysiology
1
Histopathology
7
Phenotypes
9
Pathograph
5
Genes
8
Treatments
4
Subtypes
0
Differentials
0
Datasets
0
Trials
0
Models
🏷

Classifications

Harrison's Chapter
cancer solid tumor
ICD-O Morphology
Carcinoma
🔗

Mappings

MONDO
MONDO:0007256 hepatocellular carcinoma Not Yet Curated
skos:exactMatch MONDO
MONDO provides an exact disease term for hepatocellular carcinoma.
NCIT
NCIT:C3099 Hepatocellular Carcinoma
skos:exactMatch NCIT
NCIT provides an exact neoplasm term for hepatocellular carcinoma.
ICD-10-CM
ICD10CM:C22.0 Liver cell carcinoma
skos:exactMatch ICD-10-CM
ICD-10-CM provides an exact code for liver cell carcinoma / hepatocellular carcinoma.
NCIT
NCIT:C3099 Hepatocellular Carcinoma
skos:exactMatch NCIT
NCIT provides an exact neoplasm term for hepatocellular carcinoma.

Subtypes

4
Viral Hepatitis-Associated HCC
HCC arising in the context of chronic hepatitis B or C infection. HBV can be directly oncogenic through viral integration, while HCV promotes HCC primarily through cirrhosis and chronic inflammation.
Alcohol-Related HCC
HCC arising in alcohol-related liver disease and cirrhosis. Associated with specific molecular features and generally presents at more advanced stage.
MASLD-Associated HCC
HCC arising in metabolic dysfunction-associated steatotic liver disease (formerly NAFLD/NASH). Increasingly common subtype that can occur even without cirrhosis. May have distinct immune microenvironment features affecting immunotherapy response.
Fibrolamellar HCC NCIT:C4131
Rare variant occurring in younger patients without cirrhosis. Characterized by DNAJB1-PRKACA fusion. Distinct clinical behavior and treatment considerations.
NCIT: Fibrolamellar Carcinoma (skos:closeMatch) NCIT:C4131

Pathophysiology

8
Chronic Liver Injury and Cirrhosis
Most HCC arises in the context of chronic liver disease and cirrhosis. Persistent hepatocyte death and regeneration in an inflammatory environment promotes accumulation of genetic alterations. Cirrhosis itself is a premalignant condition with ongoing oxidative stress and genomic instability.
hepatocyte link
liver link
Show evidence (1 reference)
PMID:41567639 PARTIAL
"HCC typically arises in patients with chronic liver disease, including hepatitis, cirrhosis, and non-alcoholic fatty liver diseases."
This abstract states that HCC commonly arises in chronic liver disease and cirrhosis, supporting the mechanism described.
Telomere Dysfunction and Genomic Instability
Chronic hepatocyte proliferation leads to telomere shortening, causing genomic instability. TERT promoter mutations, which are the most common HCC mutations, reactivate telomerase to enable unlimited replication. This creates a checkpoint bypass allowing survival of genetically unstable cells.
telomere maintenance link ⚠ ABNORMAL
Accumulation of Driver Mutations
Multiple driver genes are recurrently mutated in HCC, including TERT promoter (60%), TP53 (30%), CTNNB1 (30%), AXIN1 (10%), and ARID1A (10%). These mutations affect telomere maintenance, cell cycle control, WNT signaling, and chromatin remodeling.
DNA repair link ↓ DECREASED
WNT/Beta-Catenin Pathway Activation
Activating mutations in CTNNB1 (beta-catenin) or inactivating mutations in AXIN1 lead to constitutive WNT pathway activation. This drives cell proliferation and is associated with a distinct molecular subclass of HCC with specific clinical features including cholestasis and immune exclusion.
Wnt signaling pathway link ↑ INCREASED
TP53 Pathway Inactivation
TP53 mutations are common in HCC, particularly in HBV-associated and aflatoxin-associated tumors. Loss of p53 function removes a critical checkpoint, allowing survival of cells with DNA damage and promoting genomic instability.
apoptotic process link ↓ DECREASED
Enhanced Hepatocyte Proliferation
Combined effects of telomerase reactivation, cell cycle checkpoint loss, and mitogenic signaling drive uncontrolled hepatocyte proliferation and tumor growth.
cell population proliferation link ↑ INCREASED
Angiogenesis and VEGF Signaling
HCC is a highly vascular tumor dependent on angiogenesis. VEGF signaling promotes new blood vessel formation supplying the tumor. VEGF also has immunosuppressive effects, contributing to the immune-excluded microenvironment. This provides the rationale for anti-VEGF therapy in combination with immunotherapy.
angiogenesis link ↑ INCREASED
Show evidence (1 reference)
PMID:19637355 SUPPORT
"Hepatocellular carcinoma (HCC) is a highly vascular tumor, and angiogenesis is believed to play a considerable role in its development and progression."
Abstract notes HCC is highly vascular and angiogenesis plays a major role, supporting this mechanism.
Immune Evasion and Immunosuppressive Microenvironment
HCC develops in a chronically inflamed liver with an inherently immunosuppressive microenvironment. Tumor cells upregulate PD-L1, VEGF-mediated immunosuppression excludes effector T cells, and recruitment of regulatory T cells, myeloid-derived suppressor cells, and tumor-associated macrophages creates an immune-tolerant niche. The combination of anti-PD-L1 with anti-VEGF addresses both the checkpoint-mediated and VEGF-mediated immunosuppression.
CD8-positive, alpha-beta T cell link
Negative Regulation of T Cell Mediated Immunity link ↑ INCREASED
Show evidence (1 reference)
PMID:32158599 SUPPORT Other
"The HCC tumor microenvironment is characterized by a dysfunction of the immune system through multiple mechanisms, including accumulation of various immunosuppressive factors, recruitment of regulatory T cells and myeloid-derived suppressor cells, and induction of T cell exhaustion accompanied..."
Review specifically describes HCC's immunosuppressive microenvironment including Treg and MDSC recruitment, T cell exhaustion, and checkpoint ligand-receptor interactions — directly supporting all claims in this node about HCC immune evasion mechanisms.

Histopathology

1
Hepatocellular Carcinoma VERY_FREQUENT
Hepatocellular carcinoma is the most common primary liver malignancy.
Show evidence (1 reference)
PMID:27785449 SUPPORT
"Hepatocellular carcinoma (HCC) is the most common primary liver malignancy"
Abstract states that HCC is the most common primary liver malignancy.

Pathograph

Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.
Pathograph: causal mechanism network for Hepatocellular Carcinoma 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
Digestive 4
Hepatomegaly FREQUENT Hepatomegaly (HP:0002240)
Ascites FREQUENT Ascites (HP:0001541)
Jaundice OCCASIONAL Jaundice (HP:0000952)
Nausea FREQUENT Nausea (HP:0002018)
Constitutional 2
Abdominal Pain FREQUENT Abdominal pain (HP:0002027)
Fatigue VERY_FREQUENT Fatigue (HP:0012378)
Growth 1
Weight Loss VERY_FREQUENT Weight loss (HP:0001824)
🧬

Genetic Associations

5
TERT Promoter (Somatic Activating Mutation)
TP53 (Somatic Loss of Function)
CTNNB1 (Somatic Activating Mutation)
AXIN1 (Somatic Loss of Function)
ARID1A (Somatic Loss of Function)
💊

Treatments

8
Atezolizumab plus Bevacizumab
Action: pharmacotherapy MAXO:0000058
Agent: atezolizumab bevacizumab
First-line standard of care for unresectable HCC based on IMbrave150 trial. Anti-PD-L1 (atezolizumab) combined with anti-VEGF (bevacizumab) demonstrated superior overall survival compared to sorafenib. Requires adequate liver function (Child-Pugh A) and no high-risk varices.
Mechanism Target:
INHIBITS Immune Evasion and Immunosuppressive Microenvironment — Atezolizumab (anti-PD-L1) blocks PD-L1-mediated T cell suppression while bevacizumab (anti-VEGF) reverses VEGF-mediated immunosuppression, together restoring anti-tumor immunity in HCC.
Show evidence (1 reference)
PMID:39687036 SUPPORT Human Clinical
"Atezolizumab plus bevacizumab significantly improved overall survival (OS) and progression-free survival (PFS) versus sorafenib"
Superior outcomes with combined anti-PD-L1/anti-VEGF demonstrate that targeting both checkpoint-mediated and VEGF-mediated immunosuppression is effective in HCC.
INHIBITS Angiogenesis and VEGF Signaling — Bevacizumab directly inhibits VEGF-driven angiogenesis that sustains HCC tumor growth.
Show evidence (1 reference)
PMID:39687036 SUPPORT
"Atezolizumab plus bevacizumab significantly improved overall survival (OS) and progression-free survival (PFS) versus sorafenib"
IMbrave150 abstract reports improved overall and progression-free survival with atezolizumab plus bevacizumab versus sorafenib.
Durvalumab plus Tremelimumab
Action: pharmacotherapy MAXO:0000058
Agent: durvalumab tremelimumab
Alternative first-line immunotherapy option. HIMALAYA trial demonstrated durvalumab (anti-PD-L1) with single priming dose of tremelimumab (anti-CTLA-4) improves survival compared to sorafenib. Option for patients who cannot receive bevacizumab.
Mechanism Target:
INHIBITS Immune Evasion and Immunosuppressive Microenvironment — Durvalumab (anti-PD-L1) blocks adaptive immune resistance while tremelimumab (anti-CTLA-4) priming dose expands the T cell repertoire, together overcoming the immunosuppressive HCC microenvironment.
Sorafenib
Action: pharmacotherapy MAXO:0000058
Agent: sorafenib
Multi-kinase inhibitor targeting RAF, VEGFR, and PDGFR. Was first systemic therapy to improve survival in HCC. Now used in second line or when immunotherapy is contraindicated.
Lenvatinib
Action: pharmacotherapy MAXO:0000058
Agent: lenvatinib
Multi-kinase inhibitor with activity against VEGFR, FGFR, PDGFR, RET, and KIT. Non-inferior to sorafenib in first line. Alternative when immunotherapy not appropriate.
Surgical Resection
Action: hepatic resection Ontology label: Hepatectomy NCIT:C15249
Potentially curative for early-stage HCC in patients with preserved liver function (Child-Pugh A). Limited by underlying cirrhosis in many patients. Requires adequate future liver remnant.
Liver Transplantation
Action: organ transplantation MAXO:0010039
Potentially curative treatment that addresses both tumor and underlying cirrhosis. Milan criteria (single tumor 5 cm or less or up to 3 tumors each 3 cm or less, no vascular invasion, no metastases) guide patient selection. Limited by organ availability.
Transarterial Chemoembolization (TACE)
Action: chemotherapy MAXO:0000647
Locoregional therapy delivering chemotherapy directly to tumor via hepatic artery followed by embolization. Standard for intermediate-stage HCC (BCLC-B). Can be used as bridge to transplant or with systemic therapy.
Radiofrequency/Microwave Ablation
Action: ablation therapy MAXO:0000452
Thermal ablation for small tumors (typically less than 3 cm). Effective alternative to resection for early-stage HCC, particularly in patients with limited liver function.
🔬

Biochemical Markers

3
Alpha-Fetoprotein (AFP)
Liver Function Tests
PIVKA-II (DCP)
{ }

Source YAML

click to show
name: Hepatocellular Carcinoma
creation_date: '2026-01-26T02:55:13Z'
updated_date: '2026-04-13T00:40:00Z'
description: >-
  Hepatocellular carcinoma (HCC) is the most common primary liver malignancy, typically arising
  in the setting of chronic liver disease and cirrhosis. Major risk factors include chronic
  hepatitis B or C infection, alcohol-related liver disease, and metabolic dysfunction-associated
  steatotic liver disease (MASLD/NAFLD). HCC pathogenesis involves multiple molecular pathways
  including WNT/beta-catenin, TP53, telomere maintenance, and chromatin remodeling. The
  combination of atezolizumab (anti-PD-L1) plus bevacizumab (anti-VEGF) has established
  immunotherapy as first-line treatment for advanced HCC, based on the IMbrave150 trial.
categories:
- Gastrointestinal Cancer
- Hepatobiliary Cancer
- Liver Cancer
parents:
- liver carcinoma
has_subtypes:
- name: Viral Hepatitis-Associated HCC
  description: >-
    HCC arising in the context of chronic hepatitis B or C infection. HBV can be directly
    oncogenic through viral integration, while HCV promotes HCC primarily through cirrhosis
    and chronic inflammation.
- name: Alcohol-Related HCC
  description: >-
    HCC arising in alcohol-related liver disease and cirrhosis. Associated with specific
    molecular features and generally presents at more advanced stage.
- name: MASLD-Associated HCC
  description: >-
    HCC arising in metabolic dysfunction-associated steatotic liver disease (formerly NAFLD/NASH).
    Increasingly common subtype that can occur even without cirrhosis. May have distinct
    immune microenvironment features affecting immunotherapy response.
- name: Fibrolamellar HCC
  description: >-
    Rare variant occurring in younger patients without cirrhosis. Characterized by DNAJB1-PRKACA
    fusion. Distinct clinical behavior and treatment considerations.
  mappings:
    ncit_mappings:
    - term:
        id: NCIT:C4131
        label: Fibrolamellar Carcinoma
      mapping_predicate: skos:closeMatch
      mapping_source: NCIT
      mapping_justification: NCIT provides a closely aligned fibrolamellar carcinoma term for this HCC subtype.
pathophysiology:
- name: Chronic Liver Injury and Cirrhosis
  description: >-
    Most HCC arises in the context of chronic liver disease and cirrhosis. Persistent
    hepatocyte death and regeneration in an inflammatory environment promotes accumulation
    of genetic alterations. Cirrhosis itself is a premalignant condition with ongoing
    oxidative stress and genomic instability.
  evidence:
  - reference: PMID:41567639
    reference_title: "Identification of novel germline and somatic mutations associated with hepatocellular carcinoma by next-generation sequencing."
    supports: PARTIAL
    snippet: HCC typically arises in patients with chronic liver disease, including hepatitis, cirrhosis, and non-alcoholic fatty liver diseases.
    explanation: This abstract states that HCC commonly arises in chronic liver disease and cirrhosis, supporting the mechanism described.
  cell_types:
  - preferred_term: hepatocyte
    term:
      id: CL:0000182
      label: hepatocyte
  locations:
  - preferred_term: liver
    term:
      id: UBERON:0002107
      label: liver
  downstream:
  - target: Telomere Dysfunction and Genomic Instability
    description: Repeated hepatocyte division leads to telomere shortening
  - target: Accumulation of Driver Mutations
    description: Chronic regeneration promotes mutation accumulation
- name: Telomere Dysfunction and Genomic Instability
  description: >-
    Chronic hepatocyte proliferation leads to telomere shortening, causing genomic instability.
    TERT promoter mutations, which are the most common HCC mutations, reactivate telomerase
    to enable unlimited replication. This creates a checkpoint bypass allowing survival
    of genetically unstable cells.
  biological_processes:
  - preferred_term: telomere maintenance
    modifier: ABNORMAL
    term:
      id: GO:0000723
      label: telomere maintenance
  downstream:
  - target: WNT/Beta-Catenin Pathway Activation
    description: Genomic instability promotes acquisition of pathway-activating mutations
- name: Accumulation of Driver Mutations
  description: >-
    Multiple driver genes are recurrently mutated in HCC, including TERT promoter (60%),
    TP53 (30%), CTNNB1 (30%), AXIN1 (10%), and ARID1A (10%). These mutations affect
    telomere maintenance, cell cycle control, WNT signaling, and chromatin remodeling.
  biological_processes:
  - preferred_term: DNA repair
    modifier: DECREASED
    term:
      id: GO:0006281
      label: DNA repair
- name: WNT/Beta-Catenin Pathway Activation
  description: >-
    Activating mutations in CTNNB1 (beta-catenin) or inactivating mutations in AXIN1
    lead to constitutive WNT pathway activation. This drives cell proliferation and is
    associated with a distinct molecular subclass of HCC with specific clinical features
    including cholestasis and immune exclusion.
  biological_processes:
  - preferred_term: Wnt signaling pathway
    modifier: INCREASED
    term:
      id: GO:0016055
      label: Wnt signaling pathway
  downstream:
  - target: Enhanced Hepatocyte Proliferation
    description: WNT signaling drives cell proliferation and stemness
- name: TP53 Pathway Inactivation
  description: >-
    TP53 mutations are common in HCC, particularly in HBV-associated and aflatoxin-associated
    tumors. Loss of p53 function removes a critical checkpoint, allowing survival of cells
    with DNA damage and promoting genomic instability.
  biological_processes:
  - preferred_term: apoptotic process
    modifier: DECREASED
    term:
      id: GO:0006915
      label: apoptotic process
- name: Enhanced Hepatocyte Proliferation
  description: >-
    Combined effects of telomerase reactivation, cell cycle checkpoint loss, and
    mitogenic signaling drive uncontrolled hepatocyte proliferation and tumor growth.
  biological_processes:
  - preferred_term: cell population proliferation
    modifier: INCREASED
    term:
      id: GO:0008283
      label: cell population proliferation
- name: Angiogenesis and VEGF Signaling
  description: >-
    HCC is a highly vascular tumor dependent on angiogenesis. VEGF signaling promotes
    new blood vessel formation supplying the tumor. VEGF also has immunosuppressive
    effects, contributing to the immune-excluded microenvironment. This provides the
    rationale for anti-VEGF therapy in combination with immunotherapy.
  evidence:
  - reference: PMID:19637355
    reference_title: "Vascular endothelial growth factor in the management of hepatocellular carcinoma: a review of literature."
    supports: SUPPORT
    snippet: "Hepatocellular carcinoma (HCC) is a highly vascular tumor, and angiogenesis is believed to play a considerable role in its development and progression."
    explanation: "Abstract notes HCC is highly vascular and angiogenesis plays a major role, supporting this mechanism."
  biological_processes:
  - preferred_term: angiogenesis
    modifier: INCREASED
    term:
      id: GO:0001525
      label: angiogenesis
  downstream:
  - target: Immune Evasion and Immunosuppressive Microenvironment
    description: VEGF-mediated immunosuppression contributes to T cell exclusion and checkpoint upregulation
- name: Immune Evasion and Immunosuppressive Microenvironment
  conforms_to: "immune_checkpoint_blockade#Adaptive Immune Resistance"
  description: >-
    HCC develops in a chronically inflamed liver with an inherently
    immunosuppressive microenvironment. Tumor cells upregulate PD-L1,
    VEGF-mediated immunosuppression excludes effector T cells, and
    recruitment of regulatory T cells, myeloid-derived suppressor cells,
    and tumor-associated macrophages creates an immune-tolerant niche.
    The combination of anti-PD-L1 with anti-VEGF addresses both the
    checkpoint-mediated and VEGF-mediated immunosuppression.
  cell_types:
  - preferred_term: CD8-positive, alpha-beta T cell
    term:
      id: CL:0000625
      label: CD8-positive, alpha-beta T cell
  biological_processes:
  - preferred_term: Negative Regulation of T Cell Mediated Immunity
    term:
      id: GO:0002710
      label: negative regulation of T cell mediated immunity
    modifier: INCREASED
  evidence:
  - reference: PMID:32158599
    supports: SUPPORT
    evidence_source: OTHER
    snippet: >-
      The HCC tumor microenvironment is characterized by a dysfunction of
      the immune system through multiple mechanisms, including accumulation
      of various immunosuppressive factors, recruitment of regulatory T cells
      and myeloid-derived suppressor cells, and induction of T cell exhaustion
      accompanied with the interaction between immune checkpoint ligands and
      receptors.
    explanation: >-
      Review specifically describes HCC's immunosuppressive microenvironment
      including Treg and MDSC recruitment, T cell exhaustion, and checkpoint
      ligand-receptor interactions — directly supporting all claims in this
      node about HCC immune evasion mechanisms.
histopathology:
- name: Hepatocellular Carcinoma
  finding_term:
    preferred_term: Hepatocellular Carcinoma
    term:
      id: NCIT:C3099
      label: Hepatocellular Carcinoma
  frequency: VERY_FREQUENT
  description: Hepatocellular carcinoma is the most common primary liver malignancy.
  evidence:
  - reference: PMID:27785449
    reference_title: "Hepatocellular carcinoma: a review."
    supports: SUPPORT
    snippet: "Hepatocellular carcinoma (HCC) is the most common primary liver malignancy"
    explanation: Abstract states that HCC is the most common primary liver malignancy.

phenotypes:
- category: Hepatic
  name: Hepatomegaly
  frequency: FREQUENT
  description: >-
    Liver enlargement from tumor mass. May be palpable as a hard, irregular mass in the
    right upper quadrant.
  phenotype_term:
    preferred_term: Hepatomegaly
    term:
      id: HP:0002240
      label: Hepatomegaly
- category: Hepatic
  name: Ascites
  frequency: FREQUENT
  description: >-
    Abdominal fluid accumulation from portal hypertension (cirrhosis) and/or tumor-related
    factors. Presence indicates advanced disease and decompensated liver function.
  phenotype_term:
    preferred_term: Ascites
    term:
      id: HP:0001541
      label: Ascites
- category: Hepatic
  name: Jaundice
  frequency: OCCASIONAL
  description: >-
    Yellowing of skin and sclera from elevated bilirubin. May result from biliary obstruction
    by tumor, hepatic failure, or diffuse tumor infiltration.
  phenotype_term:
    preferred_term: Jaundice
    term:
      id: HP:0000952
      label: Jaundice
- category: Gastrointestinal
  name: Abdominal Pain
  frequency: FREQUENT
  description: >-
    Right upper quadrant pain or discomfort from liver capsule distension or tumor growth.
    Sudden severe pain may indicate tumor rupture.
  phenotype_term:
    preferred_term: Abdominal pain
    term:
      id: HP:0002027
      label: Abdominal pain
- category: Constitutional
  name: Weight Loss
  frequency: VERY_FREQUENT
  description: >-
    Unintentional weight loss is common in HCC due to cancer cachexia, reduced oral intake,
    and altered metabolism.
  phenotype_term:
    preferred_term: Weight loss
    term:
      id: HP:0001824
      label: Weight loss
- category: Constitutional
  name: Fatigue
  frequency: VERY_FREQUENT
  description: >-
    Fatigue from liver dysfunction, anemia, and cancer-related factors.
  phenotype_term:
    preferred_term: Fatigue
    term:
      id: HP:0012378
      label: Fatigue
- category: Gastrointestinal
  name: Nausea
  frequency: FREQUENT
  description: >-
    Nausea and anorexia from liver dysfunction and advanced disease.
  phenotype_term:
    preferred_term: Nausea
    term:
      id: HP:0002018
      label: Nausea
biochemical:
- name: Alpha-Fetoprotein (AFP)
  notes: >-
    Serum AFP is elevated in approximately 60% of HCC cases. Levels greater than 400 ng/mL
    are highly specific for HCC in the setting of cirrhosis. Used for diagnosis (with
    imaging) and monitoring treatment response. AFP-L3 fraction improves specificity.
- name: Liver Function Tests
  notes: >-
    Elevated transaminases, alkaline phosphatase, and bilirubin may occur. Pattern depends
    on underlying liver disease and tumor burden. Child-Pugh score assesses hepatic reserve
    and guides treatment decisions.
- name: PIVKA-II (DCP)
  notes: >-
    Des-gamma-carboxy prothrombin is an alternative biomarker to AFP. May be elevated
    when AFP is normal. Useful in combination with AFP for surveillance and diagnosis.
genetic:
- name: TERT Promoter
  association: Somatic Activating Mutation
  notes: >-
    TERT promoter mutations (C228T, C250T) are the most common genetic alterations in HCC,
    present in approximately 60% of cases. These mutations create binding sites for ETS
    transcription factors, reactivating telomerase expression and enabling unlimited
    cell division.
- name: TP53
  association: Somatic Loss of Function
  notes: >-
    TP53 mutations occur in approximately 30% of HCC, enriched in HBV-associated and
    aflatoxin-associated tumors. The R249S hotspot mutation is specifically associated
    with aflatoxin B1 exposure.
- name: CTNNB1
  association: Somatic Activating Mutation
  notes: >-
    CTNNB1 (beta-catenin) mutations occur in approximately 30% of HCC, causing constitutive
    WNT pathway activation. Associated with distinct clinical features including
    cholestasis and immune exclusion, potentially affecting immunotherapy response.
- name: AXIN1
  association: Somatic Loss of Function
  notes: >-
    AXIN1 inactivating mutations occur in approximately 10% of HCC, also activating
    WNT signaling. AXIN1 and CTNNB1 mutations are typically mutually exclusive.
- name: ARID1A
  association: Somatic Loss of Function
  notes: >-
    ARID1A mutations affect chromatin remodeling and occur in approximately 10% of HCC.
    Part of the SWI/SNF complex alterations seen across multiple cancer types.
treatments:
- name: Atezolizumab plus Bevacizumab
  description: >-
    First-line standard of care for unresectable HCC based on IMbrave150 trial. Anti-PD-L1
    (atezolizumab) combined with anti-VEGF (bevacizumab) demonstrated superior overall
    survival compared to sorafenib. Requires adequate liver function (Child-Pugh A) and
    no high-risk varices.
  evidence:
  - reference: PMID:39687036
    reference_title: "Efficacy and Safety of Atezolizumab plus Bevacizumab versus Sorafenib in Hepatocellular Carcinoma with Main Trunk and/or Contralateral Portal Vein Invasion in IMbrave150."
    supports: SUPPORT
    snippet: "Atezolizumab plus bevacizumab significantly improved overall survival (OS) and progression-free survival (PFS) versus sorafenib"
    explanation: "IMbrave150 abstract reports improved overall and progression-free survival with atezolizumab plus bevacizumab versus sorafenib."
  treatment_term:
    preferred_term: pharmacotherapy
    term:
      id: MAXO:0000058
      label: pharmacotherapy
    therapeutic_agent:
    - preferred_term: atezolizumab
      term:
        id: NCIT:C106250
        label: Atezolizumab
    - preferred_term: bevacizumab
      term:
        id: NCIT:C2039
        label: Bevacizumab
  target_mechanisms:
  - target: Immune Evasion and Immunosuppressive Microenvironment
    treatment_effect: INHIBITS
    description: >-
      Atezolizumab (anti-PD-L1) blocks PD-L1-mediated T cell suppression
      while bevacizumab (anti-VEGF) reverses VEGF-mediated immunosuppression,
      together restoring anti-tumor immunity in HCC.
    evidence:
    - reference: PMID:39687036
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: "Atezolizumab plus bevacizumab significantly improved overall survival (OS) and progression-free survival (PFS) versus sorafenib"
      explanation: >-
        Superior outcomes with combined anti-PD-L1/anti-VEGF demonstrate that
        targeting both checkpoint-mediated and VEGF-mediated immunosuppression
        is effective in HCC.
  - target: Angiogenesis and VEGF Signaling
    treatment_effect: INHIBITS
    description: >-
      Bevacizumab directly inhibits VEGF-driven angiogenesis that sustains
      HCC tumor growth.
- name: Durvalumab plus Tremelimumab
  description: >-
    Alternative first-line immunotherapy option. HIMALAYA trial demonstrated durvalumab
    (anti-PD-L1) with single priming dose of tremelimumab (anti-CTLA-4) improves survival
    compared to sorafenib. Option for patients who cannot receive bevacizumab.
  treatment_term:
    preferred_term: pharmacotherapy
    term:
      id: MAXO:0000058
      label: pharmacotherapy
    therapeutic_agent:
    - preferred_term: durvalumab
      term:
        id: NCIT:C103194
        label: Durvalumab
    - preferred_term: tremelimumab
      term:
        id: NCIT:C49085
        label: Tremelimumab
  target_mechanisms:
  - target: Immune Evasion and Immunosuppressive Microenvironment
    treatment_effect: INHIBITS
    description: >-
      Durvalumab (anti-PD-L1) blocks adaptive immune resistance while
      tremelimumab (anti-CTLA-4) priming dose expands the T cell repertoire,
      together overcoming the immunosuppressive HCC microenvironment.
- name: Sorafenib
  description: >-
    Multi-kinase inhibitor targeting RAF, VEGFR, and PDGFR. Was first systemic therapy
    to improve survival in HCC. Now used in second line or when immunotherapy is
    contraindicated.
  treatment_term:
    preferred_term: pharmacotherapy
    term:
      id: MAXO:0000058
      label: pharmacotherapy
    therapeutic_agent:
    - preferred_term: sorafenib
      term:
        id: CHEBI:50924
        label: sorafenib
- name: Lenvatinib
  description: >-
    Multi-kinase inhibitor with activity against VEGFR, FGFR, PDGFR, RET, and KIT.
    Non-inferior to sorafenib in first line. Alternative when immunotherapy not appropriate.
  treatment_term:
    preferred_term: pharmacotherapy
    term:
      id: MAXO:0000058
      label: pharmacotherapy
    therapeutic_agent:
    - preferred_term: lenvatinib
      term:
        id: CHEBI:85994
        label: lenvatinib
- name: Surgical Resection
  description: >-
    Potentially curative for early-stage HCC in patients with preserved liver function
    (Child-Pugh A). Limited by underlying cirrhosis in many patients. Requires adequate
    future liver remnant.
  treatment_term:
    preferred_term: hepatic resection
    term:
      id: NCIT:C15249
      label: Hepatectomy
- name: Liver Transplantation
  description: >-
    Potentially curative treatment that addresses both tumor and underlying cirrhosis.
    Milan criteria (single tumor 5 cm or less or up to 3 tumors each 3 cm or less, no
    vascular invasion, no metastases) guide patient selection. Limited by organ availability.
  treatment_term:
    preferred_term: organ transplantation
    term:
      id: MAXO:0010039
      label: organ transplantation
- name: Transarterial Chemoembolization (TACE)
  description: >-
    Locoregional therapy delivering chemotherapy directly to tumor via hepatic artery
    followed by embolization. Standard for intermediate-stage HCC (BCLC-B). Can be used
    as bridge to transplant or with systemic therapy.
  treatment_term:
    preferred_term: chemotherapy
    term:
      id: MAXO:0000647
      label: chemotherapy
- name: Radiofrequency/Microwave Ablation
  description: >-
    Thermal ablation for small tumors (typically less than 3 cm). Effective alternative
    to resection for early-stage HCC, particularly in patients with limited liver function.
  treatment_term:
    preferred_term: ablation therapy
    term:
      id: MAXO:0000452
      label: ablation therapy
disease_term:
  preferred_term: hepatocellular carcinoma
  term:
    id: MONDO:0007256
    label: hepatocellular carcinoma
mappings:
  mondo_mappings:
  - term:
      id: MONDO:0007256
      label: hepatocellular carcinoma
    mapping_predicate: skos:exactMatch
    mapping_source: MONDO
    mapping_justification: MONDO provides an exact disease term for hepatocellular carcinoma.
  icd10cm_mappings:
  - term:
      id: ICD10CM:C22.0
      label: Liver cell carcinoma
    mapping_predicate: skos:exactMatch
    mapping_source: ICD-10-CM
    mapping_justification: ICD-10-CM provides an exact code for liver cell carcinoma / hepatocellular carcinoma.
  ncit_mappings:
  - term:
      id: NCIT:C3099
      label: Hepatocellular Carcinoma
    mapping_predicate: skos:exactMatch
    mapping_source: NCIT
    mapping_justification: NCIT provides an exact neoplasm term for hepatocellular carcinoma.

classifications:
  icdo_morphology:
    classification_value: Carcinoma
  harrisons_chapter:
  - classification_value: cancer
  - classification_value: solid tumor