Epigenetic silencing of MLH1 in endometrial cancers is associated with larger tumor volume, increased rate of lymph node positivity and reduced recurrence-free survival
•MLH1 methylated endometrial tumors have poor prognostic features including larger size.•Tumor volume and mismatch repair class are associated with lymph node involvement.•Women with MLH1 methylated tumors have reduced recurrence-free survival.•Recurrence rate by MMR class differed dramatically in a...
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| Veröffentlicht in: | Gynecologic oncology 2017-09, Vol.146 (3), p.588-595 |
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| creator | Cosgrove, Casey M. Cohn, David E. Hampel, Heather Frankel, Wendy L. Jones, Dan McElroy, Joseph P. Suarez, Adrian A. Zhao, Weiqiang Chen, Wei Salani, Ritu Copeland, Larry J. O'Malley, David M. Fowler, Jeffrey M. Yilmaz, Ahmet Chassen, Alexis S. Pearlman, Rachel Goodfellow, Paul J. Backes, Floor J. |
| description | •MLH1 methylated endometrial tumors have poor prognostic features including larger size.•Tumor volume and mismatch repair class are associated with lymph node involvement.•Women with MLH1 methylated tumors have reduced recurrence-free survival.•Recurrence rate by MMR class differed dramatically in advanced stage endometrial cancer.•MMR defective tumors with MLH1 methylation may exhibit chemoresistance.
To determine the relationship between mismatch repair (MMR) classification and clinicopathologic features including tumor volume, and explore outcomes by MMR class in a contemporary cohort.
Single institution cohort evaluating MMR classification for endometrial cancers (EC). MMR immunohistochemistry (IHC)±microsatellite instability (MSI) testing and reflex MLH1 methylation testing was performed. Tumors with MMR abnormalities by IHC or MSI and MLH1 methylation were classified as epigenetic MMR deficiency while those without MLH1 methylation were classified as probable MMR mutations. Clinicopathologic characteristics were analyzed.
466 endometrial cancers were classified; 75% as MMR proficient, 20% epigenetic MMR defects, and 5% as probable MMR mutations. Epigenetic MMR defects were associated with advanced stage, higher grade, presence of lymphovascular space invasion, and older age. MMR class was significantly associated with tumor volume, an association not previously reported. The epigenetic MMR defect tumors median volume was 10,220mm3 compared to 3321mm3 and 2,846mm3, for MMR proficient and probable MMR mutations respectively (P |
| doi_str_mv | 10.1016/j.ygyno.2017.07.003 |
| format | Article |
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To determine the relationship between mismatch repair (MMR) classification and clinicopathologic features including tumor volume, and explore outcomes by MMR class in a contemporary cohort.
Single institution cohort evaluating MMR classification for endometrial cancers (EC). MMR immunohistochemistry (IHC)±microsatellite instability (MSI) testing and reflex MLH1 methylation testing was performed. Tumors with MMR abnormalities by IHC or MSI and MLH1 methylation were classified as epigenetic MMR deficiency while those without MLH1 methylation were classified as probable MMR mutations. Clinicopathologic characteristics were analyzed.
466 endometrial cancers were classified; 75% as MMR proficient, 20% epigenetic MMR defects, and 5% as probable MMR mutations. Epigenetic MMR defects were associated with advanced stage, higher grade, presence of lymphovascular space invasion, and older age. MMR class was significantly associated with tumor volume, an association not previously reported. The epigenetic MMR defect tumors median volume was 10,220mm3 compared to 3321mm3 and 2,846mm3, for MMR proficient and probable MMR mutations respectively (P<0.0001). Higher tumor volume was associated with lymph node involvement. Endometrioid EC cases with epigenetic MMR defects had significantly reduced recurrence-free survival (RFS). Among advanced stage (III/IV) endometrioid EC the epigenetic MMR defect group was more likely to recur compared to the MMR proficient group (47.7% vs 3.4%) despite receiving similar adjuvant therapy. In contrast, there was no difference in the number of early stage recurrences for the different MMR classes.
MMR testing that includes MLH1 methylation analysis defines a subset of tumors that have worse prognostic features and reduced RFS.</description><identifier>ISSN: 0090-8258</identifier><identifier>EISSN: 1095-6859</identifier><identifier>DOI: 10.1016/j.ygyno.2017.07.003</identifier><identifier>PMID: 28709704</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Age Factors ; Aged ; Disease-Free Survival ; DNA Methylation ; DNA mismatch repair ; DNA Mismatch Repair - genetics ; Endometrial cancer ; Endometrial Neoplasms - chemistry ; Endometrial Neoplasms - genetics ; Endometrial Neoplasms - pathology ; Epigenesis, Genetic ; Epigenomics ; Female ; Gene Silencing ; Humans ; Lymph node excision ; Lymphatic Metastasis ; Lynch syndrome ; Microsatellite Instability ; Middle Aged ; Mutation ; MutL Protein Homolog 1 - analysis ; MutL Protein Homolog 1 - genetics ; Neoplasm Grading ; Neoplasm Invasiveness - genetics ; Neoplasm Recurrence, Local - genetics ; Neoplasm Staging ; Tumor Burden - genetics</subject><ispartof>Gynecologic oncology, 2017-09, Vol.146 (3), p.588-595</ispartof><rights>2017 Elsevier Inc.</rights><rights>Copyright © 2017 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c459t-7dd93558b49bd20a8808fb8bcaf2ad33eab70c554e2e3222ce73db54c402026a3</citedby><cites>FETCH-LOGICAL-c459t-7dd93558b49bd20a8808fb8bcaf2ad33eab70c554e2e3222ce73db54c402026a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0090825817309800$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28709704$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cosgrove, Casey M.</creatorcontrib><creatorcontrib>Cohn, David E.</creatorcontrib><creatorcontrib>Hampel, Heather</creatorcontrib><creatorcontrib>Frankel, Wendy L.</creatorcontrib><creatorcontrib>Jones, Dan</creatorcontrib><creatorcontrib>McElroy, Joseph P.</creatorcontrib><creatorcontrib>Suarez, Adrian A.</creatorcontrib><creatorcontrib>Zhao, Weiqiang</creatorcontrib><creatorcontrib>Chen, Wei</creatorcontrib><creatorcontrib>Salani, Ritu</creatorcontrib><creatorcontrib>Copeland, Larry J.</creatorcontrib><creatorcontrib>O'Malley, David M.</creatorcontrib><creatorcontrib>Fowler, Jeffrey M.</creatorcontrib><creatorcontrib>Yilmaz, Ahmet</creatorcontrib><creatorcontrib>Chassen, Alexis S.</creatorcontrib><creatorcontrib>Pearlman, Rachel</creatorcontrib><creatorcontrib>Goodfellow, Paul J.</creatorcontrib><creatorcontrib>Backes, Floor J.</creatorcontrib><title>Epigenetic silencing of MLH1 in endometrial cancers is associated with larger tumor volume, increased rate of lymph node positivity and reduced recurrence-free survival</title><title>Gynecologic oncology</title><addtitle>Gynecol Oncol</addtitle><description>•MLH1 methylated endometrial tumors have poor prognostic features including larger size.•Tumor volume and mismatch repair class are associated with lymph node involvement.•Women with MLH1 methylated tumors have reduced recurrence-free survival.•Recurrence rate by MMR class differed dramatically in advanced stage endometrial cancer.•MMR defective tumors with MLH1 methylation may exhibit chemoresistance.
To determine the relationship between mismatch repair (MMR) classification and clinicopathologic features including tumor volume, and explore outcomes by MMR class in a contemporary cohort.
Single institution cohort evaluating MMR classification for endometrial cancers (EC). MMR immunohistochemistry (IHC)±microsatellite instability (MSI) testing and reflex MLH1 methylation testing was performed. Tumors with MMR abnormalities by IHC or MSI and MLH1 methylation were classified as epigenetic MMR deficiency while those without MLH1 methylation were classified as probable MMR mutations. Clinicopathologic characteristics were analyzed.
466 endometrial cancers were classified; 75% as MMR proficient, 20% epigenetic MMR defects, and 5% as probable MMR mutations. Epigenetic MMR defects were associated with advanced stage, higher grade, presence of lymphovascular space invasion, and older age. MMR class was significantly associated with tumor volume, an association not previously reported. The epigenetic MMR defect tumors median volume was 10,220mm3 compared to 3321mm3 and 2,846mm3, for MMR proficient and probable MMR mutations respectively (P<0.0001). Higher tumor volume was associated with lymph node involvement. Endometrioid EC cases with epigenetic MMR defects had significantly reduced recurrence-free survival (RFS). Among advanced stage (III/IV) endometrioid EC the epigenetic MMR defect group was more likely to recur compared to the MMR proficient group (47.7% vs 3.4%) despite receiving similar adjuvant therapy. In contrast, there was no difference in the number of early stage recurrences for the different MMR classes.
MMR testing that includes MLH1 methylation analysis defines a subset of tumors that have worse prognostic features and reduced RFS.</description><subject>Age Factors</subject><subject>Aged</subject><subject>Disease-Free Survival</subject><subject>DNA Methylation</subject><subject>DNA mismatch repair</subject><subject>DNA Mismatch Repair - genetics</subject><subject>Endometrial cancer</subject><subject>Endometrial Neoplasms - chemistry</subject><subject>Endometrial Neoplasms - genetics</subject><subject>Endometrial Neoplasms - pathology</subject><subject>Epigenesis, Genetic</subject><subject>Epigenomics</subject><subject>Female</subject><subject>Gene Silencing</subject><subject>Humans</subject><subject>Lymph node excision</subject><subject>Lymphatic Metastasis</subject><subject>Lynch syndrome</subject><subject>Microsatellite Instability</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>MutL Protein Homolog 1 - analysis</subject><subject>MutL Protein Homolog 1 - genetics</subject><subject>Neoplasm Grading</subject><subject>Neoplasm Invasiveness - genetics</subject><subject>Neoplasm Recurrence, Local - genetics</subject><subject>Neoplasm Staging</subject><subject>Tumor Burden - genetics</subject><issn>0090-8258</issn><issn>1095-6859</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUGP0zAQhSMEYpeFX4CEfORAythOmuQA0mq1sEhFXOBsOfaknSqxi-0E9R_xM3HpsoIL0kg--HtvRu8VxUsOKw58_Xa_Om6Pzq8E8GYFeUA-Ki45dHW5buvucXEJ0EHZirq9KJ7FuIdMABdPiwvRNtA1UF0WP28PtEWHiQyLNKIz5LbMD-zz5o4zcgyd9ROmQHpkRjuDITKKTMfoDemElv2gtGOjDlsMLM2TD2zx4zzhmyw3AXXMTMjkyXU8Tocdc94iO_hIiRZKR6ZdJtDO5kSimUPId2A5BEQW57DQosfnxZNBjxFf3L9XxbcPt19v7srNl4-fbq43panqLpWNtZ2s67avut4K0G0L7dC3vdGD0FZK1H0Dpq4rFCiFEAYbafu6MhUIEGstr4r3Z9_D3E9oDboU9KgOgSYdjsprUv_-ONqprV9UvQYueZsNXt8bBP99xpjURNHgOGqHfo6Kd7mwTop1lVF5Rk3wMQYcHtZwUKeO1V797lidOlaQB2RWvfr7wgfNn1Iz8O4MYM5pIQwqGjolaimnm5T19N8FvwBqkb8R</recordid><startdate>20170901</startdate><enddate>20170901</enddate><creator>Cosgrove, Casey M.</creator><creator>Cohn, David E.</creator><creator>Hampel, Heather</creator><creator>Frankel, Wendy L.</creator><creator>Jones, Dan</creator><creator>McElroy, Joseph P.</creator><creator>Suarez, Adrian A.</creator><creator>Zhao, Weiqiang</creator><creator>Chen, Wei</creator><creator>Salani, Ritu</creator><creator>Copeland, Larry J.</creator><creator>O'Malley, David M.</creator><creator>Fowler, Jeffrey M.</creator><creator>Yilmaz, Ahmet</creator><creator>Chassen, Alexis S.</creator><creator>Pearlman, Rachel</creator><creator>Goodfellow, Paul J.</creator><creator>Backes, Floor J.</creator><general>Elsevier Inc</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170901</creationdate><title>Epigenetic silencing of MLH1 in endometrial cancers is associated with larger tumor volume, increased rate of lymph node positivity and reduced recurrence-free survival</title><author>Cosgrove, Casey M. ; Cohn, David E. ; Hampel, Heather ; Frankel, Wendy L. ; Jones, Dan ; McElroy, Joseph P. ; Suarez, Adrian A. ; Zhao, Weiqiang ; Chen, Wei ; Salani, Ritu ; Copeland, Larry J. ; O'Malley, David M. ; Fowler, Jeffrey M. ; Yilmaz, Ahmet ; Chassen, Alexis S. ; Pearlman, Rachel ; Goodfellow, Paul J. ; Backes, Floor J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c459t-7dd93558b49bd20a8808fb8bcaf2ad33eab70c554e2e3222ce73db54c402026a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Age Factors</topic><topic>Aged</topic><topic>Disease-Free Survival</topic><topic>DNA Methylation</topic><topic>DNA mismatch repair</topic><topic>DNA Mismatch Repair - genetics</topic><topic>Endometrial cancer</topic><topic>Endometrial Neoplasms - chemistry</topic><topic>Endometrial Neoplasms - genetics</topic><topic>Endometrial Neoplasms - pathology</topic><topic>Epigenesis, Genetic</topic><topic>Epigenomics</topic><topic>Female</topic><topic>Gene Silencing</topic><topic>Humans</topic><topic>Lymph node excision</topic><topic>Lymphatic Metastasis</topic><topic>Lynch syndrome</topic><topic>Microsatellite Instability</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>MutL Protein Homolog 1 - analysis</topic><topic>MutL Protein Homolog 1 - genetics</topic><topic>Neoplasm Grading</topic><topic>Neoplasm Invasiveness - genetics</topic><topic>Neoplasm Recurrence, Local - genetics</topic><topic>Neoplasm Staging</topic><topic>Tumor Burden - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cosgrove, Casey M.</creatorcontrib><creatorcontrib>Cohn, David E.</creatorcontrib><creatorcontrib>Hampel, Heather</creatorcontrib><creatorcontrib>Frankel, Wendy L.</creatorcontrib><creatorcontrib>Jones, Dan</creatorcontrib><creatorcontrib>McElroy, Joseph P.</creatorcontrib><creatorcontrib>Suarez, Adrian A.</creatorcontrib><creatorcontrib>Zhao, Weiqiang</creatorcontrib><creatorcontrib>Chen, Wei</creatorcontrib><creatorcontrib>Salani, Ritu</creatorcontrib><creatorcontrib>Copeland, Larry J.</creatorcontrib><creatorcontrib>O'Malley, David M.</creatorcontrib><creatorcontrib>Fowler, Jeffrey M.</creatorcontrib><creatorcontrib>Yilmaz, Ahmet</creatorcontrib><creatorcontrib>Chassen, Alexis S.</creatorcontrib><creatorcontrib>Pearlman, Rachel</creatorcontrib><creatorcontrib>Goodfellow, Paul J.</creatorcontrib><creatorcontrib>Backes, Floor J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Gynecologic oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cosgrove, Casey M.</au><au>Cohn, David E.</au><au>Hampel, Heather</au><au>Frankel, Wendy L.</au><au>Jones, Dan</au><au>McElroy, Joseph P.</au><au>Suarez, Adrian A.</au><au>Zhao, Weiqiang</au><au>Chen, Wei</au><au>Salani, Ritu</au><au>Copeland, Larry J.</au><au>O'Malley, David M.</au><au>Fowler, Jeffrey M.</au><au>Yilmaz, Ahmet</au><au>Chassen, Alexis S.</au><au>Pearlman, Rachel</au><au>Goodfellow, Paul J.</au><au>Backes, Floor J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epigenetic silencing of MLH1 in endometrial cancers is associated with larger tumor volume, increased rate of lymph node positivity and reduced recurrence-free survival</atitle><jtitle>Gynecologic oncology</jtitle><addtitle>Gynecol Oncol</addtitle><date>2017-09-01</date><risdate>2017</risdate><volume>146</volume><issue>3</issue><spage>588</spage><epage>595</epage><pages>588-595</pages><issn>0090-8258</issn><eissn>1095-6859</eissn><abstract>•MLH1 methylated endometrial tumors have poor prognostic features including larger size.•Tumor volume and mismatch repair class are associated with lymph node involvement.•Women with MLH1 methylated tumors have reduced recurrence-free survival.•Recurrence rate by MMR class differed dramatically in advanced stage endometrial cancer.•MMR defective tumors with MLH1 methylation may exhibit chemoresistance.
To determine the relationship between mismatch repair (MMR) classification and clinicopathologic features including tumor volume, and explore outcomes by MMR class in a contemporary cohort.
Single institution cohort evaluating MMR classification for endometrial cancers (EC). MMR immunohistochemistry (IHC)±microsatellite instability (MSI) testing and reflex MLH1 methylation testing was performed. Tumors with MMR abnormalities by IHC or MSI and MLH1 methylation were classified as epigenetic MMR deficiency while those without MLH1 methylation were classified as probable MMR mutations. Clinicopathologic characteristics were analyzed.
466 endometrial cancers were classified; 75% as MMR proficient, 20% epigenetic MMR defects, and 5% as probable MMR mutations. Epigenetic MMR defects were associated with advanced stage, higher grade, presence of lymphovascular space invasion, and older age. MMR class was significantly associated with tumor volume, an association not previously reported. The epigenetic MMR defect tumors median volume was 10,220mm3 compared to 3321mm3 and 2,846mm3, for MMR proficient and probable MMR mutations respectively (P<0.0001). Higher tumor volume was associated with lymph node involvement. Endometrioid EC cases with epigenetic MMR defects had significantly reduced recurrence-free survival (RFS). Among advanced stage (III/IV) endometrioid EC the epigenetic MMR defect group was more likely to recur compared to the MMR proficient group (47.7% vs 3.4%) despite receiving similar adjuvant therapy. In contrast, there was no difference in the number of early stage recurrences for the different MMR classes.
MMR testing that includes MLH1 methylation analysis defines a subset of tumors that have worse prognostic features and reduced RFS.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>28709704</pmid><doi>10.1016/j.ygyno.2017.07.003</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Age Factors Aged Disease-Free Survival DNA Methylation DNA mismatch repair DNA Mismatch Repair - genetics Endometrial cancer Endometrial Neoplasms - chemistry Endometrial Neoplasms - genetics Endometrial Neoplasms - pathology Epigenesis, Genetic Epigenomics Female Gene Silencing Humans Lymph node excision Lymphatic Metastasis Lynch syndrome Microsatellite Instability Middle Aged Mutation MutL Protein Homolog 1 - analysis MutL Protein Homolog 1 - genetics Neoplasm Grading Neoplasm Invasiveness - genetics Neoplasm Recurrence, Local - genetics Neoplasm Staging Tumor Burden - genetics |
| title | Epigenetic silencing of MLH1 in endometrial cancers is associated with larger tumor volume, increased rate of lymph node positivity and reduced recurrence-free survival |
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