Multiple primary melanoma.

BACKGROUND: Incidence rates of cutaneous malignant melanoma (CMM) have been increasing for decades among Caucasian populations worldwide. Multiple factors identify persons at increased risk of CMM, including those with a family history of melanoma and those with atypical moles. Approximately 6-12% of melanomas are familial and approximately 12% of patients with familial melanoma have multiple primary melanomas. OBJECTIVE: To report a case of a patient with atypical moles and with 17 multiple primary melanomas. To review the literature on multiple primary melanomas as well as to review the genetics and treatment of melanoma. CONCLUSION: Patients with numerous atypical moles and a family or personal history of melanoma are at greatest risk for developing CMM. Patients from this population tend to develop CMM approximately 10 years earlier than the general population and have an increased risk for developing multiple primary melanomas. Since genetic tests capable of detecting individuals with an inherited susceptibility to CMM are not available, it is important to identify those patients with an increased risk and monitor them closely with regular total-body examinations.

A c-rasHa mutation in the metastasis of a human papillomavirus (HPV)-18 positive penile squamous cell carcinoma suggests a cooperative effect between HPV-18 and c-rasHa activation in malignant progression.

BACKGROUND: Human papillomaviruses (HPV) have been implicated in the etiology of anogenital squamous epithelial tumors. Of the 65 HPV strains, subtypes HPV-16 and HPV-18 frequently are associated with malignant conditions and are capable of transforming keratinocytes in vitro. However, additional cellular changes are necessary to confer tumorigenicity to HPV-infected cells. Secondary events implicated in the progression to malignancy include loss of tumor suppressor genes such as p53 and/or activation of cellular oncogenes such as c-rasHa. METHODS: Polymerase chain reaction (PCR) was used to identify HPV-16 or HPV-18 genetic sequence in primary penile squamous cell carcinoma and two inguinal lymph node metastases. p53 and c-rasHa loci were analyzed by sequencing of PCR-amplified genomic DNA. RESULTS: HPV-18 but not HPV-16 infection was found in the primary carcinoma and in inguinal metastases occurring 5 and 7 years after the initial lesion. Sequence analysis did not identify any p53 mutations in the primary carcinoma or its metastases. However, although the primary lesion and the 5-year metastasis encoded wild-type c-rasHa, the 7-year metastasis had a missense mutation within c-rasHa codon 61. CONCLUSIONS: To the authors' knowledge, this is the first report of an activating c-rasHa mutation associated with squamous cell carcinoma of the penis. The presence of activated c-rasHa in the second metastasis but not in the first metastasis or the primary lesion suggests that activation of c-rasHa may be a late event in the malignant progression of HPV-18-associated penile squamous cell carcinoma. Analysis of additional samples from primary lesions and their resultant metastases is necessary to elucidate the incidence and significance of c-rasHa activation in penile squamous cell carcinoma.

Basal cell carcinoma on the neck.

BACKGROUND: In our Mohs surgery practice, a large number of basal cell carcinomas (BCCs) occurring on the neck were noted to be of the superficial type. OBJECTIVE: Our purpose was to examine a series of consecutive cases of BCC on the neck. METHODS: We reviewed all cases of BCC on the neck that were treated in our Mohs surgery unit from 1988 to 1993. Permanent histologic sections of the BCCs, obtained by excisional debulking of the tumors, were examined and the BCCs were typed histologically. Each histologic type was correlated with the patient's age, race, sex, its location on the neck, and its status as either a primary or recurrent lesion. RESULTS: In total, 97 BCCs on the neck from 93 patients were examined. All patients were Caucasians with an average age of 62.7 years. A peak incidence in the fifth decade occurred in males while this peak occurred in the eighth decade for females. Males outnumbered females 3.4:1. The type and incidence of each BCC was studied with the following results: superficial (38.1%), mixed-superficial (30.0%), nodular (15.5%), infiltrative (7.2%), morpheaform (5.1%), adenoid (2.1%), keratotic (1.0%), and metatypical (1.0%). Fifty-one percent of the tumors were primary and 49% were recurrent. The most common location on the neck was the skin overlying the superior aspect of the sternocleidomastoid muscles. CONCLUSION: BCCs occurring on the neck were most commonly of the superficial type.