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1
Definitions
6
Pathophys.
1
Histopath.
5
Phenotypes
13
Pathograph
7
Genes
5
Treatments
3
Subtypes
3
Trials
1
Deep Research
📘

Definitions

1
Clinicopathologic definition
Vulvar carcinoma is a vulvar epithelial cancer, most commonly squamous cell carcinoma, diagnosed by biopsy of a suspicious vulvar lesion and staged with clinical, pathologic, and imaging assessment of local and nodal disease.
CASE_DEFINITION General adult gynecologic oncology definition
Show evidence (2 references)
PMID:38791925 SUPPORT Human Clinical
"Vulvar carcinoma is a rare cancer affecting the genital tract, constituting 4% of gynecological tumors. Vulvar squamous cell carcinoma (VSCC) is the most common type. Diagnosis relies on biopsy during vulvoscopy, plus imaging such as ultrasonography (USG), magnetic resonance imaging (MRI) and..."
This review defines vulvar carcinoma as a rare gynecologic cancer, identifies VSCC as the most common type, and summarizes biopsy and imaging-based preoperative assessment.
DOI:10.1055/a-1545-4279 SUPPORT Human Clinical
"The 2020 WHO classification is focused on the distinction between HPV-associated and HPV-independent squamous cell carcinoma of the lower female genital organs."
The WHO classification review supports HPV-associated versus HPV-independent classification for lower female genital squamous cell carcinoma, including vulvar squamous carcinoma.

Subtypes

3
HPV-associated vulvar squamous cell carcinoma
Molecular subtype associated with high-risk human papillomavirus, p16INK4A positivity, and generally better prognosis than HPV-independent disease.
Show evidence (1 reference)
PMID:37840151 SUPPORT Human Clinical
"Vulva squamous cell carcinoma (VSCC) develops through two separate molecular pathways-one involving high-risk human papilloma virus infection (HPV-associated), and the other without HPV infection (HPV-independent) often involving TP53 mutation. HPV-associated VSCC generally has a better..."
The cohort paper directly supports HPV-associated VSCC as a distinct molecular pathway and links it to better progression-free survival.
HPV-independent TP53-altered vulvar squamous cell carcinoma
Molecular subtype not driven by HPV, commonly keratinizing, enriched for TP53 alteration and other somatic lesions, and often associated with differentiated VIN and lichen sclerosus.
Show evidence (1 reference)
PMID:37840151 SUPPORT Human Clinical
"Vulva squamous cell carcinoma (VSCC) develops through two separate molecular pathways-one involving high-risk human papilloma virus infection (HPV-associated), and the other without HPV infection (HPV-independent) often involving TP53 mutation."
This abstract explicitly distinguishes the HPV-independent pathway and notes frequent TP53 mutation involvement.
HPV-independent p53-wild-type vulvar squamous cell carcinoma
Uncommon HPV-independent molecular subtype lacking abnormal p53 immunophenotype, with intermediate prognosis between HPV-associated and HPV-independent TP53-altered disease.
Show evidence (1 reference)
DOI:10.3390/cancers16244216 SUPPORT Human Clinical
"These three molecular subtypes of VSCC (HPVa, HPVi p53 abnormal, and HPVi p53 wild type), as well as their precursor lesions, cannot be diagnosed based on a routine histopathological examination or immunostaining for p53 and p16 as surrogate markers for TP53 mutation and high-risk HPV infection,..."
The review explicitly describes HPV-independent p53-wild-type VSCC as a third molecular subtype requiring p16 and p53 immunostaining.

Pathophysiology

6
HPV-Associated Tumor Suppressor Disruption
Persistent high-risk HPV infection defines one major VSCC pathway. Viral oncogene activity is reflected by p16INK4A positivity and produces cell cycle deregulation in vulvar squamous epithelium.
vulvar keratinocyte link
response to virus link G1/S transition of mitotic cell cycle link ↑ INCREASED
vulva link
Show evidence (1 reference)
PMID:37840151 SUPPORT Human Clinical
"p16INK4A immunohistochemistry, mRNA ISH, and DNA PCR had excellent concordance in terms of HPV detection."
Concordance of p16 with HPV detection supports p16-marked HPV-associated biology as a major VSCC pathway.
Lichen Sclerosus Inflammatory Microenvironment
Lichen sclerosus creates chronic vulvar inflammation, tissue remodeling, oxidative stress, scarring, and symptoms that can precede or accompany HPV-independent vulvar squamous carcinogenesis.
vulvar keratinocyte link
extracellular matrix organization link ⚠ ABNORMAL
vulva link
Show evidence (2 references)
DOI:10.3389/fmed.2023.1106318 SUPPORT Human Clinical
"Oxidative stress with lipid and DNA peroxidation provides an enabling microenvironment to autoimmunity and carcinogenesis."
The review supports oxidative stress and immune-mediated tissue injury as a carcinogenesis-enabling microenvironment in lichen sclerosus.
DOI:10.3389/fmed.2023.1106318 SUPPORT Human Clinical
"In addition to genital scarring, and sexual and urinary dysfunction, LS may also lead to squamous cell carcinoma."
This explicitly links lichen sclerosus to squamous cell carcinoma risk.
HPV-Independent Somatic Driver Accumulation
HPV-independent VSCC is enriched for TERT promoter, TP53, CDKN2A, NOTCH1, and FAT1 alterations, supporting a tumor-suppressor and differentiation failure pathway distinct from HPV-driven tumors.
vulvar keratinocyte link
TP53 link TERT link CDKN2A link NOTCH1 link FAT1 link
apoptotic process link ↓ DECREASED cell population proliferation link ↑ INCREASED
Show evidence (2 references)
PMID:34650187 SUPPORT Human Clinical
"Other common abnormalities in HPV-independent tumors were TP53 mutations (13/15, 87%), CDKN2A alterations (10/15, 67%), and NOTCH1 and FAT1 mutations (7/15, 47% each)."
Sequencing of vulvovaginal squamous carcinomas identifies recurrent TP53, CDKN2A, NOTCH1, and FAT1 alterations in HPV-independent tumors.
PMID:34650187 SUPPORT Human Clinical
"Cancer cell fraction analysis of HPV-independent squamous carcinomas suggests that TERT and/or NOTCH1 alterations along with TP53 alterations can be the initiating event in these tumors."
The paper places TERT, NOTCH1, and TP53 alterations early in the HPV-independent carcinogenic pathway.
PIK3CA-Activated HPV-Associated Signaling
HPV-associated vulvovaginal squamous carcinomas are enriched for PIK3CA activating mutations, implicating PI3K pathway activation in a subset of HPV-driven tumors.
PIK3CA link
cell population proliferation link ↑ INCREASED
Show evidence (1 reference)
PMID:34650187 SUPPORT Human Clinical
"HPV-associated vulvovaginal squamous cell carcinoma had PIK3CA activating mutations (7/11, 64%) as the most common genomic event"
This sequencing cohort supports PIK3CA activation as a recurrent event in HPV-associated vulvovaginal squamous carcinoma.
HRAS/RAS-MAPK Signaling Activation
HRAS mutations occur in a subset of VSCC and implicate RAS/MAPK signaling as an additional proliferation pathway in vulvar squamous carcinoma.
HRAS link
MAPK cascade link ↑ INCREASED cell population proliferation link ↑ INCREASED
Show evidence (1 reference)
DOI:10.1038/s41598-024-63913-z SUPPORT Human Clinical
"Somatic mutations were identified by targeted or panel sequencing, and TP53 was identified as the most common mutation (52–81%), followed by HRAS (7–26%), CDKN2A (21–24%), and PIK3CA (5–10%)."
The Japanese VSCC sequencing cohort identifies recurrent HRAS mutations, supporting a RAS/MAPK-linked somatic driver mechanism.
Clonal Squamous Cell Proliferation
HPV-driven cell-cycle deregulation or HPV-independent somatic driver accumulation leads to clonal proliferation and invasive squamous carcinoma in the vulvar epithelium.
vulvar keratinocyte link
cell population proliferation link ↑ INCREASED
vulva link

Histopathology

1
Squamous Cell Carcinoma
Vulvar squamous cell carcinoma is the most common histologic type of vulvar carcinoma.
Show evidence (1 reference)
PMID:38791925 SUPPORT Human Clinical
"Vulvar squamous cell carcinoma (VSCC) is the most common type."
This review supports squamous cell carcinoma as the dominant vulvar carcinoma histology.

Pathograph

Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.
Pathograph: causal mechanism network for Vulvar 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

5
Integument 3
Biopsy-Requiring Vulvar Lesion Localized skin lesion (HP:0011355)
Show evidence (1 reference)
PMID:38791925 SUPPORT Human Clinical
"Diagnosis relies on biopsy during vulvoscopy, plus imaging such as ultrasonography (USG), magnetic resonance imaging (MRI) and positron emission tomography (PET)."
The need for vulvoscopy-directed biopsy supports a visible or clinically suspicious vulvar lesion as the diagnostic presentation.
Vulvar Ulcer Skin ulcer (HP:0200042)
Show evidence (1 reference)
DOI:10.1002/ijgo.13881 SUPPORT Human Clinical
"While vulvar cancer may be asymptomatic, most women present with vulvar pruritus or pain, or have noticed a lump or ulcer."
The clinical update identifies ulcer as a presenting feature; the HPO binding uses the broader skin-ulcer term because local HPO did not provide a vulvar-specific ulcer term.
Vulvar Pruritus Pruritus (HP:0000989)
Show evidence (1 reference)
DOI:10.3389/fmed.2023.1106318 PARTIAL Human Clinical
"The typical clinical picture includes chronic whitish atrophic patches along with itching and soreness in the vulvar, perianal and penile regions."
This supports pruritus in lichen sclerosus, an important associated precursor/risk setting for HPV-independent vulvar carcinoma.
Constitutional 1
Vulvar Pain or Soreness Pain (HP:0012531)
Show evidence (1 reference)
DOI:10.3389/fmed.2023.1106318 PARTIAL Human Clinical
"The typical clinical picture includes chronic whitish atrophic patches along with itching and soreness in the vulvar, perianal and penile regions."
This supports vulvar soreness in lichen sclerosus, a clinically relevant associated dermatosis in the HPV-independent disease pathway.
Neoplasm 1
Vulvar Lump or Mass Neoplasm (HP:0002664)
Show evidence (1 reference)
DOI:10.1002/ijgo.13881 SUPPORT Human Clinical
"While vulvar cancer may be asymptomatic, most women present with vulvar pruritus or pain, or have noticed a lump or ulcer."
The clinical update identifies a noticed lump as a presenting feature of vulvar cancer; the HPO binding uses the broad neoplasm term because local HPO did not provide a vulvar-specific mass term.
🧬

Genetic Associations

7
TP53 (Somatic Mutation)
Show evidence (1 reference)
PMID:37840151 SUPPORT Human Clinical
"The TP53 mutation status was identified as an independent prognostic factor of worse progression-free survival (p = 0.024) after adjustment for FIGO stage."
This cohort supports TP53 mutation as a prognostic somatic alteration in VSCC.
PIK3CA (Somatic Activating Mutation)
Show evidence (1 reference)
PMID:34650187 SUPPORT Human Clinical
"HPV-associated vulvovaginal squamous cell carcinoma had PIK3CA activating mutations (7/11, 64%) as the most common genomic event"
This supports PIK3CA activation as a recurrent molecular event in the HPV-associated pathway.
TERT (Somatic Promoter Alteration)
Show evidence (1 reference)
PMID:34650187 SUPPORT Human Clinical
"TERT gene alterations, mainly TERT promoter mutations (14/15 cases, 93%) featured significantly in HPV-independent carcinomas."
This supports TERT promoter alteration as a frequent HPV-independent VSCC driver event.
CDKN2A (Somatic Alteration)
Show evidence (1 reference)
PMID:34650187 SUPPORT Human Clinical
"Other common abnormalities in HPV-independent tumors were TP53 mutations (13/15, 87%), CDKN2A alterations (10/15, 67%), and NOTCH1 and FAT1 mutations (7/15, 47% each)."
This supports CDKN2A alteration as a recurrent somatic event in the HPV-independent molecular subgroup.
NOTCH1 (Somatic Mutation)
Show evidence (1 reference)
PMID:34650187 SUPPORT Human Clinical
"Other common abnormalities in HPV-independent tumors were TP53 mutations (13/15, 87%), CDKN2A alterations (10/15, 67%), and NOTCH1 and FAT1 mutations (7/15, 47% each)."
This supports NOTCH1 mutation as a recurrent somatic event in HPV-independent vulvovaginal squamous carcinoma.
FAT1 (Somatic Mutation)
Show evidence (1 reference)
PMID:34650187 SUPPORT Human Clinical
"Other common abnormalities in HPV-independent tumors were TP53 mutations (13/15, 87%), CDKN2A alterations (10/15, 67%), and NOTCH1 and FAT1 mutations (7/15, 47% each)."
This supports FAT1 mutation as a recurrent somatic event in HPV-independent vulvovaginal squamous carcinoma.
HRAS (Somatic Mutation)
Show evidence (1 reference)
DOI:10.1038/s41598-024-63913-z SUPPORT Human Clinical
"Somatic mutations were identified by targeted or panel sequencing, and TP53 was identified as the most common mutation (52–81%), followed by HRAS (7–26%), CDKN2A (21–24%), and PIK3CA (5–10%)."
This supports HRAS as a recurrent somatic mutation in Japanese VSCC sequencing cohorts.
💊

Treatments

5
Local Excision With Sentinel Node Biopsy
Action: surgical procedure MAXO:0000004
Early-stage vulvar cancer is treated by local excision of the primary tumor with sentinel node biopsy when nodal assessment is indicated, reducing morbidity compared with inguinofemoral lymphadenectomy in appropriate patients.
Show evidence (1 reference)
DOI:10.6004/jnccn.2024.7002 SUPPORT Human Clinical
"Early-stage vulvar cancer is managed by a local excision of the primary tumor and, if indicated, a sentinel node (SN) biopsy to assess the need for further groin treatment."
This review supports local excision and sentinel node biopsy as standard early-stage management.
Definitive or Adjuvant Radiotherapy
Action: radiation therapy MAXO:0000014
Radiotherapy is used in vulvar cancer management for local-regional disease control, including definitive, adjuvant, or groin-treatment contexts depending on stage and nodal status.
Show evidence (1 reference)
DOI:10.6004/jnccn.2024.7002 SUPPORT Human Clinical
"Inguinofemoral radiotherapy is a good alternative to IFL in patients with micrometastases in the SN, with comparable efficacy and less treatment-related morbidity."
The sentinel-node review supports radiotherapy as a morbidity-sparing groin-treatment option for selected node-positive early VSCC.
Guideline-Based Multidisciplinary Treatment
Action: therapeutic procedure Ontology label: Therapeutic Procedure NCIT:C49236
Management commonly requires coordinated gynecologic oncology, pathology, imaging, radiation oncology, medical oncology, reconstructive surgery, and supportive-care input.
Show evidence (1 reference)
DOI:10.3390/cancers17020186 SUPPORT Human Clinical
"From the systematic comparison of the main international guidelines, a strong heterogeneity emerged in the diagnostic and therapeutic recommendations as well as for the multidisciplinary approach that today is essential."
This guideline comparison supports multidisciplinary management as an essential part of vulvar cancer care.
Platinum-Based Chemotherapy
Action: chemotherapy MAXO:0000647
Agent: platinum compound
First-line platinum-based chemotherapy is used for advanced or recurrent vulvar squamous cell carcinoma not amenable to curative surgery.
Show evidence (1 reference)
clinicaltrials:NCT07101848 SUPPORT Human Clinical
"This is a phase II, randomized study that will include 42 participants who have received 4 to 6 cycles of first-line platinum-based chemotherapy for advanced vulvar squamous cell carcinoma (SCC) not amenable to curative surgical treatment (FIGO 2018 stages III-IV - International Federation of..."
The trial summary explicitly requires prior first-line platinum-based chemotherapy for advanced VSCC, supporting this systemic treatment context.
HPV Vaccination
Action: vaccination MAXO:0001017
Agent: human papillomavirus vaccine
Prophylactic HPV vaccination is a prevention strategy intended to reduce the future burden of HPV-related cancers, including HPV-associated vulvar cancer.
Show evidence (1 reference)
"Designing and implementing targeted interventions to increase uptake and completion of HPV vaccination series across counties with low HPV vaccination rates may help to reduce future the burden of HPV-related cancers."
This population-based study supports HPV vaccination uptake as a strategy to reduce future HPV-related cancer burden, which includes HPV-associated vulvar carcinoma.
🔬

Biochemical Markers

2
p16 Immunohistochemistry
Show evidence (1 reference)
PMID:37840151 SUPPORT Human Clinical
"Immunohistochemistry for p53, Ki67 and p16INK4A (a surrogate marker for HPV infection) was performed on formalin-fixed paraffin-embedded tissues from a cohort of surgically treated VSCC patients to identify molecular subtypes of VSCC."
The study supports p16INK4A immunohistochemistry as an HPV-associated subtype marker in VSCC.
p53 Immunohistochemistry
Show evidence (1 reference)
PMID:37840151 SUPPORT Human Clinical
"The results of p53 and p16INK4A immunohistochemistry confirmed three VSCC subtypes associated with different prognosis."
This supports combined p53 and p16 immunohistochemistry for molecular stratification of VSCC.
🔬

Clinical Trials

3
NCT05903833 PHASE_II RECRUITING
Phase II trial of pembrolizumab plus lenvatinib in recurrent, persistent, metastatic, or locally advanced vulvar cancer not amenable to curative surgery or radiotherapy. ClinicalTrials.gov listed status as RECRUITING on 2026-05-07.
Target Phenotypes: Recurrent, persistent, metastatic, or locally advanced vulvar cancer
Show evidence (1 reference)
"Evaluation of efficacy and safety of pembrolizumab in combination with lenvatinib in patients with recurrent, persistent, metastatic or locally advanced vulva cancer."
This ClinicalTrials.gov summary directly describes the study population and pembrolizumab-lenvatinib intervention.
NCT07101848 PHASE_II NOT_RECRUITING
Phase II randomized trial of cemiplimab maintenance plus best supportive care versus best supportive care after first-line platinum chemotherapy in advanced or recurrent vulvar squamous cell carcinoma. ClinicalTrials.gov listed status as NOT_YET_RECRUITING on 2026-05-07, represented here by the schema's NOT_RECRUITING status enum.
Target Phenotypes: Advanced or recurrent vulvar squamous cell carcinoma
Show evidence (1 reference)
"This is a phase II, randomized study that will include 42 participants who have received 4 to 6 cycles of first-line platinum-based chemotherapy for advanced vulvar squamous cell carcinoma (SCC) not amenable to curative surgical treatment (FIGO 2018 stages III-IV - International Federation of..."
This ClinicalTrials.gov summary supports the trial design and population for cemiplimab maintenance in advanced or recurrent VSCC.
NCT07290894 PHASE_II RECRUITING
Phase II single-arm, multi-cohort trial of lenvatinib plus pembrolizumab in patients with vulvar cancer. ClinicalTrials.gov listed status as RECRUITING on 2026-05-07.
Target Phenotypes: Vulvar cancer
Show evidence (1 reference)
"MITO VULVA-1 is a prospective, single arm, multi-cohorts, phase II trial that aims to assess the activity and the safety of Lenvatinib plus Pembrolizumab in patients with vulvar cancer."
This ClinicalTrials.gov summary directly supports the MITO VULVA-01 trial and intervention for patients with vulvar cancer.
{ }

Source YAML

click to show
name: Vulvar Carcinoma
creation_date: "2026-05-07T18:59:34Z"
updated_date: "2026-05-07T19:58:48Z"
synonyms:
- Vulvar cancer
- Carcinoma of the vulva
- Vulvar squamous cell carcinoma
- VSCC
description: >-
  Vulvar carcinoma is a rare epithelial malignancy of the vulva. Vulvar
  squamous cell carcinoma is the dominant histologic subtype, and current
  molecular classification separates HPV-associated tumors from
  HPV-independent tumors, the latter often involving TP53 pathway disruption
  and chronic vulvar dermatoses such as lichen sclerosus.
categories:
- Gynecologic Malignancy
- Solid Tumor
- HPV-Related Cancer
parents:
- vulva cancer
disease_term:
  preferred_term: vulvar carcinoma
  term:
    id: MONDO:0005215
    label: vulvar carcinoma
definitions:
- name: Clinicopathologic definition
  definition_type: CASE_DEFINITION
  description: >-
    Vulvar carcinoma is a vulvar epithelial cancer, most commonly squamous
    cell carcinoma, diagnosed by biopsy of a suspicious vulvar lesion and
    staged with clinical, pathologic, and imaging assessment of local and
    nodal disease.
  scope: General adult gynecologic oncology definition
  evidence:
  - reference: PMID:38791925
    reference_title: "Current Preoperative Management of Vulvar Squamous Cell Carcinoma: An Overview."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Vulvar carcinoma is a rare cancer affecting the genital tract,
      constituting 4% of gynecological tumors. Vulvar squamous cell carcinoma
      (VSCC) is the most common type. Diagnosis relies on biopsy during
      vulvoscopy, plus imaging such as ultrasonography (USG), magnetic
      resonance imaging (MRI) and positron emission tomography (PET).
    explanation: >-
      This review defines vulvar carcinoma as a rare gynecologic cancer,
      identifies VSCC as the most common type, and summarizes biopsy and
      imaging-based preoperative assessment.
  - reference: DOI:10.1055/a-1545-4279
    reference_title: "2020 WHO Classification of Female Genital Tumors"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The 2020 WHO classification is focused on the distinction between
      HPV-associated and HPV-independent squamous cell carcinoma of the lower
      female genital organs.
    explanation: >-
      The WHO classification review supports HPV-associated versus
      HPV-independent classification for lower female genital squamous cell
      carcinoma, including vulvar squamous carcinoma.
has_subtypes:
- name: HPV-Associated VSCC
  display_name: HPV-associated vulvar squamous cell carcinoma
  description: >-
    Molecular subtype associated with high-risk human papillomavirus,
    p16INK4A positivity, and generally better prognosis than HPV-independent
    disease.
  evidence:
  - reference: PMID:37840151
    reference_title: "TP53 mutation and human papilloma virus status as independent prognostic factors in a Norwegian cohort of vulva squamous cell carcinoma."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Vulva squamous cell carcinoma (VSCC) develops through two separate
      molecular pathways-one involving high-risk human papilloma virus
      infection (HPV-associated), and the other without HPV infection
      (HPV-independent) often involving TP53 mutation. HPV-associated VSCC
      generally has a better progression-free survival than HPV-independent
      VSCC.
    explanation: >-
      The cohort paper directly supports HPV-associated VSCC as a distinct
      molecular pathway and links it to better progression-free survival.
- name: HPV-Independent TP53-Altered VSCC
  display_name: HPV-independent TP53-altered vulvar squamous cell carcinoma
  description: >-
    Molecular subtype not driven by HPV, commonly keratinizing, enriched for
    TP53 alteration and other somatic lesions, and often associated with
    differentiated VIN and lichen sclerosus.
  evidence:
  - reference: PMID:37840151
    reference_title: "TP53 mutation and human papilloma virus status as independent prognostic factors in a Norwegian cohort of vulva squamous cell carcinoma."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Vulva squamous cell carcinoma (VSCC) develops through two separate
      molecular pathways-one involving high-risk human papilloma virus
      infection (HPV-associated), and the other without HPV infection
      (HPV-independent) often involving TP53 mutation.
    explanation: >-
      This abstract explicitly distinguishes the HPV-independent pathway and
      notes frequent TP53 mutation involvement.
- name: HPV-Independent p53-Wild-Type VSCC
  display_name: HPV-independent p53-wild-type vulvar squamous cell carcinoma
  description: >-
    Uncommon HPV-independent molecular subtype lacking abnormal p53
    immunophenotype, with intermediate prognosis between HPV-associated and
    HPV-independent TP53-altered disease.
  evidence:
  - reference: DOI:10.3390/cancers16244216
    reference_title: "Molecular Subtypes of Vulvar Squamous Cell Carcinoma: The Significance of HPV-Independent/p53 Wild Type"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      These three molecular subtypes of VSCC (HPVa, HPVi p53 abnormal, and HPVi
      p53 wild type), as well as their precursor lesions, cannot be diagnosed
      based on a routine histopathological examination or immunostaining for p53
      and p16 as surrogate markers for TP53 mutation and high-risk HPV
      infection, respectively, are required.
    explanation: >-
      The review explicitly describes HPV-independent p53-wild-type VSCC as a
      third molecular subtype requiring p16 and p53 immunostaining.
infectious_agent:
- name: High-Risk Human Papillomavirus
  description: >-
    High-risk HPV infection drives the HPV-associated pathway of vulvar
    squamous cell carcinoma through viral oncogene effects and is commonly
    assessed by p16 immunohistochemistry or HPV RNA/DNA testing.
  infectious_agent_term:
    preferred_term: Human papillomavirus 16
    term:
      id: NCBITaxon:333760
      label: Human papillomavirus 16
  evidence:
  - reference: PMID:37840151
    reference_title: "TP53 mutation and human papilloma virus status as independent prognostic factors in a Norwegian cohort of vulva squamous cell carcinoma."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Immunohistochemistry for p53, Ki67 and p16INK4A (a surrogate marker for
      HPV infection) was performed on formalin-fixed paraffin-embedded tissues
      from a cohort of surgically treated VSCC patients to identify molecular
      subtypes of VSCC. Presence of HPV infection was detected by HPV DNA PCR
      and HPV mRNA in situ hybridization (ISH).
    explanation: >-
      This cohort operationalizes HPV-associated VSCC using p16, HPV DNA PCR,
      and HPV mRNA ISH, supporting high-risk HPV as the infectious driver in
      this molecular subtype.
pathophysiology:
- name: HPV-Associated Tumor Suppressor Disruption
  description: >-
    Persistent high-risk HPV infection defines one major VSCC pathway. Viral
    oncogene activity is reflected by p16INK4A positivity and produces cell
    cycle deregulation in vulvar squamous epithelium.
  evidence:
  - reference: PMID:37840151
    reference_title: "TP53 mutation and human papilloma virus status as independent prognostic factors in a Norwegian cohort of vulva squamous cell carcinoma."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      p16INK4A immunohistochemistry, mRNA ISH, and DNA PCR had excellent
      concordance in terms of HPV detection.
    explanation: >-
      Concordance of p16 with HPV detection supports p16-marked HPV-associated
      biology as a major VSCC pathway.
  cell_types:
  - preferred_term: vulvar keratinocyte
    term:
      id: CL:0000312
      label: keratinocyte
  locations:
  - preferred_term: vulva
    term:
      id: UBERON:0000997
      label: mammalian vulva
  biological_processes:
  - preferred_term: response to virus
    term:
      id: GO:0009615
      label: response to virus
  - preferred_term: G1/S transition of mitotic cell cycle
    modifier: INCREASED
    term:
      id: GO:0000082
      label: G1/S transition of mitotic cell cycle
  downstream:
  - target: Clonal Squamous Cell Proliferation
    description: HPV-associated cell-cycle deregulation promotes expansion of transformed vulvar keratinocytes.
- name: Lichen Sclerosus Inflammatory Microenvironment
  description: >-
    Lichen sclerosus creates chronic vulvar inflammation, tissue remodeling,
    oxidative stress, scarring, and symptoms that can precede or accompany
    HPV-independent vulvar squamous carcinogenesis.
  evidence:
  - reference: DOI:10.3389/fmed.2023.1106318
    reference_title: "Lichen sclerosus: The 2023 update"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Oxidative stress with lipid and DNA peroxidation provides an enabling
      microenvironment to autoimmunity and carcinogenesis.
    explanation: >-
      The review supports oxidative stress and immune-mediated tissue injury
      as a carcinogenesis-enabling microenvironment in lichen sclerosus.
  - reference: DOI:10.3389/fmed.2023.1106318
    reference_title: "Lichen sclerosus: The 2023 update"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      In addition to genital scarring, and sexual and urinary dysfunction, LS
      may also lead to squamous cell carcinoma.
    explanation: >-
      This explicitly links lichen sclerosus to squamous cell carcinoma risk.
  cell_types:
  - preferred_term: vulvar keratinocyte
    term:
      id: CL:0000312
      label: keratinocyte
  locations:
  - preferred_term: vulva
    term:
      id: UBERON:0000997
      label: mammalian vulva
  biological_processes:
  - preferred_term: extracellular matrix organization
    modifier: ABNORMAL
    term:
      id: GO:0030198
      label: extracellular matrix organization
  downstream:
  - target: HPV-Independent Somatic Driver Accumulation
    description: Chronic inflammatory and oxidative injury can create a permissive context for somatic driver selection.
- name: HPV-Independent Somatic Driver Accumulation
  description: >-
    HPV-independent VSCC is enriched for TERT promoter, TP53, CDKN2A, NOTCH1,
    and FAT1 alterations, supporting a tumor-suppressor and differentiation
    failure pathway distinct from HPV-driven tumors.
  evidence:
  - reference: PMID:34650187
    reference_title: "Molecular landscape of vulvovaginal squamous cell carcinoma: new insights into molecular mechanisms of HPV-associated and HPV-independent squamous cell carcinoma."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Other common abnormalities in HPV-independent tumors were TP53 mutations
      (13/15, 87%), CDKN2A alterations (10/15, 67%), and NOTCH1 and FAT1
      mutations (7/15, 47% each).
    explanation: >-
      Sequencing of vulvovaginal squamous carcinomas identifies recurrent
      TP53, CDKN2A, NOTCH1, and FAT1 alterations in HPV-independent tumors.
  - reference: PMID:34650187
    reference_title: "Molecular landscape of vulvovaginal squamous cell carcinoma: new insights into molecular mechanisms of HPV-associated and HPV-independent squamous cell carcinoma."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Cancer cell fraction analysis of HPV-independent squamous carcinomas
      suggests that TERT and/or NOTCH1 alterations along with TP53 alterations
      can be the initiating event in these tumors.
    explanation: >-
      The paper places TERT, NOTCH1, and TP53 alterations early in the
      HPV-independent carcinogenic pathway.
  genes:
  - preferred_term: TP53
    term:
      id: hgnc:11998
      label: TP53
  - preferred_term: TERT
    term:
      id: hgnc:11730
      label: TERT
  - preferred_term: CDKN2A
    term:
      id: hgnc:1787
      label: CDKN2A
  - preferred_term: NOTCH1
    term:
      id: hgnc:7881
      label: NOTCH1
  - preferred_term: FAT1
    term:
      id: hgnc:3595
      label: FAT1
  cell_types:
  - preferred_term: vulvar keratinocyte
    term:
      id: CL:0000312
      label: keratinocyte
  biological_processes:
  - preferred_term: apoptotic process
    modifier: DECREASED
    term:
      id: GO:0006915
      label: apoptotic process
  - preferred_term: cell population proliferation
    modifier: INCREASED
    term:
      id: GO:0008283
      label: cell population proliferation
  downstream:
  - target: Clonal Squamous Cell Proliferation
    description: Somatic driver alterations support malignant clonal expansion in vulvar keratinocytes.
- name: PIK3CA-Activated HPV-Associated Signaling
  description: >-
    HPV-associated vulvovaginal squamous carcinomas are enriched for PIK3CA
    activating mutations, implicating PI3K pathway activation in a subset of
    HPV-driven tumors.
  evidence:
  - reference: PMID:34650187
    reference_title: "Molecular landscape of vulvovaginal squamous cell carcinoma: new insights into molecular mechanisms of HPV-associated and HPV-independent squamous cell carcinoma."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      HPV-associated vulvovaginal squamous cell carcinoma had PIK3CA
      activating mutations (7/11, 64%) as the most common genomic event
    explanation: >-
      This sequencing cohort supports PIK3CA activation as a recurrent event
      in HPV-associated vulvovaginal squamous carcinoma.
  genes:
  - preferred_term: PIK3CA
    term:
      id: hgnc:8975
      label: PIK3CA
  biological_processes:
  - preferred_term: cell population proliferation
    modifier: INCREASED
    term:
      id: GO:0008283
      label: cell population proliferation
  downstream:
  - target: Clonal Squamous Cell Proliferation
    description: PI3K pathway activation supports tumor cell growth and survival.
- name: HRAS/RAS-MAPK Signaling Activation
  description: >-
    HRAS mutations occur in a subset of VSCC and implicate RAS/MAPK signaling as
    an additional proliferation pathway in vulvar squamous carcinoma.
  evidence:
  - reference: DOI:10.1038/s41598-024-63913-z
    reference_title: "Genomic profiles of Japanese patients with vulvar squamous cell carcinoma"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Somatic mutations were identified by targeted or panel sequencing, and TP53
      was identified as the most common mutation (52–81%), followed by HRAS
      (7–26%), CDKN2A (21–24%), and PIK3CA (5–10%).
    explanation: >-
      The Japanese VSCC sequencing cohort identifies recurrent HRAS mutations,
      supporting a RAS/MAPK-linked somatic driver mechanism.
  genes:
  - preferred_term: HRAS
    term:
      id: hgnc:5173
      label: HRAS
  biological_processes:
  - preferred_term: MAPK cascade
    modifier: INCREASED
    term:
      id: GO:0000165
      label: MAPK cascade
  - preferred_term: cell population proliferation
    modifier: INCREASED
    term:
      id: GO:0008283
      label: cell population proliferation
  downstream:
  - target: Clonal Squamous Cell Proliferation
    description: HRAS-driven MAPK signaling can promote transformed keratinocyte proliferation.
- name: Clonal Squamous Cell Proliferation
  description: >-
    HPV-driven cell-cycle deregulation or HPV-independent somatic driver
    accumulation leads to clonal proliferation and invasive squamous carcinoma
    in the vulvar epithelium.
  cell_types:
  - preferred_term: vulvar keratinocyte
    term:
      id: CL:0000312
      label: keratinocyte
  locations:
  - preferred_term: vulva
    term:
      id: UBERON:0000997
      label: mammalian vulva
  biological_processes:
  - preferred_term: cell population proliferation
    modifier: INCREASED
    term:
      id: GO:0008283
      label: cell population proliferation
histopathology:
- name: Squamous Cell Carcinoma
  finding_term:
    preferred_term: Squamous Cell Carcinoma
    term:
      id: NCIT:C2929
      label: Squamous Cell Carcinoma
  diagnostic: true
  description: >-
    Vulvar squamous cell carcinoma is the most common histologic type of
    vulvar carcinoma.
  evidence:
  - reference: PMID:38791925
    reference_title: "Current Preoperative Management of Vulvar Squamous Cell Carcinoma: An Overview."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Vulvar squamous cell carcinoma (VSCC) is the most common type.
    explanation: >-
      This review supports squamous cell carcinoma as the dominant vulvar
      carcinoma histology.
phenotypes:
- category: Gynecologic
  name: Biopsy-Requiring Vulvar Lesion
  diagnostic: true
  description: >-
    A persistent or suspicious vulvar lesion requires biopsy to establish or
    exclude vulvar carcinoma.
  phenotype_term:
    preferred_term: vulvar lesion
    term:
      id: HP:0011355
      label: Localized skin lesion
  evidence:
  - reference: PMID:38791925
    reference_title: "Current Preoperative Management of Vulvar Squamous Cell Carcinoma: An Overview."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Diagnosis relies on biopsy during vulvoscopy, plus imaging such as
      ultrasonography (USG), magnetic resonance imaging (MRI) and positron
      emission tomography (PET).
    explanation: >-
      The need for vulvoscopy-directed biopsy supports a visible or clinically
      suspicious vulvar lesion as the diagnostic presentation.
- category: Gynecologic
  name: Vulvar Lump or Mass
  description: >-
    Patients with vulvar cancer may notice a vulvar lump or mass as part of the
    presenting lesion complex.
  phenotype_term:
    preferred_term: vulvar lump or mass
    term:
      id: HP:0002664
      label: Neoplasm
  evidence:
  - reference: DOI:10.1002/ijgo.13881
    reference_title: "Cancer of the vulva: 2021 update"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      While vulvar cancer may be asymptomatic, most women present with vulvar
      pruritus or pain, or have noticed a lump or ulcer.
    explanation: >-
      The clinical update identifies a noticed lump as a presenting feature of
      vulvar cancer; the HPO binding uses the broad neoplasm term because local
      HPO did not provide a vulvar-specific mass term.
- category: Dermatologic
  name: Vulvar Ulcer
  description: >-
    Ulceration can be part of the presenting vulvar lesion complex in vulvar
    cancer.
  phenotype_term:
    preferred_term: vulvar ulcer
    term:
      id: HP:0200042
      label: Skin ulcer
  evidence:
  - reference: DOI:10.1002/ijgo.13881
    reference_title: "Cancer of the vulva: 2021 update"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      While vulvar cancer may be asymptomatic, most women present with vulvar
      pruritus or pain, or have noticed a lump or ulcer.
    explanation: >-
      The clinical update identifies ulcer as a presenting feature; the HPO
      binding uses the broader skin-ulcer term because local HPO did not provide
      a vulvar-specific ulcer term.
- category: Dermatologic
  name: Vulvar Pruritus
  description: >-
    Itching is common in lichen sclerosus and other vulvar dermatoses that can
    underlie HPV-independent vulvar carcinogenesis.
  phenotype_term:
    preferred_term: Vulvar pruritus
    term:
      id: HP:0000989
      label: Pruritus
  evidence:
  - reference: DOI:10.3389/fmed.2023.1106318
    reference_title: "Lichen sclerosus: The 2023 update"
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The typical clinical picture includes chronic whitish atrophic patches
      along with itching and soreness in the vulvar, perianal and penile
      regions.
    explanation: >-
      This supports pruritus in lichen sclerosus, an important associated
      precursor/risk setting for HPV-independent vulvar carcinoma.
- category: Dermatologic
  name: Vulvar Pain or Soreness
  description: >-
    Vulvar soreness or pain may occur in associated dermatoses and can
    contribute to impaired sexual and urinary function.
  phenotype_term:
    preferred_term: Vulvar pain
    term:
      id: HP:0012531
      label: Pain
  evidence:
  - reference: DOI:10.3389/fmed.2023.1106318
    reference_title: "Lichen sclerosus: The 2023 update"
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The typical clinical picture includes chronic whitish atrophic patches
      along with itching and soreness in the vulvar, perianal and penile
      regions.
    explanation: >-
      This supports vulvar soreness in lichen sclerosus, a clinically relevant
      associated dermatosis in the HPV-independent disease pathway.
genetic:
- name: TP53
  association: Somatic Mutation
  gene_term:
    preferred_term: TP53
    term:
      id: hgnc:11998
      label: TP53
  notes: >-
    TP53 mutations are frequent in HPV-independent VSCC and correlate with
    poorer progression-free survival.
  evidence:
  - reference: PMID:37840151
    reference_title: "TP53 mutation and human papilloma virus status as independent prognostic factors in a Norwegian cohort of vulva squamous cell carcinoma."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The TP53 mutation status was identified as an independent prognostic
      factor of worse progression-free survival (p = 0.024) after adjustment
      for FIGO stage.
    explanation: >-
      This cohort supports TP53 mutation as a prognostic somatic alteration in
      VSCC.
- name: PIK3CA
  association: Somatic Activating Mutation
  gene_term:
    preferred_term: PIK3CA
    term:
      id: hgnc:8975
      label: PIK3CA
  notes: >-
    PIK3CA activating mutations are enriched in HPV-associated vulvovaginal
    squamous carcinomas.
  evidence:
  - reference: PMID:34650187
    reference_title: "Molecular landscape of vulvovaginal squamous cell carcinoma: new insights into molecular mechanisms of HPV-associated and HPV-independent squamous cell carcinoma."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      HPV-associated vulvovaginal squamous cell carcinoma had PIK3CA
      activating mutations (7/11, 64%) as the most common genomic event
    explanation: >-
      This supports PIK3CA activation as a recurrent molecular event in the
      HPV-associated pathway.
- name: TERT
  association: Somatic Promoter Alteration
  gene_term:
    preferred_term: TERT
    term:
      id: hgnc:11730
      label: TERT
  notes: >-
    TERT promoter alterations are highly enriched in HPV-independent
    vulvovaginal squamous carcinomas.
  evidence:
  - reference: PMID:34650187
    reference_title: "Molecular landscape of vulvovaginal squamous cell carcinoma: new insights into molecular mechanisms of HPV-associated and HPV-independent squamous cell carcinoma."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      TERT gene alterations, mainly TERT promoter mutations (14/15 cases, 93%)
      featured significantly in HPV-independent carcinomas.
    explanation: >-
      This supports TERT promoter alteration as a frequent HPV-independent
      VSCC driver event.
- name: CDKN2A
  association: Somatic Alteration
  gene_term:
    preferred_term: CDKN2A
    term:
      id: hgnc:1787
      label: CDKN2A
  notes: >-
    CDKN2A alterations occur in HPV-independent tumors and remove an important
    cell-cycle restraint.
  evidence:
  - reference: PMID:34650187
    reference_title: "Molecular landscape of vulvovaginal squamous cell carcinoma: new insights into molecular mechanisms of HPV-associated and HPV-independent squamous cell carcinoma."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Other common abnormalities in HPV-independent tumors were TP53 mutations
      (13/15, 87%), CDKN2A alterations (10/15, 67%), and NOTCH1 and FAT1
      mutations (7/15, 47% each).
    explanation: >-
      This supports CDKN2A alteration as a recurrent somatic event in the
      HPV-independent molecular subgroup.
- name: NOTCH1
  association: Somatic Mutation
  gene_term:
    preferred_term: NOTCH1
    term:
      id: hgnc:7881
      label: NOTCH1
  notes: >-
    NOTCH1 mutations are recurrent in HPV-independent vulvovaginal squamous
    carcinomas and may occur early with TP53 alterations.
  evidence:
  - reference: PMID:34650187
    reference_title: "Molecular landscape of vulvovaginal squamous cell carcinoma: new insights into molecular mechanisms of HPV-associated and HPV-independent squamous cell carcinoma."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Other common abnormalities in HPV-independent tumors were TP53 mutations
      (13/15, 87%), CDKN2A alterations (10/15, 67%), and NOTCH1 and FAT1
      mutations (7/15, 47% each).
    explanation: >-
      This supports NOTCH1 mutation as a recurrent somatic event in
      HPV-independent vulvovaginal squamous carcinoma.
- name: FAT1
  association: Somatic Mutation
  gene_term:
    preferred_term: FAT1
    term:
      id: hgnc:3595
      label: FAT1
  notes: >-
    FAT1 mutations recur in HPV-independent vulvovaginal squamous carcinomas.
  evidence:
  - reference: PMID:34650187
    reference_title: "Molecular landscape of vulvovaginal squamous cell carcinoma: new insights into molecular mechanisms of HPV-associated and HPV-independent squamous cell carcinoma."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Other common abnormalities in HPV-independent tumors were TP53 mutations
      (13/15, 87%), CDKN2A alterations (10/15, 67%), and NOTCH1 and FAT1
      mutations (7/15, 47% each).
    explanation: >-
      This supports FAT1 mutation as a recurrent somatic event in
      HPV-independent vulvovaginal squamous carcinoma.
- name: HRAS
  association: Somatic Mutation
  gene_term:
    preferred_term: HRAS
    term:
      id: hgnc:5173
      label: HRAS
  notes: >-
    HRAS mutations occur in a subset of VSCC and support RAS/MAPK pathway
    involvement.
  evidence:
  - reference: DOI:10.1038/s41598-024-63913-z
    reference_title: "Genomic profiles of Japanese patients with vulvar squamous cell carcinoma"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Somatic mutations were identified by targeted or panel sequencing, and TP53
      was identified as the most common mutation (52–81%), followed by HRAS
      (7–26%), CDKN2A (21–24%), and PIK3CA (5–10%).
    explanation: >-
      This supports HRAS as a recurrent somatic mutation in Japanese VSCC
      sequencing cohorts.
biochemical:
- name: p16 Immunohistochemistry
  notes: >-
    p16INK4A immunohistochemistry is used as a surrogate marker for HPV
    infection in VSCC molecular subtyping.
  evidence:
  - reference: PMID:37840151
    reference_title: "TP53 mutation and human papilloma virus status as independent prognostic factors in a Norwegian cohort of vulva squamous cell carcinoma."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Immunohistochemistry for p53, Ki67 and p16INK4A (a surrogate marker for
      HPV infection) was performed on formalin-fixed paraffin-embedded tissues
      from a cohort of surgically treated VSCC patients to identify molecular
      subtypes of VSCC.
    explanation: >-
      The study supports p16INK4A immunohistochemistry as an HPV-associated
      subtype marker in VSCC.
- name: p53 Immunohistochemistry
  notes: >-
    p53 immunohistochemistry is used to infer TP53 mutation status and helps
    stratify HPV-independent VSCC prognosis.
  evidence:
  - reference: PMID:37840151
    reference_title: "TP53 mutation and human papilloma virus status as independent prognostic factors in a Norwegian cohort of vulva squamous cell carcinoma."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The results of p53 and p16INK4A immunohistochemistry confirmed three
      VSCC subtypes associated with different prognosis.
    explanation: >-
      This supports combined p53 and p16 immunohistochemistry for molecular
      stratification of VSCC.
treatments:
- name: Local Excision With Sentinel Node Biopsy
  description: >-
    Early-stage vulvar cancer is treated by local excision of the primary
    tumor with sentinel node biopsy when nodal assessment is indicated, reducing
    morbidity compared with inguinofemoral lymphadenectomy in appropriate
    patients.
  evidence:
  - reference: DOI:10.6004/jnccn.2024.7002
    reference_title: "Update on the Sentinel Node Procedure in Vulvar Cancer"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Early-stage vulvar cancer is managed by a local excision of the primary
      tumor and, if indicated, a sentinel node (SN) biopsy to assess the need
      for further groin treatment.
    explanation: >-
      This review supports local excision and sentinel node biopsy as standard
      early-stage management.
  treatment_term:
    preferred_term: surgical procedure
    term:
      id: MAXO:0000004
      label: surgical procedure
- name: Definitive or Adjuvant Radiotherapy
  description: >-
    Radiotherapy is used in vulvar cancer management for local-regional disease
    control, including definitive, adjuvant, or groin-treatment contexts
    depending on stage and nodal status.
  evidence:
  - reference: DOI:10.6004/jnccn.2024.7002
    reference_title: "Update on the Sentinel Node Procedure in Vulvar Cancer"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Inguinofemoral radiotherapy is a good alternative to IFL in patients
      with micrometastases in the SN, with comparable efficacy and less
      treatment-related morbidity.
    explanation: >-
      The sentinel-node review supports radiotherapy as a morbidity-sparing
      groin-treatment option for selected node-positive early VSCC.
  treatment_term:
    preferred_term: radiation therapy
    term:
      id: MAXO:0000014
      label: radiation therapy
- name: Guideline-Based Multidisciplinary Treatment
  description: >-
    Management commonly requires coordinated gynecologic oncology, pathology,
    imaging, radiation oncology, medical oncology, reconstructive surgery, and
    supportive-care input.
  evidence:
  - reference: DOI:10.3390/cancers17020186
    reference_title: "Management of Patients with Vulvar Cancers: A Systematic Comparison of International Guidelines (NCCN-ASCO-ESGO-BGCS-IGCS-FIGO-French Guidelines-RCOG)"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      From the systematic comparison of the main international guidelines, a
      strong heterogeneity emerged in the diagnostic and therapeutic
      recommendations as well as for the multidisciplinary approach that today
      is essential.
    explanation: >-
      This guideline comparison supports multidisciplinary management as an
      essential part of vulvar cancer care.
  treatment_term:
    preferred_term: therapeutic procedure
    term:
      id: NCIT:C49236
      label: Therapeutic Procedure
- name: Platinum-Based Chemotherapy
  description: >-
    First-line platinum-based chemotherapy is used for advanced or recurrent
    vulvar squamous cell carcinoma not amenable to curative surgery.
  evidence:
  - reference: clinicaltrials:NCT07101848
    reference_title: "A PHASE II, RANDOMIZED TRIAL TO ASSESS MAINTENANCE THERAPY WITH CEMIPLIMAB VERSUS BEST SUPPORTIVE CARE AFTER 1ST LINE PLATINUM-BASED CHEMOTHERAPY IN ADVANCED/RECURRENT VULVAR CANCER"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      This is a phase II, randomized study that will include 42 participants who
      have received 4 to 6 cycles of first-line platinum-based chemotherapy for
      advanced vulvar squamous cell carcinoma (SCC) not amenable to curative
      surgical treatment (FIGO 2018 stages III-IV - International Federation of
      Gynecology and Obstetrics) /
    explanation: >-
      The trial summary explicitly requires prior first-line platinum-based
      chemotherapy for advanced VSCC, supporting this systemic treatment context.
  treatment_term:
    preferred_term: chemotherapy
    term:
      id: MAXO:0000647
      label: chemotherapy
    therapeutic_agent:
    - preferred_term: platinum compound
      term:
        id: NCIT:C1450
        label: Platinum Compound
- name: HPV Vaccination
  description: >-
    Prophylactic HPV vaccination is a prevention strategy intended to reduce the
    future burden of HPV-related cancers, including HPV-associated vulvar cancer.
  evidence:
  - reference: DOI:10.1001/jamanetworkopen.2024.31807
    reference_title: "Human Papillomavirus Vaccination and Human Papillomavirus–Related Cancer Rates"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Designing and implementing targeted interventions to increase uptake and
      completion of HPV vaccination series across counties with low HPV
      vaccination rates may help to reduce future the burden of HPV-related
      cancers.
    explanation: >-
      This population-based study supports HPV vaccination uptake as a strategy
      to reduce future HPV-related cancer burden, which includes HPV-associated
      vulvar carcinoma.
  treatment_term:
    preferred_term: vaccination
    term:
      id: MAXO:0001017
      label: vaccination
    therapeutic_agent:
    - preferred_term: human papillomavirus vaccine
      term:
        id: NCIT:C1951
        label: Human Papilloma Virus Vaccine
clinical_trials:
- name: NCT05903833
  phase: PHASE_II
  status: RECRUITING
  description: >-
    Phase II trial of pembrolizumab plus lenvatinib in recurrent, persistent,
    metastatic, or locally advanced vulvar cancer not amenable to curative
    surgery or radiotherapy. ClinicalTrials.gov listed status as RECRUITING on
    2026-05-07.
  target_phenotypes:
  - preferred_term: Recurrent, persistent, metastatic, or locally advanced vulvar cancer
  evidence:
  - reference: clinicaltrials:NCT05903833
    reference_title: "Pembrolizumab in Combination With Lenvatinib in Pts With Recurrent, Persistent, Metastatic or Locally Advanced Vulvar Cancer Not Amenable to Curative Surgery or Radiotherapy"
    supports: SUPPORT
    snippet: >-
      Evaluation of efficacy and safety of pembrolizumab in combination with
      lenvatinib in patients with recurrent, persistent, metastatic or locally
      advanced vulva cancer.
    explanation: >-
      This ClinicalTrials.gov summary directly describes the study population
      and pembrolizumab-lenvatinib intervention.
- name: NCT07101848
  phase: PHASE_II
  status: NOT_RECRUITING
  description: >-
    Phase II randomized trial of cemiplimab maintenance plus best supportive
    care versus best supportive care after first-line platinum chemotherapy in
    advanced or recurrent vulvar squamous cell carcinoma. ClinicalTrials.gov
    listed status as NOT_YET_RECRUITING on 2026-05-07, represented here by the
    schema's NOT_RECRUITING status enum.
  target_phenotypes:
  - preferred_term: Advanced or recurrent vulvar squamous cell carcinoma
  evidence:
  - reference: clinicaltrials:NCT07101848
    reference_title: "A PHASE II, RANDOMIZED TRIAL TO ASSESS MAINTENANCE THERAPY WITH CEMIPLIMAB VERSUS BEST SUPPORTIVE CARE AFTER 1ST LINE PLATINUM-BASED CHEMOTHERAPY IN ADVANCED/RECURRENT VULVAR CANCER"
    supports: SUPPORT
    snippet: >-
      This is a phase II, randomized study that will include 42 participants
      who have received 4 to 6 cycles of first-line platinum-based
      chemotherapy for advanced vulvar squamous cell carcinoma (SCC) not
      amenable to curative surgical treatment (FIGO 2018 stages III-IV -
      International Federation of Gynecology and Obstetrics) /
    explanation: >-
      This ClinicalTrials.gov summary supports the trial design and population
      for cemiplimab maintenance in advanced or recurrent VSCC.
- name: NCT07290894
  phase: PHASE_II
  status: RECRUITING
  description: >-
    Phase II single-arm, multi-cohort trial of lenvatinib plus pembrolizumab in
    patients with vulvar cancer. ClinicalTrials.gov listed status as RECRUITING
    on 2026-05-07.
  target_phenotypes:
  - preferred_term: Vulvar cancer
  evidence:
  - reference: clinicaltrials:NCT07290894
    reference_title: "Pembrolizumab Plus Lenvatinib in Vulvar Cancer Patients: MITO VULVA-01 Study."
    supports: SUPPORT
    snippet: >-
      MITO VULVA-1 is a prospective, single arm, multi-cohorts, phase II trial
      that aims to assess the activity and the safety of Lenvatinib plus
      Pembrolizumab in patients with vulvar cancer.
    explanation: >-
      This ClinicalTrials.gov summary directly supports the MITO VULVA-01 trial
      and intervention for patients with vulvar cancer.
📚

References & Deep Research

Deep Research

1
Falcon
Vulvar Carcinoma (Vulvar Cancer): Disease Characteristics Research Report
Edison Scientific Literature 60 citations 2026-05-07T15:26:17.300658

Vulvar Carcinoma (Vulvar Cancer): Disease Characteristics Research Report

Target Disease

  • Disease name: Vulvar carcinoma (vulvar cancer)
  • Category: Malignant neoplasm of the vulva (female genital tract cancer)
  • MONDO ID: Not available from the retrieved sources in this run (would require dedicated ontology lookup).

1. Disease Information

Overview (what is the disease?)

Vulvar carcinoma is an uncommon malignant tumor arising in vulvar tissues; vulvar squamous cell carcinoma (VSCC) is the predominant histologic subtype (≈90% of vulvar cancers in multiple reviews). (corte2024currentpreoperativemanagement pages 1-2)

Key identifiers and terminologies

  • ICD-10: C51 (vulval/vulvar cancer) is explicitly used in health system cost and epidemiology analyses. (steinkasserer2023characterizationofpatients pages 1-2)
  • ICD-O-3 site coding: HPV-related cancer epidemiology work referenced ICD-O-3 site codes including C51.0 for vulvar cancer. (adekanmbi2024humanpapillomavirusvaccination pages 1-2)
  • MeSH (term): A 2024 imaging review searched PubMed using MeSH terms including “vulval neoplasm” (and “diagnostic imaging”). (ha2024imaginginvulval pages 1-2)
  • FIGO staging: The FIGO 2021 revision is data-derived and explicitly allows incorporation of cross-sectional imaging findings into staging. (olawaiye2021figostagingfor pages 1-2)

Common synonyms / alternative names

  • Vulvar carcinoma; vulval cancer; vulvar cancer; vulvar squamous cell carcinoma (VSCC) (dominant histology). (corte2024currentpreoperativemanagement pages 1-2)

Evidence-source note (individual patient vs aggregated)

This report is derived from aggregated disease-level resources (reviews, guidelines syntheses, cohort/registry studies, and clinical trial registry entries) plus some single-center retrospective cohorts and experimental model studies. (corte2024currentpreoperativemanagement pages 1-2, dongre2024tp53mutationand pages 1-2, meng2024overallsurvivalassociated pages 1-2, dongre2020establishmentofa pages 1-7)


2. Etiology

Core causal pathways (current understanding)

Modern classification recognizes two main etiologic pathways for VSCC: 1. HPV-associated VSCC: often basaloid/warty morphology; typically p16 “block” positive; generally occurs in younger patients and is associated with precursor high-grade squamous intraepithelial lesions (HSIL/usual VIN). (dongre2024tp53mutationand pages 1-2, horn2024molecularsubtypesof pages 12-14, hohn20212020whoclassification pages 4-6) 2. HPV-independent VSCC: often keratinizing morphology; frequently linked to chronic inflammatory vulvar dermatoses (notably lichen sclerosus) and to differentiated VIN (dVIN); commonly shows aberrant p53 patterns consistent with TP53 alteration; generally associated with poorer prognosis. (dongre2024tp53mutationand pages 1-2, horn2024molecularsubtypesof pages 12-14, horn2024molecularsubtypesof pages 16-18)

A recent focus is the less common HPV-independent/p53-wild-type subtype, emphasizing that not all HPV-independent tumors are p53-abnormal. (horn2024molecularsubtypesof pages 12-14)

Risk factors

Infectious: high-risk HPV infection is a major risk factor for HPV-associated disease; HPV16 is predominant among HPV-positive high-grade vulvar lesions in one 2024 review (HPV16 ≈80% of HPV-positive cases). (scurtu2024squamouscellcarcinoma pages 5-7)

Inflammatory/dermatologic: lichen sclerosus (LS) is strongly associated with HPV-independent precancers and cancer and can lead to SCC development; LS causes chronic inflammation and tissue remodeling that may support carcinogenesis. (luca2023lichensclerosusthe pages 1-2, scurtu2024squamouscellcarcinoma pages 5-7)

Precursor lesions: differentiated VIN (dVIN) is a high-risk HPV-independent precursor; one 2024 review reports much higher progression for dVIN than HSIL (43.2% vs 9.7%). (scurtu2024squamouscellcarcinoma pages 4-5)

Host factors: immunosuppression is highlighted as a critical cofactor for HPV-associated lesions in a recent review. (scurtu2024squamouscellcarcinoma pages 5-7)

Protective factors

HPV vaccination: Multiple sources support prophylactic HPV vaccination as a key protective factor against HPV-associated disease, with very high efficacy in HPV-naïve individuals. - A large 2024 cross-sectional study notes vaccine efficacy “close to 100%” for preventing HPV-associated cancers among those without prior infection with vaccine HPV types. (adekanmbi2024humanpapillomavirusvaccination pages 1-2) - A 2024 review of HPV vaccine strategies states that vaccination blocks transmission and prevents HPV-related cancers and reports global implementation but limited coverage (143 member states by end of 2023; ~15% of young girls vaccinated). (cai2024humanpapillomavirusrelatedcancer pages 1-2)

Management of lichen sclerosus (risk reduction plausibility): LS reviews and cohorts emphasize the need for early diagnosis, adequate treatment, and follow-up to reduce malignant evolution risk. - A 2024 LS review reports markedly elevated vulvar cancer risk in LS (example population-based SIR 33.6 for vulvar cancer) and suggests that consistent long-term potent topical corticosteroid (TCS) use may reduce recurrence compared with historical recurrence rates. (popa2024vulvarlichensclerosus pages 21-22)

Gene–environment interactions

Direct quantitative gene–environment interaction estimates were not present in the retrieved evidence. Mechanistically, LS-associated chronic inflammation/oxidative stress provides an enabling microenvironment for carcinogenesis and can co-occur with TP53 pathway alterations typical of HPV-independent disease. (luca2023lichensclerosusthe pages 1-2, scurtu2024squamouscellcarcinoma pages 5-7)


3. Phenotypes (clinical presentation, signs/symptoms, QoL)

Common presenting symptoms/signs (VSCC)

Recent clinical updates emphasize that presentation ranges from asymptomatic lesions detected on exam to symptomatic disease with: - vulvar pruritus (itching) - pain/burning - lump/mass - ulcer These features are highlighted in recent clinical overviews and updates. (corte2024currentpreoperativemanagement pages 1-2, olawaiye2021cancerofthe pages 1-2)

Age of onset / demographics

VSCC predominantly affects postmenopausal women with mean/median ages often >65–70 years in clinical series and reviews; HPV-associated cases skew younger. (corte2024currentpreoperativemanagement pages 1-2, cebollaverdugo2024multidisciplinaryvulvarcancer pages 2-4, dongre2024tp53mutationand pages 1-2)

Quality-of-life impacts

Major QoL burdens stem from symptoms (pain/pruritus), genital functional impairment, and treatment morbidity. - Conservative approaches (e.g., sentinel node biopsy) are emphasized to reduce long-term morbidity such as chronic lymphedema, wound issues, and sexual dysfunction. (cebollaverdugo2024multidisciplinaryvulvarcancer pages 2-4, kolk2024updateonthe pages 1-2)

Suggested HPO terms (examples)

(These are ontology suggestions; HPO IDs are provided where commonly used—verify in HPO browser for exact IDs.) - Pruritus (HP:0000989) - Vulvar pain (term exists in HPO; verify exact ID) - Genital ulcer (HP:0000211, general mucosal ulceration; vulvar-specific term should be checked) - Vulvar mass (term exists; verify exact ID) - Lymphedema (HP:0001004) (treatment complication) (cebollaverdugo2024multidisciplinaryvulvarcancer pages 2-4) - Dyspareunia (HP:0000148) (common in LS and survivorship context) (luca2023lichensclerosusthe pages 1-2)


4. Genetic / Molecular Information

Molecular classification and defining biomarkers

WHO-era classification of vulvar SCC emphasizes HPV association using p16 as a surrogate marker and p53 immunophenotyping for HPV-independent disease (with a recognized “uncertain” group). (hohn20212020whoclassification pages 4-6, horn2024molecularsubtypesof pages 16-18)

  • HPV-associated: p16 block-positive; often p53 wild-type pattern; typically better prognosis/radiosensitivity. (hohn20212020whoclassification pages 4-6)
  • HPV-independent: often p16 negative/non-block; frequently p53 aberrant (overexpression, null, cytoplasmic) consistent with TP53 alteration. (horn2024molecularsubtypesof pages 16-18)

Recurrent somatic alterations (VSCC)

2024 Japanese VSCC genomic profiling: TP53 (52–81%), HRAS (7–26%), CDKN2A (21–24%), PIK3CA (5–10%). (fujii2024genomicprofilesof pages 1-2)

HPV-status–linked molecular profiles (tumor sequencing cohort): HPV-independent tumors show high rates of TP53, TERT promoter, CDKN2A, NOTCH1, FAT1 alterations, while HPV-associated tumors are enriched for activating PIK3CA mutations (PI3K pathway). (salama2022molecularlandscapeof pages 1-3)

Mechanistic/pathway summary (causal chain)

  • HPV-associated pathway: viral oncoproteins (E6/E7/E5) enable immune evasion and drive carcinogenesis; E6/E7 disrupt tumor suppressor pathways, with downstream cell-cycle dysregulation and p16 overexpression. (scurtu2024squamouscellcarcinoma pages 5-7)
  • HPV-independent pathway: chronic inflammation (e.g., LS) and precursor dVIN are linked to TP53 mutagenic processes, NOTCH1 loss-of-function, and RTK/RAS/PI3K signaling (including HRAS involvement), driving clonal expansion and invasion. (scurtu2024squamouscellcarcinoma pages 5-7, fujii2024genomicprofilesof pages 1-2)

Suggested GO biological process terms (examples)

  • Epithelial cell proliferation (GO:0050673)
  • Keratinocyte differentiation (GO:0030216)
  • Cell cycle regulation (GO:0051726)
  • DNA damage response (GO:0006974)
  • Regulation of apoptotic process (GO:0042981)
  • Response to virus (GO:0009615) (HPV-associated)

Suggested CL (cell type) terms (examples)

  • Keratinocyte (CL:0000312)
  • Fibroblast / cancer-associated fibroblast (CL:0000057; CAF is a functional state) (dongre2020establishmentofa pages 1-7)
  • CD8-positive, alpha-beta T cell (CL:0000625) (prognostic immune infiltrate context) (zhang2023anintegratedmodel pages 1-2)

5. Environmental Information

Infectious agents

  • High-risk HPV is a key infectious driver of the HPV-associated VSCC pathway. (dongre2024tp53mutationand pages 1-2, scurtu2024squamouscellcarcinoma pages 5-7)

Lifestyle factors

  • Smoking is cited as a risk factor in clinical updates and reviews. (olawaiye2021cancerofthe pages 1-2)

Non-infectious inflammatory conditions

  • Chronic inflammatory vulvar dermatoses, especially lichen sclerosus, are strongly linked to HPV-independent carcinogenesis and functional morbidity. (luca2023lichensclerosusthe pages 1-2)

6. Mechanism / Pathophysiology

Key mechanisms and pathways

  • PI3K/AKT/mTOR signaling: implicated particularly in HPV-associated tumors via PIK3CA activating mutations, and in a subset of HPV-independent cases. (salama2022molecularlandscapeof pages 1-3, fujii2024genomicprofilesof pages 1-2)
  • RAS/MAPK signaling: HRAS mutations occur in a subset of VSCC. (fujii2024genomicprofilesof pages 1-2)
  • TP53 tumor suppressor pathway: frequently altered in HPV-independent VSCC and linked to worse prognosis. (dongre2024tp53mutationand pages 1-2, fujii2024genomicprofilesof pages 1-2)
  • NOTCH pathway: frequently altered in HPV-independent disease in sequencing cohorts, consistent with altered squamous differentiation programs. (salama2022molecularlandscapeof pages 1-3)

Tumor microenvironment and stromal dependence

Experimental evidence supports a strong role for tumor–stroma interaction: a LS-associated VSCC cell line (VCC1) showed fibroblast-dependent invasion and tumor formation in 3D organotypic models and xenografts. (dongre2020establishmentofa pages 1-7)


7. Anatomical Structures Affected

Organ / tissue level

  • Primary site: vulva (labia majora/minora, clitoris, perineum, mons). (corte2024currentpreoperativemanagement pages 1-2)
  • Regional spread: lymphatic drainage primarily to inguinofemoral nodes, secondarily to pelvic nodes. (olawaiye2021cancerofthe pages 1-2)

Suggested UBERON terms (examples)

  • Vulva (UBERON:0000997)
  • Labium majus (UBERON:0003185)
  • Labium minus (UBERON:0003186)
  • Clitoris (UBERON:0002256)
  • Inguinal lymph node (UBERON:0001542)

8. Temporal Development

  • Onset: typically adult/geriatric; HPV-associated pathway tends to present earlier than HPV-independent. (dongre2024tp53mutationand pages 1-2)
  • Progression and precursors: HSIL/uVIN and dVIN are recognized precursors; dVIN has higher malignant potential and faster progression than HSIL in comparative data summarized by reviews. (scurtu2024squamouscellcarcinoma pages 4-5)

9. Inheritance and Population

Epidemiology (selected recent statistics)

  • A 2024 imaging review cites 47,000 global vulvar cancer cases in 2022. (ha2024imaginginvulval pages 1-2)
  • A single-center “patterns of care” study cites GLOBOCAN 2020 estimates (45,240 cases; 17,427 deaths). (singhal2024patternsofcare pages 1-2)

Genetic inheritance is not applicable in a Mendelian sense for most vulvar carcinoma; this is primarily a sporadic, multifactorial cancer with somatic driver alterations.


10. Diagnostics

Diagnostic approach

  • Biopsy of any suspicious vulvar lesion is emphasized as essential for diagnosis; vulvoscopy is a key clinical tool. (corte2024currentpreoperativemanagement pages 1-2, olawaiye2021cancerofthe pages 1-2)

Biomarkers used in practice

  • p16 immunohistochemistry is used as a surrogate for HPV association; diffuse “block” staining supports HPV-associated neoplasia. (dongre2024tp53mutationand pages 1-2, hohn20212020whoclassification pages 4-6)
  • p53 immunohistochemistry helps identify HPV-independent/TP53-altered tumors and precursor lesions such as dVIN. (horn2024molecularsubtypesof pages 16-18)

Imaging (preoperative and staging)

Imaging recommendations vary by stage and clinical question; a 2024 preoperative management review identifies MRI and PET as gold-standard imaging for local extension and nodal evaluation, with expert-performed ultrasound increasingly used for groin node assessment. (corte2024currentpreoperativemanagement pages 1-2)

The FIGO 2021 staging revision explicitly allows staging to incorporate cross-sectional imaging findings. (olawaiye2021figostagingfor pages 1-2)

The following table (from the 2024 imaging review) summarizes FIGO 2021 staging.

(ha2024imaginginvulval media e360c86b)

Differential diagnosis (selected)

Vulvar lesions that can mimic malignant or premalignant disease include inflammatory dermatoses (e.g., lichen sclerosus) and premalignant vulvar intraepithelial lesions; biopsy is required when neoplasia is suspected. (luca2023lichensclerosusthe pages 1-2)


11. Outcome / Prognosis

Prognostic factors

  • Nodal status is critical: one systematic review states 5-year OS is >80% node-negative, <40% with inguinal node involvement, and 10–15% with pelvic nodes. (ferrari2024adjuvantradiotherapyfor pages 1-2)
  • Molecular subtype impacts prognosis: TP53 mutation status is an independent adverse prognostic factor for progression-free survival, and transcriptionally active hrHPV is associated with improved outcomes in a 2024 cohort. (dongre2024tp53mutationand pages 1-2)

Recent quantitative survival / outcome statistics

  • SEER-derived survival cited in a guideline comparison: 5-year survival 85.6% localized, 47.5% regional, 23.3% distant (stage IVB). (restaino2025managementofpatients pages 2-4)
  • A single-center cohort (n=82) reported: disease-specific recurrence 32.9%, mortality 30.5%, median DFS 17 months, median OS 27 months. (singhal2024patternsofcare pages 1-2)
  • In metastatic vulvar cancer (SEER 2000–2019), chemoradiotherapy improved OS vs radiotherapy alone (matched cohort HR 0.7367, 95% CI 0.5906–0.9190). (meng2024overallsurvivalassociated pages 1-2)

12. Treatment

Current standard-of-care (real-world implementations)

Surgery - Early-stage disease: local excision / radical local excision with attention to margins, plus groin staging when indicated. (kolk2024updateonthe pages 1-2, ferrari2024adjuvantradiotherapyfor pages 1-2)

Sentinel lymph node biopsy (SLNB) - SLNB is an established, less morbid alternative to inguinofemoral lymphadenectomy in selected early-stage VSCC; it reduces complications such as lymphedema while maintaining oncologic safety. (kolk2024updateonthe pages 1-2)

Radiotherapy / chemoradiotherapy - Adjuvant radiotherapy for nodal disease has limited RCT evidence but suggests reduction in cancer-related deaths and groin recurrences; one RCT reported 6-year cancer-related deaths 29% vs 51% (HR 0.49) and groin recurrences 5.3% vs 24.1% favoring radiotherapy. (ferrari2024adjuvantradiotherapyfor pages 1-2) - For locally advanced unresectable disease, multiple guideline sets recommend definitive chemoradiation. (restaino2025managementofpatients pages 14-16)

Systemic therapy and immunotherapy (emerging) - Modern guidance notes emerging immunotherapy options for advanced disease, but evidence remains limited and often extrapolated from other SCC sites; clinical trials are ongoing. (restaino2025managementofpatients pages 2-4)

Active / planned clinical trials (selected)

  • NCT07101848 (BRAVA VULVAR): Phase II randomized maintenance cemiplimab vs best supportive care after 1st-line platinum chemotherapy in advanced/recurrent vulvar cancer; primary endpoint PFS at week 24; not yet recruiting; estimated start 2025-11-01. URL: https://clinicaltrials.gov/study/NCT07101848 (NCT07101848 chunk 1)
  • NCT05903833: Phase II single-arm pembrolizumab + lenvatinib in recurrent/metastatic/locally advanced VSCC not amenable to curative surgery/radiotherapy; primary endpoint ORR within 24 weeks; recruiting; start 2025-06-24. URL: https://clinicaltrials.gov/study/NCT05903833 (NCT05903833 chunk 1)
  • NCT07290894 (MITO VULVA-01): Phase II single-arm multi-cohort pembrolizumab + lenvatinib across unresectable locally advanced, chemo-naïve metastatic, and post-chemo recurrent/metastatic cohorts; primary endpoint ORR by RECIST 1.1; recruiting; start 2026-03-12. URL: https://clinicaltrials.gov/study/NCT07290894 (NCT07290894 chunk 1)

MAXO (Medical Action Ontology) suggestions (examples)

(Provide as ontology suggestions; confirm IDs in MAXO.) - Surgical excision / wide local excision; radical vulvectomy - Sentinel lymph node biopsy - External beam radiotherapy - Concurrent chemoradiotherapy - Immune checkpoint inhibitor therapy (anti–PD-1)


13. Prevention

Primary prevention

  • HPV vaccination is the primary preventive tool for HPV-associated vulvar precancers/cancers, with very high efficacy in HPV-naïve individuals and broad global adoption but incomplete coverage. (adekanmbi2024humanpapillomavirusvaccination pages 1-2, cai2024humanpapillomavirusrelatedcancer pages 1-2)

Secondary/tertiary prevention

  • There is no population screening program for vulvar cancer; prevention relies on early identification and management of predisposing conditions/precursors and biopsy of suspicious lesions. (olawaiye2021cancerofthe pages 1-2)
  • For LS, long-term potent topical corticosteroids are standard and cohorts/reviews emphasize surveillance; LS has strong symptom burden and elevated malignancy risk. (luca2023lichensclerosusthe pages 1-2, popa2024vulvarlichensclerosus pages 21-22)

14. Other Species / Natural Disease

No naturally occurring non-human species disease data were identified in the retrieved sources for vulvar carcinoma specifically.


15. Model Organisms / Experimental Models

Cell lines, organotypic models, xenografts

  • A LS-associated VSCC cell line (VCC1) was established and shown to have fibroblast-dependent tumorigenic and invasive behavior in 3D collagen co-culture/organotypic assays and xenografts, highlighting cancer-associated fibroblast contributions. URL: https://doi.org/10.1016/j.yexcr.2019.111684 (Published Jan 2020). (dongre2020establishmentofa pages 1-7)
  • The A431 cell line is used as a vulvar SCC model in mechanistic studies; one report shows miR-4712-5p promotes proliferation/invasion by targeting PTEN and activating AKT/cyclin D1 signaling. URL: https://doi.org/10.3892/or.2019.7320 (Published Sep 2019). (yang2019microrna47125ppromotesproliferation pages 1-2)

Suggested uses

  • Tumor–stroma interaction experiments (CAF co-culture)
  • Pathway perturbation (PI3K/AKT, RAS/MAPK)
  • Immunotherapy biomarker exploration (PD-L1, TILs) and radiosensitivity hypotheses by subtype

Summary artifact (identifiers, subtypes, genomics)

Section Item Summary Notes/Citations
Identifiers/terminology Standard disease name Vulvar carcinoma / vulval cancer; most cases are vulvar squamous cell carcinoma (VSCC), the predominant histology (~90%). ICD-10 C51 is reported for vulval cancer; VSCC predominance noted in recent reviews (corte2024currentpreoperativemanagement pages 1-2)
Identifiers/terminology Controlled vocabulary / search term A 2024 imaging review explicitly used the MeSH search terms “vulval neoplasm” and “diagnostic imaging.” Useful for literature retrieval, though no MeSH UID was provided in retrieved text (ha2024imaginginvulval pages 1-2)
Identifiers/terminology Staging/classification FIGO 2021 is the current staging framework for vulvar carcinoma and permits incorporation of cross-sectional imaging into staging. Data-derived revision; imaging incorporation specifically noted (olawaiye2021figostagingfor pages 1-2, ha2024imaginginvulval pages 1-2, faruqiUnknownyear2021figostaging pages 1-5)
Identifiers/terminology ICD-related coding context Additional ICD-related references in retrieved literature include ICD-10 groupings for vulvar cancer and ICD-O-3 site code C51.0 in HPV-related cancer analyses. ICD-10 C51 reported in economic analysis; ICD-O-3 C51.0 cited in HPV-related cancer rate study (steinkasserer2023characterizationofpatients pages 1-2, adekanmbi2024humanpapillomavirusvaccination pages 1-2)
Molecular subtype HPV-associated VSCC Typically younger women; often basaloid/warty morphology; precursor lesions are HSIL/uVIN (usual-type VIN); usually block-positive p16, generally non-aberrant/wild-type p53 pattern; often better prognosis and better radiotherapy response. HPV-associated tumors usually occur in younger patients and have improved prognosis/radiosensitivity (dongre2024tp53mutationand pages 1-2, horn2024molecularsubtypesof pages 12-14, hohn20212020whoclassification pages 4-6, scurtu2024squamouscellcarcinoma pages 5-7)
Molecular subtype HPV-independent, p53-abnormal VSCC Typically older/postmenopausal women; usually keratinizing morphology; precursor lesions are dVIN and often lichen sclerosus; usually p16 negative/non-block with aberrant p53 (overexpression, null, or cytoplasmic pattern); generally worse prognosis and less radiosensitive. Strongly associated with TP53 alterations, poorer outcomes, and lower radiosensitivity (dongre2024tp53mutationand pages 1-2, hohn20212020whoclassification pages 4-6, horn2024molecularsubtypesof pages 16-18)
Molecular subtype HPV-independent, p53-wild-type VSCC Uncommon third molecular subtype within HPV-independent disease; lacks HPV association and lacks classic p53-abnormal pattern; still falls within the HPV-independent spectrum but is molecularly distinct and under active study. Recent 2024 review emphasizes diagnostic/treatment significance of this subtype (horn2024molecularsubtypesof pages 12-14, horn2024molecularsubtypesof pages 1-5)
Biomarker framework p16 / p53 interpretation p16 is a surrogate marker of HPV-driven disease; p53 IHC helps identify HPV-independent/TP53-altered disease. Combined p16/p53 stratification supports classification into clinically meaningful subgroups. WHO/CAP-aligned approach summarized in recent reviews and cohort work (dongre2024tp53mutationand pages 1-2, hohn20212020whoclassification pages 4-6, horn2024molecularsubtypesof pages 16-18, hohn20212020whoclassification pages 1-2)
Genomics: 2024 Japanese cohort TP53 Most common alteration in Japanese VSCC cohorts: 52–81%. 2024 Scientific Reports cohort; predominantly HPV-independent tumors (fujii2024genomicprofilesof pages 1-2)
Genomics: 2024 Japanese cohort HRAS Recurrent alteration: 7–26%. Suggests RTK/RAS pathway involvement in a subset (fujii2024genomicprofilesof pages 1-2)
Genomics: 2024 Japanese cohort CDKN2A Recurrent alteration: 21–24%. Cell-cycle dysregulation signal (fujii2024genomicprofilesof pages 1-2)
Genomics: 2024 Japanese cohort PIK3CA Recurrent alteration: 5–10%. Supports PI3K pathway targetability in a subset (fujii2024genomicprofilesof pages 1-2)
Genomics: 2022 MSK cohort HPV-associated profile Enriched for PIK3CA activating mutations 7/11 (64%); NOTCH-pathway alterations also present 6/11 (55%) but involving different genes than HPV-independent tumors. HPV-associated tumors favor PI3K-pathway activation (salama2022molecularlandscapeof pages 4-6, salama2022molecularlandscapeof pages 8-10, salama2022molecularlandscapeof pages 1-3)
Genomics: 2022 MSK cohort HPV-independent profile Strong enrichment for TERT alterations 14/15 (93%), TP53 13/15 (87%), CDKN2A 10/15 (67%), NOTCH1 7/15 (47%), FAT1 7/15 (47%); NOTCH-pathway alterations overall 10/15 (67%). Distinct molecular program from HPV-associated tumors; TERT/TP53/CDKN2A/NOTCH1 argue against HPV-driven etiology (salama2022molecularlandscapeof pages 4-6, salama2022molecularlandscapeof pages 8-10, salama2022molecularlandscapeof pages 1-3)
Genomics: additional recent cohort HPV-independent vs HPV-associated differences In an additional recent cohort, HPV-negative tumors showed TP53 86% vs 0%, POLE 50% vs 6%, NOTCH1 43% vs 19%, CDKN2A 36% vs 0%; HPV-associated tumors more often had CNVs, especially cMYC, plus CDK2/CDK4 amplifications. Useful supporting comparison for subtype-specific molecular architecture (farkas2025pathologicalvariantsin pages 8-9, farkas2025pathologicalvariantsin pages 7-8)

Table: This table compiles core identifiers, current subtype terminology, biomarker definitions, and recurrent genomic alterations for vulvar carcinoma/VSCC. It is useful as a compact reference for disease ontology, clinicopathologic stratification, and precision-oncology annotation.

References

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