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Presents information on family cancer syndromes. Names of the hereditary diseases; Incidence of the diseases; What are the diagnosis of the syndromes; Mutations of the syndromes.

Traditionally, cisplatin has not been regarded among chemotherapeutic drugs as a carcinogenic risk to humans because it is not a classical alkylating agent. A review of recently published experimental data indicates that cisplatin is mutagenic, clastogenic, capable of inducing cell transformation, able to act as an initiator in classical mouse skin initiation/promotion experiments, and carcinogenic in laboratory animals. Notably, it causes myeloid leukemia in BD IX rats. These observations demonstrate that cisplatin should be considered a potent carcinogen in experimental settings. A review of the literature identified 65 instances of subsequent cancer in patients receiving cisplatin-based chemotherapy for an initial malignancy. The majority of second cancers were acute nonlymphocytic leukemias or myelodysplasia. In only one instance was cisplatin the sole antineoplastic drug given to patients. The routine use of cisplatin in conjunction with other known or suspected human carcinogens makes it impossible to use these anecdotal reports as a basis for assessing cisplatin‘s carcinogenicity in humans. Two quantitative epidemiologic studies have addressed this question: One suggested that the combination of cisplatin and doxorubicin is leukemogenic in humans, while the other implicated etoposide rather than cisplatin as the leukemogen. Formal epidemiologic studies of appropriate cohorts of cisplatin-treated patients are needed to resolve the question of its carcinogenicity in humans. [J Natl Cancer Inst 84: 306–312, 1992) [ABSTRACT FROM PUBLISHER]

The article comments on a study conducted by Timothy R. Rebbeck and colleagues concerning meta-analysis of risk reduction estimates associated with risk-reducing salpingo-oophorectomy (RRSO) in BRCA1 and BRCA2 mutation carriers. The study found that RRSO is strongly associated with reductions in the risk of breast and ovarian/fallopian cancers.

The author reflects on the importance of data sharing in genetic research as demonstrated by the study conducted by S.L. Zheng and others on the association of single-nucleotide polymorphisms (SNPs) on the risk of prostate cancer. He declares that the rapid posting of Human Genome Project data in the public domain ensured timely access to large quantities of genetic data for analyses. He believes that readily accessible genotype datasets are critical for the continued advance of genetic research.