Serous psammocarcinoma of the ovary and peritoneum
01 Apr 1990-International Journal of Gynecological Pathology (Int J Gynecol Pathol)-Vol. 9, Iss: 2, pp 110-121
TL;DR: The clinical behavior of psammocarcinoma more closely resembles that of borderline serous tumors than of serous carcinomas of the usual type, following a protracted course and being associated with a relatively favorable prognosis.
Abstract: We report 11 cases of serous psammocarcinoma, a rare variant of serous carcinoma characterized by massive psammoma body formation and low-grade cytological features. The patients ranged in age from 36 to 76 (mean of 57) years. The tumors were stage three in every case (three stage IIIA, seven stage IIIB, and one stage IIIC). Eight of the patients had ovarian psammocarcinomas with ovarian tumors measuring 5-22 (mean of 11) cm in diameter; the other three patients had primary peritoneal psammocarcinomas. The surfaces of the ovarian tumors were smooth and intact in seven of eight ovarian psammocarcinomas. Cysts were present in six of eight ovarian tumors, and the solid portions were typically gritty or granular. Necrosis was not seen. Microscopically there was destructive invasion of ovarian stroma or vascular invasion in the ovarian tumors; the extraovarian tumor implants were invasive of intraperitoneal viscera in five cases. The epithelium was arranged in small nests with no areas of solid epithelial proliferation, and at least 75% of the epithelial nests were associated with psammoma body formation. No more than moderate nuclear atypicality was identified in any case. No mitotic figures were found in 10 of the tumors, with a single mitotic figure identified in the other tumor. Follow-up data for more than 1 year was available for six patients, with two patients lost to follow-up and three patients followed without evidence of recurrence for less than 1 year. One patient died of tumor 6 1/2 years after presentation, and five patients were alive without evidence of recurrent tumor 3-10 (mean of 8.3) years after presentation. Although based on a small number of cases, these data suggest that the clinical behavior of psammocarcinoma more closely resembles that of borderline serous tumors than of serous carcinomas of the usual type, following a protracted course and being associated with a relatively favorable prognosis.
Citations
More filters
TL;DR: A group of serous neoplasms that have distinctive morphologic features and that are often associated with progressive, invasive disease are described, characterized by a filigree pattern of highly complex micropapillae arising directly from large, bulbous papillary structures.
Abstract: According to the International Federation of Gynecology and Obstetrics (FIGO) and the World Health Organization (WHO), stromal invasion, defined as destructive infiltrative growth, is the sole criterion used to distinguish serous borderline tumors from invasive serous carcinomas of the ovary. Although this criterion effectively identifies most malignant tumors, it does not permit the identification of a small subset of well-differentiated ovarian carcinomas that do not display destructive infiltrative growth but that may be associated with malignant behavior. In this study, we describe a group of such serous neoplasms that have distinctive morphologic features and that are often associated with progressive, invasive disease. We have designated these tumors micropapillary serous carcinomas (MPSC). They are characterized by a filigree pattern of highly complex micropapillae arising directly from large, bulbous papillary structures. The micropapillae are covered by round to cuboidal cells with a high nuclear-to-cytoplasmic ratio. Typical serous borderline tumors tend to display a hierarchical pattern of branching terminating in small papillae or tufts, and the cells covering the papillae tend to be more columnar and often ciliated compared with cells of MPSC. We reviewed more than 400 cases of serous ovarian borderline tumors and well-differentiated serous carcinomas and identified 26 cases of MPSC. Seventeen tumors lacked destructive infiltrative growth (noninvasive), and nine contained areas of invasion ranging from minimal to extensive. Eight of the 26 tumors were stage I, and none of the patients developed recurrence whether or not their tumors had demonstrable invasion. In contrast, of the 16 women presenting with stage II disease or higher and who had more than 1 year of follow-up, eight (50%) have either died of intra-abdominal carcinomatosis or are alive with carcinoma. Twenty-four (92%) of MPSCs contained areas of serous borderline tumor. The frequent association of MPSCs with serous borderline tumors suggests that MPSCs arise from the latter and may account for the few cases of serous borderline tumors that have been associated with progression to invasive carcinoma.
314 citations
TL;DR: The finding that at least 60% of serous borderline tumours harbour mutations in two members of the ERK‐MAP‐kinase pathway compared with 12% of high‐grade serous carcinomas (BRAF 0%, KRAS 12%) indicates that the majority of serious borderline tumoured tumours do not progress to serious carcinomas.
Abstract: Genes of the RAF family, which mediate cellular responses to growth signals, encode kinases that are regulated by RAS and participate in the RAS/RAF/MEK/ERK/MAP-kinase pathway. Activating mutations in BRAF have recently been identified in melanomas, colorectal cancers, and thyroid and ovarian tumours. In the present study, an extensive characterization of BRAF and KRAS mutations has been performed in 264 epithelial and non-epithelial ovarian neoplasms. The epithelial tumours ranged from adenomas and borderline neoplasms to invasive carcinomas including serous, mucinous, clear cell, and endometrioid lesions. It is shown that BRAF mutations in ovarian tumours occur exclusively in low-grade serous neoplasms (33 of 91, 36%); these included serous borderline tumours (typical and micropapillary variants), an invasive micropapillary carcinoma and a psammocarcinoma. KRAS mutations were identified in 26 of 91 (29.5%) low-grade serous tumours, 7 of 49 (12%) high-grade serous carcinomas, 2 of 6 mucinous adenomas, 22 of 28 mucinous borderline tumours, and 10 of 18 mucinous carcinomas. Of note, two serous borderline tumours were found to harbour both BRAF and KRAS mutations. The finding that at least 60% of serous borderline tumours harbour mutations in two members of the ERK-MAP-kinase pathway (BRAF 36%, KRAS 30%) compared with 12% of high-grade serous carcinomas (BRAF 0%, KRAS 12%) indicates that the majority of serous borderline tumours do not progress to serous carcinomas. Furthermore, no BRAF mutations were detected in the other 173 ovarian tumours in this study.
251 citations
Cites background from "Serous psammocarcinoma of the ovary..."
...A BRAF mutation was also identified in another type of low-grade serous neoplasm, namely a psammocarcinoma [16]; analysis of a large group of this sub-type is essential before the significance of this finding can be evaluated....
[...]
01 Jan 1994
TL;DR: For practical reasons, pure mullerian mesenchymal tumors are noted briefly in this chapter, completing the spectrum that traditionally has encompassed endometrioid stromal sarcomas and malignant mixed Mullerian tumors.
Abstract: The ovaries do not arise from the mullerian ducts, yet they are commonly the site of a range of neoplasms seen elsewhere in the mullerian duct derivatives. These loosely associated, principally epithelial, neoplasms are generally accepted as originating from the surface epithelium (modified mesothelium) and subjacent stroma of the ovaries. In the second version of the World Health Organization (WHO) classification of ovarian tumors, these neoplasms are designated as surface epithelial-stromal tumors. The epithelial elements resemble those within tumors found in the fallopian tubes, uterus, cervix, and upper vagina. Transitional cell (formerly Brenner) tumors, as well as those mucinous tumors of “intestinal” differentiation, are retained in a classification of best fit. For practical reasons, pure mullerian mesenchymal tumors are noted briefly in this chapter, completing the spectrum that traditionally has encompassed endometrioid stromal sarcomas and malignant mixed mullerian tumors. Their approximate relative frequencies are shown in Table 18.1.
183 citations
01 Jan 1994
TL;DR: This chapter considers the wide range of nonneoplastic and neoplastic lesions that involve the peritoneum, and in some cases the retroperitoneal lymph nodes, of females.
Abstract: This chapter considers the wide range of nonneoplastic and neoplastic lesions that involve the peritoneum, and in some cases the retroperitoneal lymph nodes, of females. The first half of the chapter deals with inflammatory lesions, tumor-like lesions (including mesothelial hyperplasia), mesothelial neoplasms, miscellaneous primary tumors, and metastatic tumors. The second half of the chapter is devoted to a large group of lesions that share a potential origin from the secondary mullerian system, the prototypical example of which is endometriosis.
183 citations
TL;DR: It is suggested that rather than being the outcome of dystrophic calcification of dead or dying tissue, PBs may indeed represent an active biologic process ultimately leading to degeneration/death of tumor cells and retardation of growth of the neoplasm.
Abstract: Psammoma bodies (PBs) are concentric lamellated calcified structures, observed most commonly in papillary thyroid carcinoma (PTC), meningioma, and papillary serous cystadenocarcinoma of ovary but have rarely been reported in other neoplasms and nonneoplastic lesions. PBs are said to represent a process of dystrophic calcification. Despite numerous ancillary studies over a span of three and half decades, formation of PBs remains a poorly understood mechanism. Ultrastructural study of PTC has shown that thickening of the base lamina in vascular stalk of neoplastic papillae followed by thrombosis, calcification, and tumor cell necrosis leads to formation of PBs. Studies on serous cystadenocarcinoma of ovary and meningioma, however, revealed that collagen production by neoplastic cells and subsequent calcification was responsible for the formation of PBs. The existence of some precursor forms of PBs was reported in meningiomas and more recently in PTC, which were mostly in the form of extracellular hyaline globules surrounded by well-preserved neoplastic cells or in a smaller number of cases intracytoplasmic bodies liberated from intact tumor cells. Cellular degeneration and necrosis, leading to the disappearance of neoplastic cells, were noticed by us only around PBs but not around the precursor forms. Based on the above findings, it is suggested that rather than being the outcome of dystrophic calcification of dead or dying tissue, PBs may indeed represent an active biologic process ultimately leading to degeneration/death of tumor cells and retardation of growth of the neoplasm. It may also serve as a barrier against the spread of neoplasm.
120 citations