Hereditary ovarian cancer accounts for at least 5% of the estimated 22,000 new cases of this disease during 2009. During this same time, over 15,000 will die from malignancy ascribed to ovarian origin. The bulk of these hereditary cases fits the hereditary breast-ovarian cancer syndrome, while virtually all of the remainder will be consonant with the Lynch syndrome, disorders which are autosomal dominantly inherited. Advances in molecular genetics have led to the identification of BRCA1 and BRCA2 gene mutations which predispose to the hereditary breast-ovarian cancer syndrome, and mutations in mismatch repair genes, the most common of which are MSH2 and MLH1, which predispose to Lynch syndrome. These discoveries enable relatively certain diagnosis, limited only by their variable penetrance, so that identification of mutation carriers through a comprehensive cancer family history might be possible. This paper reviews the subject of hereditary ovarian cancer, with particular attention to its molecular genetic basis, its pathology, and its phenotypic/genotypic heterogeneity.

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Metastasis into a thyroid neoplasm—tumor-to-tumor metastasis—is exceedingly rare. We describe the 28th documented case of a tumor metastatic to a thyroid neoplasm and review the literature on tumor-to-tumor metastasis involving a thyroid neoplasm as recipient. All cases showed a recipient thyroid neoplasm with an abrupt transition to a morphologically distinct neoplasm. Metastasis into primary thyroid neoplasm was synchronous in 33% of cases and metachronous in 67%. Follicular adenoma was the most common recipient thyroid neoplasm overall (16/28), and papillary thyroid carcinoma was the most common malignant recipient neoplasm (9/28). Of the 9 recipient papillary carcinomas, 6 were follicular variants. Renal cell carcinoma was the most common neoplasm to metastasize to a primary thyroid neoplasm (9/28), followed by lung (6/28), breast (5/28), and colon (3/28) carcinoma. Tumor-to-tumor metastasis should be considered whenever a dimorphic pattern is encountered in a thyroid tumor.

Prepregnancy human and guinea pig cytomegalovirus immunity reduces rates of congenital infection in subsequent pregnancies. Inbred JY-9 strain guinea pigs were used to study the role of hyperimmune anti-glycoprotein B (gB) serum in modification of congenital infection in early pregnancy. Significantly shorter duration of primary maternal viremia and fewer pregnancy losses occurred in passively immunized dams, compared with nonimmune dams. Placentas from recipients of negative control serum were smaller and had marked mononuclear cell infiltrates and focal necrosis and more viral foci than did those from recipients of anti-gB hyperimmune serum. Significantly higher intrauterine growth retardation occurred in pups of negative control serum recipients than in pups of passively immunized dams. Significantly higher proportions of pups and placentas from recipients of negative control serum were positive on viral culture than from passively immunized dams. Thus, anti-gB passive immunization decreased fetal infection and intrauterine growth retardation, shortened maternal viremia, and reduced pregnancy losses and placental inflammation and infection.