Vulvar cancer is a relatively rare malignancy affecting the external female genitalia, known collectively as the vulva. Questions often arise about its origins, specifically whether it is passed down through generations. While inherited risk is a concern, the vast majority of cases are tied to acquired factors that develop over a lifetime. Understanding the distinction between genetic predisposition and environmental influences is important for assessing personal risk and focusing on prevention.
Understanding Vulvar Cancer
Vulvar cancer forms in the tissues of the vulva, including the labia majora, labia minora, clitoris, and the openings of the urethra and vagina. Compared to other gynecological malignancies, vulvar cancer is uncommon, accounting for approximately 3% to 5% of all cancers of the female reproductive tract. The most prevalent form is squamous cell carcinoma, which arises from the thin, flat cells covering the vulvar surface and makes up about 90% of all diagnoses.
The disease typically progresses slowly, often starting as a precancerous condition referred to as vulvar intraepithelial neoplasia (VIN) or a high-grade squamous intraepithelial lesion (HSIL). These abnormal cell changes are confined to the skin’s surface and may take several years to transform into invasive cancer if left untreated. Less common types include melanoma, which originates in pigment-producing cells, and adenocarcinoma, which arises in glands beneath the skin.
Primary Acquired Risk Factors
The most significant cause of vulvar cancer is infection with the Human Papillomavirus (HPV), a sexually transmitted virus. High-risk HPV types, particularly HPV 16 and 18, are responsible for a large proportion of vulvar squamous cell carcinomas. This HPV-associated pathway often involves the development of VIN and tends to affect women at a younger age, sometimes under 50.
A distinct pathway involves chronic inflammatory skin disorders of the vulva. Lichen Sclerosus, a long-term condition causing thin, white, itchy patches of skin, is a notable example. This condition leads to constant irritation and inflammation, which can drive cellular changes and lead to HPV-negative vulvar cancer, a type more commonly seen in older women.
Advanced age is another non-modifiable risk factor; the average age for diagnosis of invasive vulvar cancer is around 70 years. The risk increases significantly after menopause, with more than half of all cases diagnosed in women over 70. This demographic often aligns with the non-HPV-associated cancers linked to chronic skin conditions.
Lifestyle habits also play a role, especially tobacco use. Smoking exposes the body to carcinogenic chemicals that increase the risk of vulvar cancer, particularly for individuals infected with high-risk HPV. Any condition that weakens the immune system, such as HIV infection or immunosuppressive medications, hinders the body’s ability to clear HPV and fight abnormal cell growth.
Assessing the Role of Genetics and Family History
Vulvar cancer is generally not categorized as a hereditary cancer like certain breast or ovarian cancers. Most cases arise from somatic mutations, which are acquired DNA changes occurring during a person’s lifetime and are not passed from parent to child. This means the primary drivers are acquired risk factors, such as HPV infection or chronic inflammatory disease, rather than an inherited genetic defect.
A family history of vulvar cancer or related conditions can slightly increase the need for vigilance. This may be due to shared environmental factors, like HPV exposure, or an unidentified genetic susceptibility that makes a person more prone to acquired risk factors. In rare instances, certain inherited disorders, such as Fanconi anemia, are linked to an elevated lifetime risk of developing vulvar cancer.
For the less common vulvar melanoma subtype, a family history of melanoma or the presence of atypical moles is considered a risk factor. While these specific genetic links exist, they account for a very small fraction of all vulvar cancer diagnoses. The vast majority of vulvar squamous cell carcinoma, the most common type, is not caused by a single gene mutation inherited at birth.
Screening and Prevention Strategies
Proactive management of risk factors is the most effective approach to preventing vulvar cancer. Primary prevention focuses on eliminating the most common acquired risk factor: high-risk HPV. The HPV vaccine is highly effective against the strains responsible for most vulvar cancers and is recommended for eligible individuals before exposure to the virus.
Cessation of smoking significantly lowers the risk, especially for those with a history of HPV infection, by allowing the immune system to function more effectively against abnormal cells. Secondary prevention centers on early detection through regular gynecological visits and self-examination. While there is no standard screening test like a Pap test for cervical cancer, an annual pelvic exam allows a healthcare provider to visually inspect the vulva for suspicious lesions.
Individuals should perform regular self-exams to become familiar with the appearance of their vulva and report any persistent changes to a doctor. These changes include chronic itching, pain, or the presence of new lumps or sores. Prompt diagnosis and treatment of precancerous lesions, like VIN, or management of chronic inflammatory conditions, such as Lichen Sclerosus, prevents progression to invasive cancer.