Overexpression of the Tumor-Suppressor Gene P53 in Human Ovarian Tumor-Tissues and Its Correlation With Clinical Stage

Imai, Satoki; Kiyozuka, Y; Nishimura, Haruo; Iwanaga, Shigeaki; Murakami, Fumihiro; Imamura, K; Noda, Tetsuo; Haga, Satomi; Yakushiji, M

doi:10.3892/ijo.4.5.1097

Cited by 5 publications

(5 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We examined 80 tumors for mutations of TP53 and K‐ras and this constitutes the single largest study of these genes in benign ovarian tumors. We detected TP53 mutations in 2/34 serous (6%) and 1/26 mucinous (4%) benign tumors, which is in contrast to most previous studies where no mutations were detected 31, 32, 33, 34. This discrepancy is most likely due to the fact that previous studies have examined insufficient numbers to detect a low frequency of mutations.…”

Section: Discussionmentioning

confidence: 99%

Cytotoxic/natural killer cell cutaneous lymphomas

Santucci

Pimpinelli

Massi

et al. 2003

Cancer

245

View full text Add to dashboard Cite

BACKGROUNDCutaneous lymphomas expressing a cytotoxic or natural killer (NK) cell phenotype represent a group of lymphoproliferative disorders for which there is currently much confusion and little consensus regarding the best nomenclature and classification.METHODSThis study analyzes 48 cases of primary cutaneous lymphoma expressing cytotoxic proteins and/or the NK cell marker, CD56. These cases were collected for a workshop of the European Organization for Research and Treatment of Cancer Cutaneous Lymphoma Task Force, to better clarify the clinical, morphologic, and phenotypic features of these uncommon tumors.RESULTSSeveral categories with different clinical and pathologic features were delineated: 1) aggressive, CD8+, epidermotropic, cytotoxic T‐cell lymphoma; 2) mycosis fungoides, cytotoxic immunophenotype variant; 3) subcutaneous panniculitis‐like T‐cell lymphoma; 4) NK/T‐cell lymphoma, nasal type; 5) CD4+, NK cell lymphoma; 6) blastoid NK cell lymphoma; (7) intravascular NK‐like lymphoma; and 8) cytotoxic, peripheral T‐cell lymphoma.CONCLUSIONSOur data show that primary cutaneous cytotoxic/NK cell lymphomas include distinct groups of diseases, clinically, histologically, and biologically. Because the finding of a cytotoxic phenotype often has prognostic significance, the routine use of cytotoxic markers in the diagnosis and classification of cutaneous lymphomas should be expanded. Cancer 2003;97:610–27. © 2003 American Cancer Society.DOI 10.1002/cncr.11107

show abstract

Section: Discussionmentioning

confidence: 99%

Cytotoxic/natural killer cell cutaneous lymphomas

Santucci

Pimpinelli

Massi

et al. 2003

Cancer

245

View full text Add to dashboard Cite

show abstract

“…We detected TP53 mutations in 2/34 serous (6%) and 1/26 mucinous (4%) benign tumors, which is in contrast to most previous studies where no mutations were detected. [31][32][33][34] This discrepancy is most likely due to the fact that previous studies have examined insufficient numbers to detect a low frequency of mutations. The only TP53 mutations previously reported in benign tumors have been in tumors contiguous with malignant carcinoma.…”

Section: Discussionmentioning

confidence: 99%

Genetic analysis of benign ovarian tumors

Thomas

Neville

Baxter

et al. 2003

Intl Journal of Cancer

View full text Add to dashboard Cite

Ovarian cancer represents a major cause of cancer death among women and yet remarkably little is known about its etiology. The paradigm established by the colorectal carcinogenesis model would suggest that ovarian cancers are likely to arise through malignant transformation of benign ovarian tumors. However, molecular genetic data that could answer this important question is lacking. In our study, we analyzed 80 benign ovarian tumors for TP53 and K-ras mutations and for LOH on chromosomes 6, 7, 9, 11 and 17 using 56 microsatellite markers. Twenty-five percent (5/20) of nonepithelial tumors and 73% (44/60) of epithelial tumors exhibited LOH on at least 1 chromosome arm. A particularly high frequency of LOH was detected among the epithelial tumors on chromosome arms 6q (17%), 7p (17%), 7q (27%) and 11p (18%), which are also regions of frequent LOH among ovarian carcinomas. No K-ras mutations were detected in any tumor but somatic TP53 mutations were detected in 2/34 (6%) serous and 1/26 (4%) mucinous epithelial tumors. In contrast to most previous studies our data is derived from a relatively large number of microdissected tumors and is likely to represent a more accurate picture of the frequency of alterations in these tumors. We conclude that LOH is common in benign ovarian tumors, suggesting that inactivation of tumor suppressor genes are pivotal in their development. The high frequency of alterations is consistent with their being precursors to malignant disease but does not unequivocally prove this continuum. It does however provide a framework for future analysis of the molecular genetic etiology of ovarian tumorigenesis.

show abstract

“…[62][63][64][65] However, a recent study utilizing microdissection 66 found TP53 mutations in 6% (2/24) of benign serous tumors. Zheng et al 67 and Wolf et al 68 found that benign cysts in continuity with serous carcinomas have similar cytogenetic and mutational changes, suggesting that such cysts already have genetic abnormalities that predispose them to malignant transformation.…”

Section: Molecular Genetic Datamentioning

confidence: 99%

Origins and molecular pathology of ovarian cancer

2005

View full text Add to dashboard Cite

Epithelial ovarian cancer comprises the majority of malignant ovarian tumors in adult women. These neoplasms are classified into distinct morphologic categories based on the appearance of the epithelium into tumors of serous, mucinous, endometrioid, clear cell, transitional, squamous, mixed and undifferentiated type. Current data indicate that each of these histologic subtypes is associated with distinct morphologic and molecular genetic alterations: high-grade serous and possibly endometrioid carcinomas most probably arise from surface epithelial inclusion glands with TP53 mutations and dysfunction of BRCA1 and/or BRCA2; low-grade serous carcinomas probably arise in a stepwise fashion in an adenoma-borderline tumor-carcinoma sequence from typical to micropapillary borderline tumors to low-grade invasive serous carcinoma via activation of the RAS-RAF signaling pathway secondary to mutations in KRAS and BRAF; mucinous carcinomas arise via an adenoma-borderline tumor-carcinoma sequence with mutations in KRAS; low-grade endometrioid carcinomas arise from endometriosis via mutations in CTNNB1 (the gene encoding b-catenin) and PTEN. Although the morphologic data strongly support an origin of clear cell carcinoma from endometriosis, there is limited data on the genetic alterations in these uncommon tumors. Thus it is likely that most low-grade, relatively indolent ovarian carcinomas of serous, mucinous and endometrioid type arise from pre-existing cystadenomas or endometriosis whereas most high-grade serous carcinomas arise without an easily identifiable precursor lesion. Modern Pathology (2005) 18, S19-S32. doi:10.1038/modpathol.3800306Keywords: ovarian cancer; ovarian borderline tumors; histogenesis; molecular pathology Epithelial ovarian cancer comprises the majority of malignant ovarian tumors in adult women. These neoplasms are classified into distinct morphologic categories based on the appearance of the epithelium into tumors of serous, mucinous, endometrioid, clear cell, transitional, squamous, mixed and undifferentiated type. 1,2 Two types of ovarian surface epithelial lesions have been described as possible precursors of these carcinomas: lesions that appear in situ in surface epithelium or surface epithelial inclusion glands (SEIG); and preexisting benign epithelial ovarian tumors and endometriosis. The morphologic and genetic data implicating each as a precursor lesion of the major histologic subtypes of ovarian carcinoma are discussed. Surface epithelium and surface epithelial inclusion glands as precursor lesions Morphologic DataTwo types of morphologic data are available regarding the malignant potential of ovarian surface epithelium and inclusion glands, alterations in these structures and studies on microscopic ovarian carcinoma.Surface epithelium and surface epithelial inclusion glands Despite the widespread acceptance of the origin of surface epithelial cancers from the ovarian surface epithelium and its inclusion glands, only rarely have putative precursor lesions been described at these sites. Two...

show abstract

Overexpression of the Tumor-Suppressor Gene P53 in Human Ovarian Tumor-Tissues and Its Correlation With Clinical Stage

Cited by 5 publications

References 0 publications

Cytotoxic/natural killer cell cutaneous lymphomas

Cytotoxic/natural killer cell cutaneous lymphomas

Genetic analysis of benign ovarian tumors

Origins and molecular pathology of ovarian cancer

Contact Info

Product

Resources

About