Vulvar cancer pathophysiology: Difference between revisions

Jump to navigation Jump to search
No edit summary
Line 3: Line 3:


==Overview==
==Overview==
==Pathogenesis of vulvar cancer==
* [[HPV|Human papillomaviruses]] subtypes 16 and 18 (High risk) play an essential role in the pathogenesis of  vulvar cancer. Once [[HPV]] enters an epithelial cell, the virus begins to make the proteins it encodes. Two of the proteins made by high-risk HPVs (E6 and E7) interfere with cell functions that normally prevent excessive growth, helping the cell to grow in an uncontrolled manner and to avoid cell death. Many times these infected cells are recognized by the immune system and eliminated. Sometimes, however, these infected cells are not destroyed, and a persistent infection results. As the persistently infected cells continue to grow, they may develop mutations in cellular genes that promote even more abnormal cell growth, leading to the formation of an area of precancerous cells and, ultimately, a cancerous tumor.
*  Vulvar carcinoma has its origins at the  it can involve the outer squamous cells, the inner glandular cells, or both. The precursor lesion is [[dysplasia]]: [[ vulvarintraepithelial neoplasia]] (VIN), which can subsequently become invasive cancer. This process can be quite slow. Longitudinal studies have shown that in patients with untreated in situ  vulvar cancer, 30% to 70% will develop invasive carcinoma over a period of 10 to 12 years. However, in about 10% of patients, lesions can progress from in situ to invasive in a period of less than 1 year. As it becomes invasive, the tumor breaks through the basement membrane and invades the  vulvar stroma. Extension of the tumor in the cervix may ultimately manifest as ulceration, exophytic tumor, or extensive infiltration of underlying tissue, including the bladder or rectum.


== Types ==
== Types ==

Revision as of 15:58, 30 September 2015

Vulvar cancer Microchapters

Home

Patient Info

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Vulvar cancer from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Staging

History and Symptoms

Physical Examination

Laboratory Findings

X Ray

CT

MRI

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Vulvar cancer pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Vulvar cancer pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Vulvar cancer pathophysiology

CDC on Vulvar cancer pathophysiology

Vulvar cancer pathophysiology in the news

Blogs on Vulvar cancer pathophysiology

Directions to Hospitals Treating Vulvar cancer

Risk calculators and risk factors for Vulvar cancer pathophysiology

Overview

Pathogenesis of vulvar cancer

  • Human papillomaviruses subtypes 16 and 18 (High risk) play an essential role in the pathogenesis of vulvar cancer. Once HPV enters an epithelial cell, the virus begins to make the proteins it encodes. Two of the proteins made by high-risk HPVs (E6 and E7) interfere with cell functions that normally prevent excessive growth, helping the cell to grow in an uncontrolled manner and to avoid cell death. Many times these infected cells are recognized by the immune system and eliminated. Sometimes, however, these infected cells are not destroyed, and a persistent infection results. As the persistently infected cells continue to grow, they may develop mutations in cellular genes that promote even more abnormal cell growth, leading to the formation of an area of precancerous cells and, ultimately, a cancerous tumor.
  • Vulvar carcinoma has its origins at the it can involve the outer squamous cells, the inner glandular cells, or both. The precursor lesion is dysplasia: vulvarintraepithelial neoplasia (VIN), which can subsequently become invasive cancer. This process can be quite slow. Longitudinal studies have shown that in patients with untreated in situ vulvar cancer, 30% to 70% will develop invasive carcinoma over a period of 10 to 12 years. However, in about 10% of patients, lesions can progress from in situ to invasive in a period of less than 1 year. As it becomes invasive, the tumor breaks through the basement membrane and invades the vulvar stroma. Extension of the tumor in the cervix may ultimately manifest as ulceration, exophytic tumor, or extensive infiltration of underlying tissue, including the bladder or rectum.



Types

Table 31-1. Histologic Subtypes of Vulvar Cancer[1][2][3][4]

1. Vulvar carcinomas

  • Squamous cell carcinoma
  • Basal cell carcinoma
  • Vulvar Paget disease
  • Adenocarcinoma
  • Transitional cell carcinoma
  • Verrucous carcinoma
  • Merkel cell tumors
  • Verrucous carcinoma

2. Vulvar malignant melanoma

3. Vulvar sarcoma

  • Leiomyosarcoma
  • Malignant fibrous histiocytoma
  • Epithelial sarcoma
Vulvar carcinomas Subtype Features on Gross Pathology Features on Histopathological Microscopic Analysis
Squamous cell carcinoma of vulva
  • Eosinophilia
  • Extra large nuclei/bizarre nuclei
  • Inflammation (lymphocytes, plasma cells)
  • Long rete ridges
  • Numerous beeds/blobs of epithelial cells that seem unlikely to be rete ridges
Basal cell carcinoma of vulva
  • Pearly nodule with telangiectasias
  • Basaloid cells - similar in appearance to basal cells:
  • Moderate blue/grey cytoplasm.
  • Dark ovoid/ellipsoid nucleus with uniform chromatin
  • Palisading of cells at the edge of the cell nests
  • Artefactual separation of cells (forming the nests) from the underlying stroma - key feature
  • Surrounded by blue (myxoid) stroma - key feature
Vulvar melanoma
  • Superficial spreading is the most common type
  • Brown/black color, but may include reddish brown or white
  • Hyperkeratotic, diffused borders with no distinct demarcation
  • Irregular and elevated
  • Presence of intraepidermal lateral spread (most characteristic feature)
  • Dermal invasion
  • Desmoplasia
  • Epidermal hyperplasia
  • Appearance of epithelioid cells with occasional spindle cells

References

  1. Hoffman, Barbara (2012). Williams gynecology. New York: McGraw-Hill Medical. ISBN 9780071716727.
  2. Malignant melanoma. Libre pathology. http://librepathology.org/wiki/index.php/Malignant_melanoma. URL Accessed on September 30, 2015
  3. Basal cell carcinoma . Libre pathology. http://librepathology.org/wiki/index.php/Basal_cell_carcinoma. URL Accessed on September 30, 2015
  4. Squamous cell carcinoma. Libre pathology. http://librepathology.org/wiki/index.php/Squamous_cell_carcinoma. URL Accessed on September 30, 2015