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Background: Molecular data suggest that peritoneal tumors in women with advanced-stage ovarian papillary serous adenocarcinoma are monoclonal in origin. Whether the same is true for ovarian tumors of low malignant potential is not known. We compared peritoneal and ovarian tumors from women with advanced-stage ovarian papillary serous tumors of low malignant potential to determine whether the peritoneal tumors arose from the same clone as the ovarian tumors., Methods: We studied the clonality of 73 peritoneal and ovarian tumors from 18 women with advanced-stage ovarian papillary serous tumors of low malignant potential. Formalin-fixed, paraffin-embedded tumors and representative normal tissues were sectioned and stained with hematoxylin-eosin, representative sections from separate tumors were manually microdissected, genomic DNA was extracted from the microdissected tumors, and the polymerase chain reaction was used to amplify a CAG polymorphic site in the human androgen receptor locus on the X chromosome to determine the inactivation pattern of the X chromosome and the clonality of the tumors., Results: The pattern of X-chromosome inactivation could be determined from the tumors of 13 of 18 patients. Of the 13 patients, seven (54%) had nonrandom inactivation of the X chromosome, and six of the seven had different inactivation patterns in the peritoneal and ovarian tumors. Three of these patients also had different patterns of nonrandom X-chromosome inactivation in tumors from each ovary. The remaining six patients had random patterns of X-chromosome inactivation in the peritoneal and ovarian tumors., Conclusions: Our data suggest that peritoneal and ovarian tumors of low malignant potential arise independently.

Recent ultrastructural, cytogenetic, and ploidy analyses indicate that seminoma acts as a precursor from which other forms of testicular germ cell tumor may originate. Ten cases of primary or metastatic testicular germ cell tumors were investigated that showed possible transformation of seminoma to yolk sac tumor. Such transformation was identified in six cases in which foci of abrupt change from seminoma to various patterns of yolk sac tumor occurred, often at the periphery of otherwise pure lobules of seminoma. Immunostains for cytokeratins, placental-like alkaline phosphatase, and alpha-fetoprotein demonstrated the expected changes in reactivity at the foci of such transformation. Four additional cases were regarded as either seminomas with artifactual microcystic change or the close association of seminoma and yolk sac tumor but lacking evidence for transformation. These data support the theory that seminoma is not an "endpoint" neoplasm but may serve a precursor role in the progression to nonseminomatous germ cell tumors.

Variability in classification in anatomic pathology does not necessarily indicate that a mistake has been made. It is usually an artifact, created when pathologists choose a single category from among two or more justifiable alternatives. This is most common when standard classifications with uniform terminology are not used. It also can occur when classification systems are not constructed so as to insure mutual exclusivity of categories. It is proposed that a proficiency test in anatomic pathology should not be considered scientifically valid until a professional organization primarily concerned with anatomic pathology has endorsed its proposed classification system as having categories that are close to 100% mutually exclusive in the hands of expert pathologists not involved in developing the system. All possible precautions should be taken to insure that the "right answers" for any proficiency test are generated in a way that excludes the possibility of multiple justifiable alternatives.

Six of 125 keloids of the earlobe demonstrated a peculiar accumulation of mucinous material within their stroma. The six patients had all received prior injections of a corticosteroid compound. The histopathologic picture is characterized by irregularly contoured pools of amorphous eosinophilic material surrounded by a variable granulomatous response of multinucleate giant cells and bubbly histiocytes. Histochemical studies demonstrated that the material is different from the hyaluronic acid-rich substances of the usual forms of cutaneous mucinoses. The lesion is similar to but distinct from that previously described to occur in nasal mucosa injected with corticosteroids. Its recognition and correlation with clinical history should prevent confusion with other entities.

We describe a retroperitoneal neoplasm in an 11-year-old girl which had a light microscopic appearance identical to that of papillary serous carcinoma of the ovary. There was no evidence of ovarian involvement. Immunohistochemical staining for amylase was positive within the cytoplasm of tumor cells. Since amylase is a marker for serous ovarian tumors, this finding supports the belief that "ovarian-type" neoplasms that occur at ectopic locations are essentially identical to their ovarian counterparts. We believe they originate from metaplasia of mesothelium. Our findings support the concept that these tumors should exhibit a biologic behavior and therapeutic response which are similar to those of an ovarian tumor of the same grade and comparable stage. The demonstration of intracytoplasmic amylase also may prove useful in differentiating peritoneal serous tumors from non-metaplastic mesothelial proliferations. We are unaware of a prior report of an extra-ovarian serous carcinoma in a child.

Yolk sac tumor and seminoma may have a similar appearance in focal areas. Small biopsies may therefore be difficult to interpret. The authors studied 20 yolk sac tumors and 21 seminomas to investigate the utility of immunohistochemical markers in this differential diagnosis. All yolk sac tumors stained positively for cytokeratin (CK) but so did 43% of seminomas. The CK positivity of yolk sac tumors was generally more diffuse and intense, however, there was an overlap in the spectrum of intensity of CK positivity in yolk sac tumor and seminoma. Alpha-fetoprotein (AFP) was a less sensitive (55%) marker for yolk sac tumor than CK, but AFP was quite specific in this differential diagnosis because no seminoma stained for AFP. Alpha-1-antitrypsin was not a very useful marker because of poor sensitivity and specificity. The interpretation of light microscopic patterns remains of paramount importance in the differentiation of solid yolk sac tumor from seminoma.

Examination by immunoperoxidase methods showed that two strumal carcinoids contained thyroxine in the follicular epithelium and colloid. Ultrastructure showed features of thyroid epithelia. Granule-containing cells replaced some follicular epithelial cells at the colloid interface. The morphology of the granules of these cells resembled those of C-cells and foregut-hindgut carcinoids. Transition between thyroid and carcinoid occurred by proliferation of interfollicular cells which subtly formed trabecular structures. Immunoperoxidase for calcitonin was positive both in the interfollicular cells of one tumor and in cells near the transition from thyroid to carcinoid pattern of the other. We conclude that thyroid tissue is a proven component of strumal carcinoid but that follicular epithelial cells may be replaced by granule-containing parafollicular cells. We suggest that the transition from thyroid to carcinoid is accomplished through an intermediate stage of calcitonin-positive cell proliferation. We emphasize, however, that these neoplasms are types of teratomas which may show several forms of differentiation. The tumor of one patient had mid-gut carcinoid elements and represents the first described strumal carcinoid with the carcinoid syndrome.