Ovarian carcinomas: at least five different diseases with distinct histological features and molecular genetics
Based on histopathology and molecular genetics, ovarian carcinomas are divided into five main types: high-grade serous (70%), endometrioid (10%), clear cell (10%), mucinous (3%), and low-grade serous (
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| Veröffentlicht in: | Human pathology 2018-10, Vol.80, p.11-27 |
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| creator | Prat, Jaime D'Angelo, Emanuela Espinosa, Iñigo |
| description | Based on histopathology and molecular genetics, ovarian carcinomas are divided into five main types: high-grade serous (70%), endometrioid (10%), clear cell (10%), mucinous (3%), and low-grade serous ( |
| doi_str_mv | 10.1016/j.humpath.2018.06.018 |
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•The main types of ovarian carcinomas differ in pathogenesis, behavior and prognosis•In high-grade serous, p53 and BRCA loss and high-copy number lead to heterogeneity•Low-grade serous result from progression of borderline tumors through KRAS mutations•Mucinous: KRAS mutations, overexpression/amplification of HER2, both, or neither•Endometrioid and clear cell arise from endometriosis through ARID1A, PTEN and PIK3CA mutations</description><identifier>ISSN: 0046-8177</identifier><identifier>EISSN: 1532-8392</identifier><identifier>DOI: 10.1016/j.humpath.2018.06.018</identifier><identifier>PMID: 29944973</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adenocarcinoma, Clear Cell - genetics ; Adenocarcinoma, Clear Cell - pathology ; Adenocarcinoma, Mucinous - genetics ; Adenocarcinoma, Mucinous - pathology ; Age ; Animals ; Chemotherapy ; Clear cell carcinoma ; Endometrial cancer ; Endometrioid carcinoma ; Endometriosis ; Female ; High-grade serous carcinoma ; Humans ; Low-grade serous carcinoma ; Lymphatic system ; Medical prognosis ; Metastasis ; Mucinous carcinoma ; Mutation ; Mutation - genetics ; Ovarian cancer ; Ovarian Neoplasms - genetics ; Ovarian Neoplasms - pathology ; Ovary ; Pathology, Molecular - methods ; Stem cells ; Tumors ; Uterine Neoplasms - genetics ; Uterine Neoplasms - pathology</subject><ispartof>Human pathology, 2018-10, Vol.80, p.11-27</ispartof><rights>2018 Elsevier Inc.</rights><rights>Copyright © 2018 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Oct 2018</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c393t-3ab9ff901bc017432f2c4709fd8bc0621cca2f53480bc1bfedda1542884caf1e3</citedby><cites>FETCH-LOGICAL-c393t-3ab9ff901bc017432f2c4709fd8bc0621cca2f53480bc1bfedda1542884caf1e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0046817718302302$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29944973$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Prat, Jaime</creatorcontrib><creatorcontrib>D'Angelo, Emanuela</creatorcontrib><creatorcontrib>Espinosa, Iñigo</creatorcontrib><title>Ovarian carcinomas: at least five different diseases with distinct histological features and molecular genetics</title><title>Human pathology</title><addtitle>Hum Pathol</addtitle><description>Based on histopathology and molecular genetics, ovarian carcinomas are divided into five main types: high-grade serous (70%), endometrioid (10%), clear cell (10%), mucinous (3%), and low-grade serous (<5%) carcinomas. These tumors, which account for over 95% of cases, represent distinct diseases with different prognoses and treatments. TP53 mutations are identified in almost all (96%) high-grade serous carcinomas (HGSCs). Early p53 loss followed by BRCA loss leads to deficiency in homologous recombination (DHR) repair, which in turn triggers chromosomal instability and widespread somatic copy number changes. An undetermined number of cases of HGSCs originate in the tubal fimbria; however, an origin from the ovarian surface epithelium cannot be totally excluded. Low-grade serous carcinomas (LGSCs) most likely represent progression of SBTs. BRAF or KRAS mutations occur in one-third to one-half of cases. Mucinous carcinomas (MCs) typically show benign-appearing, borderline, non-invasive and invasive components indicating tumor progression. KRAS mutations occur in 43.6% of cases and overexpression/amplification of HER2 in 18.8%. Endometrioid and clear cell carcinomas (EC and CCC) originate from ovarian endometriosis. Compared with their uterine counterparts, ECs have a similar frequency of β-catenin abnormalities but lower rate of microsatellite instability (MI) and PTEN alterations. ARID1A mutations occur in both ECs (30%) and CCCs (50%) and may be encountered in adjacent endometriosis. CCCs carry inactivating PTEN mutations and activating mutations in PIK3CA in 8% and 33% of cases, respectively. This review summarizes recent advances in the molecular pathology, which have greatly improved our understanding of the biology of ovarian carcinomas and are also relevant to patient management.
•The main types of ovarian carcinomas differ in pathogenesis, behavior and prognosis•In high-grade serous, p53 and BRCA loss and high-copy number lead to heterogeneity•Low-grade serous result from progression of borderline tumors through KRAS mutations•Mucinous: KRAS mutations, overexpression/amplification of HER2, both, or neither•Endometrioid and clear cell arise from endometriosis through ARID1A, PTEN and PIK3CA mutations</description><subject>Adenocarcinoma, Clear Cell - genetics</subject><subject>Adenocarcinoma, Clear Cell - pathology</subject><subject>Adenocarcinoma, Mucinous - genetics</subject><subject>Adenocarcinoma, Mucinous - pathology</subject><subject>Age</subject><subject>Animals</subject><subject>Chemotherapy</subject><subject>Clear cell carcinoma</subject><subject>Endometrial cancer</subject><subject>Endometrioid carcinoma</subject><subject>Endometriosis</subject><subject>Female</subject><subject>High-grade serous carcinoma</subject><subject>Humans</subject><subject>Low-grade serous carcinoma</subject><subject>Lymphatic system</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Mucinous carcinoma</subject><subject>Mutation</subject><subject>Mutation - genetics</subject><subject>Ovarian cancer</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - pathology</subject><subject>Ovary</subject><subject>Pathology, Molecular - methods</subject><subject>Stem cells</subject><subject>Tumors</subject><subject>Uterine Neoplasms - genetics</subject><subject>Uterine Neoplasms - pathology</subject><issn>0046-8177</issn><issn>1532-8392</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1vFDEMhiMEokvhJ4AicellhnzNFxeEqlIqVeoFzpEn43SzmkmWJLOo_56sduHApafXth7biV9C3nNWc8bbT7t6uy57yNtaMN7XrK2LvCAb3khR9XIQL8mGMdVWPe-6C_ImpR1jnDeqeU0uxDAoNXRyQ8LDAaIDTw1E43xYIH2mkOmMkDK17oB0ctZiRJ9LlEoZE_3t8vaYZedNptsShDk8OgMztQh5jYUBP9ElzGjWGSJ9RI_ZmfSWvLIwJ3x31kvy89vNj-vv1f3D7d311_vKyEHmSsI4WDswPhrGOyWFFUZ1bLBTXyqt4MaAsI1UPRsNHy1OE5S_ib5XBixHeUmuTnP3MfxaMWW9uGRwnsFjWJMWrGV9x9umKejH_9BdWKMvr9OC81Z2nVRDoZoTZWJIKaLV--gWiE-aM310RO_02RF9dESzVhcpfR_O09dxwelf118LCvDlBGA5x8Fh1Mk49AYnF9FkPQX3zIo_xouheQ</recordid><startdate>201810</startdate><enddate>201810</enddate><creator>Prat, Jaime</creator><creator>D'Angelo, Emanuela</creator><creator>Espinosa, Iñigo</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201810</creationdate><title>Ovarian carcinomas: at least five different diseases with distinct histological features and molecular genetics</title><author>Prat, Jaime ; D'Angelo, Emanuela ; Espinosa, Iñigo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c393t-3ab9ff901bc017432f2c4709fd8bc0621cca2f53480bc1bfedda1542884caf1e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adenocarcinoma, Clear Cell - genetics</topic><topic>Adenocarcinoma, Clear Cell - pathology</topic><topic>Adenocarcinoma, Mucinous - genetics</topic><topic>Adenocarcinoma, Mucinous - pathology</topic><topic>Age</topic><topic>Animals</topic><topic>Chemotherapy</topic><topic>Clear cell carcinoma</topic><topic>Endometrial cancer</topic><topic>Endometrioid carcinoma</topic><topic>Endometriosis</topic><topic>Female</topic><topic>High-grade serous carcinoma</topic><topic>Humans</topic><topic>Low-grade serous carcinoma</topic><topic>Lymphatic system</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>Mucinous carcinoma</topic><topic>Mutation</topic><topic>Mutation - genetics</topic><topic>Ovarian cancer</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Ovarian Neoplasms - pathology</topic><topic>Ovary</topic><topic>Pathology, Molecular - methods</topic><topic>Stem cells</topic><topic>Tumors</topic><topic>Uterine Neoplasms - genetics</topic><topic>Uterine Neoplasms - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Prat, Jaime</creatorcontrib><creatorcontrib>D'Angelo, Emanuela</creatorcontrib><creatorcontrib>Espinosa, Iñigo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Human pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Prat, Jaime</au><au>D'Angelo, Emanuela</au><au>Espinosa, Iñigo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ovarian carcinomas: at least five different diseases with distinct histological features and molecular genetics</atitle><jtitle>Human pathology</jtitle><addtitle>Hum Pathol</addtitle><date>2018-10</date><risdate>2018</risdate><volume>80</volume><spage>11</spage><epage>27</epage><pages>11-27</pages><issn>0046-8177</issn><eissn>1532-8392</eissn><abstract>Based on histopathology and molecular genetics, ovarian carcinomas are divided into five main types: high-grade serous (70%), endometrioid (10%), clear cell (10%), mucinous (3%), and low-grade serous (<5%) carcinomas. These tumors, which account for over 95% of cases, represent distinct diseases with different prognoses and treatments. TP53 mutations are identified in almost all (96%) high-grade serous carcinomas (HGSCs). Early p53 loss followed by BRCA loss leads to deficiency in homologous recombination (DHR) repair, which in turn triggers chromosomal instability and widespread somatic copy number changes. An undetermined number of cases of HGSCs originate in the tubal fimbria; however, an origin from the ovarian surface epithelium cannot be totally excluded. Low-grade serous carcinomas (LGSCs) most likely represent progression of SBTs. BRAF or KRAS mutations occur in one-third to one-half of cases. Mucinous carcinomas (MCs) typically show benign-appearing, borderline, non-invasive and invasive components indicating tumor progression. KRAS mutations occur in 43.6% of cases and overexpression/amplification of HER2 in 18.8%. Endometrioid and clear cell carcinomas (EC and CCC) originate from ovarian endometriosis. Compared with their uterine counterparts, ECs have a similar frequency of β-catenin abnormalities but lower rate of microsatellite instability (MI) and PTEN alterations. ARID1A mutations occur in both ECs (30%) and CCCs (50%) and may be encountered in adjacent endometriosis. CCCs carry inactivating PTEN mutations and activating mutations in PIK3CA in 8% and 33% of cases, respectively. This review summarizes recent advances in the molecular pathology, which have greatly improved our understanding of the biology of ovarian carcinomas and are also relevant to patient management.
•The main types of ovarian carcinomas differ in pathogenesis, behavior and prognosis•In high-grade serous, p53 and BRCA loss and high-copy number lead to heterogeneity•Low-grade serous result from progression of borderline tumors through KRAS mutations•Mucinous: KRAS mutations, overexpression/amplification of HER2, both, or neither•Endometrioid and clear cell arise from endometriosis through ARID1A, PTEN and PIK3CA mutations</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>29944973</pmid><doi>10.1016/j.humpath.2018.06.018</doi><tpages>17</tpages></addata></record> |
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| subjects | Adenocarcinoma, Clear Cell - genetics Adenocarcinoma, Clear Cell - pathology Adenocarcinoma, Mucinous - genetics Adenocarcinoma, Mucinous - pathology Age Animals Chemotherapy Clear cell carcinoma Endometrial cancer Endometrioid carcinoma Endometriosis Female High-grade serous carcinoma Humans Low-grade serous carcinoma Lymphatic system Medical prognosis Metastasis Mucinous carcinoma Mutation Mutation - genetics Ovarian cancer Ovarian Neoplasms - genetics Ovarian Neoplasms - pathology Ovary Pathology, Molecular - methods Stem cells Tumors Uterine Neoplasms - genetics Uterine Neoplasms - pathology |
| title | Ovarian carcinomas: at least five different diseases with distinct histological features and molecular genetics |
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