Origin and molecular pathogenesis of ovarian high-grade serous carcinoma
A new paradigm for the pathogenesis of ovarian cancer has recently been proposed which helps to explain persistent problems in describing the development and diverse morphology of these neoplasms. The paradigm incorporates recent advances in our understanding of the molecular pathogenesis of epithel...
Gespeichert in:
| Veröffentlicht in: | Annals of oncology Jg. 24 Suppl 10; S. x16 |
|---|---|
| 1. Verfasser: | |
| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
England
01.12.2013
|
| Schlagworte: | |
| ISSN: | 1569-8041, 1569-8041 |
| Online-Zugang: | Weitere Angaben |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| Abstract | A new paradigm for the pathogenesis of ovarian cancer has recently been proposed which helps to explain persistent problems in describing the development and diverse morphology of these neoplasms. The paradigm incorporates recent advances in our understanding of the molecular pathogenesis of epithelial 'ovarian' cancer with new insights into the origin of these tumors. Correlated clinicopathologic and molecular genetic studies led to the development of a dualistic model that divides all the various histologic types of epithelial ovarian carcinomas into two broad categories designated 'type I' and 'type II'. The prototypic type I tumor is low-grade serous carcinoma and the prototypic type II tumor is high-grade serous carcinomas (HGSCs). As the serous tumors comprise ∼70% of all epithelial ovarian tumors and account for the majority of deaths, the serous tumors will be the subject of this review. There are marked differences between the low-grade and high-grade serous tumors. Briefly, the former are indolent, present in stage I (tumor confined to the ovary) and develop from well-established precursors, so-called 'atypical proliferative (borderline) tumors,' which are characterized by specific mutations, including KRAS, BRAF and ERBB2; they are relatively genetically stable. In contrast, HGSCs are aggressive, present in the advanced stage, and develop from intraepithelial carcinomas in the fallopian tube. They harbor TP53 mutations in over 95% of cases, but rarely harbor the mutations detected in the low-grade serous tumors. At the time of diagnosis they demonstrate marked chromosomal aberrations but over the course of the disease these changes remain relatively stable. Along with the recent advances in understanding the molecular pathogenesis of these tumors, studies have demonstrated that the long sought for precursor of ovarian HGSC appears to develop from an occult intraepithelial carcinoma in the fimbrial region of the fallopian tube designated 'serous tubal intraepithelial carcinoma (STIC)' and involves the ovary secondarily. Another possible mechanism for the development of ''ovarian'' HGSC is implantation of normal fimbrial epithelium on the denuded ovarian surface at the site of rupture when ovulation occurs. We speculate that this tubal epithelium can result in the formation of a cortical inclusion cyst (CICs) that can then undergo malignant transformation. Thus, serous tumors may develop from inclusion cysts, as has been previously proposed, but by a process of implantation of tubal (müllerian-type) tissue rather than by a process of metaplasia from ovarian surface epithelium (OSE, mesothelial). The dualistic model serves as a framework for studying ovarian cancer and can assist investigators in organizing this complex group of neoplasms. In conjunction with the recognition that the majority of 'ovarian' carcinomas originate outside the ovary, this model also facilitates the development of new and novel approaches to prevention, screening and treatment of this devastating disease. |
|---|---|
| AbstractList | A new paradigm for the pathogenesis of ovarian cancer has recently been proposed which helps to explain persistent problems in describing the development and diverse morphology of these neoplasms. The paradigm incorporates recent advances in our understanding of the molecular pathogenesis of epithelial 'ovarian' cancer with new insights into the origin of these tumors. Correlated clinicopathologic and molecular genetic studies led to the development of a dualistic model that divides all the various histologic types of epithelial ovarian carcinomas into two broad categories designated 'type I' and 'type II'. The prototypic type I tumor is low-grade serous carcinoma and the prototypic type II tumor is high-grade serous carcinomas (HGSCs). As the serous tumors comprise ∼70% of all epithelial ovarian tumors and account for the majority of deaths, the serous tumors will be the subject of this review. There are marked differences between the low-grade and high-grade serous tumors. Briefly, the former are indolent, present in stage I (tumor confined to the ovary) and develop from well-established precursors, so-called 'atypical proliferative (borderline) tumors,' which are characterized by specific mutations, including KRAS, BRAF and ERBB2; they are relatively genetically stable. In contrast, HGSCs are aggressive, present in the advanced stage, and develop from intraepithelial carcinomas in the fallopian tube. They harbor TP53 mutations in over 95% of cases, but rarely harbor the mutations detected in the low-grade serous tumors. At the time of diagnosis they demonstrate marked chromosomal aberrations but over the course of the disease these changes remain relatively stable. Along with the recent advances in understanding the molecular pathogenesis of these tumors, studies have demonstrated that the long sought for precursor of ovarian HGSC appears to develop from an occult intraepithelial carcinoma in the fimbrial region of the fallopian tube designated 'serous tubal intraepithelial carcinoma (STIC)' and involves the ovary secondarily. Another possible mechanism for the development of ''ovarian'' HGSC is implantation of normal fimbrial epithelium on the denuded ovarian surface at the site of rupture when ovulation occurs. We speculate that this tubal epithelium can result in the formation of a cortical inclusion cyst (CICs) that can then undergo malignant transformation. Thus, serous tumors may develop from inclusion cysts, as has been previously proposed, but by a process of implantation of tubal (müllerian-type) tissue rather than by a process of metaplasia from ovarian surface epithelium (OSE, mesothelial). The dualistic model serves as a framework for studying ovarian cancer and can assist investigators in organizing this complex group of neoplasms. In conjunction with the recognition that the majority of 'ovarian' carcinomas originate outside the ovary, this model also facilitates the development of new and novel approaches to prevention, screening and treatment of this devastating disease. A new paradigm for the pathogenesis of ovarian cancer has recently been proposed which helps to explain persistent problems in describing the development and diverse morphology of these neoplasms. The paradigm incorporates recent advances in our understanding of the molecular pathogenesis of epithelial 'ovarian' cancer with new insights into the origin of these tumors. Correlated clinicopathologic and molecular genetic studies led to the development of a dualistic model that divides all the various histologic types of epithelial ovarian carcinomas into two broad categories designated 'type I' and 'type II'. The prototypic type I tumor is low-grade serous carcinoma and the prototypic type II tumor is high-grade serous carcinomas (HGSCs). As the serous tumors comprise ∼70% of all epithelial ovarian tumors and account for the majority of deaths, the serous tumors will be the subject of this review. There are marked differences between the low-grade and high-grade serous tumors. Briefly, the former are indolent, present in stage I (tumor confined to the ovary) and develop from well-established precursors, so-called 'atypical proliferative (borderline) tumors,' which are characterized by specific mutations, including KRAS, BRAF and ERBB2; they are relatively genetically stable. In contrast, HGSCs are aggressive, present in the advanced stage, and develop from intraepithelial carcinomas in the fallopian tube. They harbor TP53 mutations in over 95% of cases, but rarely harbor the mutations detected in the low-grade serous tumors. At the time of diagnosis they demonstrate marked chromosomal aberrations but over the course of the disease these changes remain relatively stable. Along with the recent advances in understanding the molecular pathogenesis of these tumors, studies have demonstrated that the long sought for precursor of ovarian HGSC appears to develop from an occult intraepithelial carcinoma in the fimbrial region of the fallopian tube designated 'serous tubal intraepithelial carcinoma (STIC)' and involves the ovary secondarily. Another possible mechanism for the development of ''ovarian'' HGSC is implantation of normal fimbrial epithelium on the denuded ovarian surface at the site of rupture when ovulation occurs. We speculate that this tubal epithelium can result in the formation of a cortical inclusion cyst (CICs) that can then undergo malignant transformation. Thus, serous tumors may develop from inclusion cysts, as has been previously proposed, but by a process of implantation of tubal (müllerian-type) tissue rather than by a process of metaplasia from ovarian surface epithelium (OSE, mesothelial). The dualistic model serves as a framework for studying ovarian cancer and can assist investigators in organizing this complex group of neoplasms. In conjunction with the recognition that the majority of 'ovarian' carcinomas originate outside the ovary, this model also facilitates the development of new and novel approaches to prevention, screening and treatment of this devastating disease.A new paradigm for the pathogenesis of ovarian cancer has recently been proposed which helps to explain persistent problems in describing the development and diverse morphology of these neoplasms. The paradigm incorporates recent advances in our understanding of the molecular pathogenesis of epithelial 'ovarian' cancer with new insights into the origin of these tumors. Correlated clinicopathologic and molecular genetic studies led to the development of a dualistic model that divides all the various histologic types of epithelial ovarian carcinomas into two broad categories designated 'type I' and 'type II'. The prototypic type I tumor is low-grade serous carcinoma and the prototypic type II tumor is high-grade serous carcinomas (HGSCs). As the serous tumors comprise ∼70% of all epithelial ovarian tumors and account for the majority of deaths, the serous tumors will be the subject of this review. There are marked differences between the low-grade and high-grade serous tumors. Briefly, the former are indolent, present in stage I (tumor confined to the ovary) and develop from well-established precursors, so-called 'atypical proliferative (borderline) tumors,' which are characterized by specific mutations, including KRAS, BRAF and ERBB2; they are relatively genetically stable. In contrast, HGSCs are aggressive, present in the advanced stage, and develop from intraepithelial carcinomas in the fallopian tube. They harbor TP53 mutations in over 95% of cases, but rarely harbor the mutations detected in the low-grade serous tumors. At the time of diagnosis they demonstrate marked chromosomal aberrations but over the course of the disease these changes remain relatively stable. Along with the recent advances in understanding the molecular pathogenesis of these tumors, studies have demonstrated that the long sought for precursor of ovarian HGSC appears to develop from an occult intraepithelial carcinoma in the fimbrial region of the fallopian tube designated 'serous tubal intraepithelial carcinoma (STIC)' and involves the ovary secondarily. Another possible mechanism for the development of ''ovarian'' HGSC is implantation of normal fimbrial epithelium on the denuded ovarian surface at the site of rupture when ovulation occurs. We speculate that this tubal epithelium can result in the formation of a cortical inclusion cyst (CICs) that can then undergo malignant transformation. Thus, serous tumors may develop from inclusion cysts, as has been previously proposed, but by a process of implantation of tubal (müllerian-type) tissue rather than by a process of metaplasia from ovarian surface epithelium (OSE, mesothelial). The dualistic model serves as a framework for studying ovarian cancer and can assist investigators in organizing this complex group of neoplasms. In conjunction with the recognition that the majority of 'ovarian' carcinomas originate outside the ovary, this model also facilitates the development of new and novel approaches to prevention, screening and treatment of this devastating disease. |
| Author | Kurman, R J |
| Author_xml | – sequence: 1 givenname: R J surname: Kurman fullname: Kurman, R J organization: Department of Gynecology |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24265397$$D View this record in MEDLINE/PubMed |
| BookMark | eNpNj01LAzEYhINU7IcevUqOXtYm2WyaHKWoFQq96Hl5N3l3G9lNatIV_PcWrOBphuFhmJmTSYgBCbnl7IEzUy4hnAK7HNxRqvKCzHilTKGZ5JN_fkrmOX8wxpQR5opMhRSqKs1qRja75DsfKARHh9ijHXtI9ADHfewwYPaZxpbGL0geAt37bl90CRzSjCmOmVpI1oc4wDW5bKHPeHPWBXl_fnpbb4rt7uV1_bgtbGn0sVDcWa0q1mLbOAt65ZBz7azUJQrTypIb3jAGElYtNiUIwznoBqvKykoLJxbk_rf3kOLniPlYDz5b7HsIeBpUc6kqrbhR7ITendGxGdDVh-QHSN_133vxA88RX5Y |
| CitedBy_id | crossref_primary_10_12677_acm_2025_1551490 crossref_primary_10_3892_ol_2022_13200 crossref_primary_10_1111_jcmm_12927 crossref_primary_10_1186_s12885_017_3843_y crossref_primary_10_5472_marumj_1056169 crossref_primary_10_1016_j_ijbiomac_2019_01_009 crossref_primary_10_3892_ol_2016_4895 crossref_primary_10_1111_hex_12661 crossref_primary_10_1186_s13000_016_0482_6 crossref_primary_10_1016_j_scib_2020_03_040 crossref_primary_10_1016_j_ygyno_2021_08_019 crossref_primary_10_1097_AOG_0000000000006016 crossref_primary_10_1016_j_ajog_2015_03_044 crossref_primary_10_1038_d41586_022_04169_3 crossref_primary_10_1007_s11912_020_00933_8 crossref_primary_10_1002_cncr_29521 crossref_primary_10_1155_2019_1870834 crossref_primary_10_1016_j_jmig_2017_01_001 crossref_primary_10_1007_s40944_024_00873_2 crossref_primary_10_1016_j_soncn_2017_02_002 crossref_primary_10_1038_bjc_2016_27 crossref_primary_10_1186_s13048_025_01766_4 crossref_primary_10_1080_14728214_2023_2218643 crossref_primary_10_1155_2015_751571 crossref_primary_10_1111_febs_15722 crossref_primary_10_3390_diagnostics12102516 crossref_primary_10_1021_acsabm_5c00777 crossref_primary_10_3390_ijms17122113 crossref_primary_10_1155_2015_219012 crossref_primary_10_1186_s12885_016_2637_y crossref_primary_10_3322_caac_21456 crossref_primary_10_3892_etm_2023_12303 crossref_primary_10_1055_s_0042_1742321 crossref_primary_10_1210_jc_2013_4249 crossref_primary_10_3390_cells9030527 crossref_primary_10_3892_mmr_2015_4485 crossref_primary_10_1007_s00129_015_3720_1 crossref_primary_10_1210_endrev_bnac013 crossref_primary_10_1007_s00261_020_02911_x crossref_primary_10_5858_arpa_2017_0004_OA crossref_primary_10_1016_j_currproblcancer_2016_11_001 crossref_primary_10_1002_cncr_34023 crossref_primary_10_1002_path_4819 crossref_primary_10_1097_AOG_0000000000001867 crossref_primary_10_1155_2014_787143 crossref_primary_10_3390_cancers12061470 crossref_primary_10_1016_j_ajog_2015_09_005 crossref_primary_10_1186_s12885_023_11453_6 crossref_primary_10_1097_IGC_0000000000000379 crossref_primary_10_3390_cancers12082054 crossref_primary_10_1002_ijc_29000 crossref_primary_10_1016_j_acepjo_2025_100093 crossref_primary_10_1016_j_humpath_2017_08_021 crossref_primary_10_1097_PAT_0000000000000291 crossref_primary_10_1016_j_tranon_2018_08_003 crossref_primary_10_3390_ijerph18115741 crossref_primary_10_1016_j_anndiagpath_2017_07_002 crossref_primary_10_1038_onc_2016_456 crossref_primary_10_1016_j_genrep_2019_100380 crossref_primary_10_3389_fonc_2025_1514460 crossref_primary_10_1073_pnas_2201423119 crossref_primary_10_1111_his_13248 crossref_primary_10_1007_s12094_018_1865_9 crossref_primary_10_1016_j_jogc_2017_03_121 crossref_primary_10_1002_cncr_32079 crossref_primary_10_1016_j_jogc_2016_12_005 crossref_primary_10_1155_2015_341723 crossref_primary_10_3322_caac_21559 crossref_primary_10_1210_endrev_bnad018 crossref_primary_10_1016_j_humpath_2015_12_011 crossref_primary_10_1038_s41417_020_00227_y crossref_primary_10_1186_s10020_021_00295_2 crossref_primary_10_1016_j_ygyno_2017_09_029 crossref_primary_10_1136_jitc_2019_000480 crossref_primary_10_3892_or_2015_4386 crossref_primary_10_1016_j_conctc_2017_10_003 crossref_primary_10_1148_rg_2016150130 crossref_primary_10_1177_2036361320979219 crossref_primary_10_1111_apm_12646 crossref_primary_10_3390_genes14040886 crossref_primary_10_1097_GRF_0000000000000316 crossref_primary_10_1038_s41420_025_02398_9 crossref_primary_10_1016_j_gore_2023_101157 crossref_primary_10_1097_IGC_0000000000001052 crossref_primary_10_1002_jmv_28898 crossref_primary_10_1038_s41417_022_00447_4 crossref_primary_10_1007_s00428_016_1918_9 crossref_primary_10_1016_j_fertnstert_2023_11_031 crossref_primary_10_1097_MD_0000000000010881 crossref_primary_10_1177_1758835920967241 crossref_primary_10_1007_s00404_020_05547_w crossref_primary_10_3390_ijms232012358 crossref_primary_10_3390_diagnostics14111069 crossref_primary_10_1186_s12014_017_9152_2 crossref_primary_10_1016_j_ajog_2017_06_004 crossref_primary_10_1097_AOG_0000000000001448 crossref_primary_10_1007_s11912_021_01088_w crossref_primary_10_1038_s41416_019_0422_9 crossref_primary_10_3390_cancers15164128 crossref_primary_10_1111_jog_12550 crossref_primary_10_1007_s40291_016_0201_8 crossref_primary_10_1111_cpr_13029 crossref_primary_10_1097_AOG_0000000000002939 crossref_primary_10_1002_cam4_5612 crossref_primary_10_1016_j_crad_2020_11_116 crossref_primary_10_1111_iep_12196 crossref_primary_10_1186_s13048_021_00825_w crossref_primary_10_3389_fcell_2022_1042734 crossref_primary_10_3390_cancers14236010 crossref_primary_10_3390_ph17081095 crossref_primary_10_1186_s12905_024_03487_0 crossref_primary_10_1053_j_semdp_2017_11_007 crossref_primary_10_3390_cancers13081875 crossref_primary_10_3390_cancers13153840 crossref_primary_10_1155_2023_8981430 crossref_primary_10_3390_cancers15030868 crossref_primary_10_1016_j_path_2019_01_007 crossref_primary_10_1016_j_jmig_2016_12_004 crossref_primary_10_1016_j_ygyno_2014_07_089 crossref_primary_10_1016_j_ygyno_2015_07_100 crossref_primary_10_1042_BST20180286 crossref_primary_10_1148_rg_2021200086 crossref_primary_10_3389_fonc_2016_00025 crossref_primary_10_1177_1066896919838347 crossref_primary_10_3390_cancers13123065 crossref_primary_10_1007_s00404_018_4941_z crossref_primary_10_1016_j_ygyno_2016_02_021 crossref_primary_10_1186_s13048_016_0271_6 crossref_primary_10_1016_j_bulcan_2025_03_019 crossref_primary_10_1007_s00292_019_0572_9 crossref_primary_10_4103_0973_1482_172130 crossref_primary_10_1016_j_neo_2018_03_007 crossref_primary_10_1111_his_13399 crossref_primary_10_1186_s13048_017_0347_y crossref_primary_10_3390_jcm12041422 crossref_primary_10_1016_j_acthis_2016_01_004 crossref_primary_10_1016_j_jmig_2016_12_007 crossref_primary_10_1016_j_mric_2022_07_002 crossref_primary_10_3892_etm_2022_11351 crossref_primary_10_1016_j_ygyno_2015_09_018 crossref_primary_10_1097_PGP_0000000000000348 crossref_primary_10_1016_j_ijbiomac_2019_07_109 crossref_primary_10_1016_j_tranon_2019_09_007 crossref_primary_10_1155_2024_1907965 crossref_primary_10_3892_br_2017_955 crossref_primary_10_1158_1940_6207_CAPR_14_0293 crossref_primary_10_1016_j_ejogrb_2025_114525 crossref_primary_10_1021_acs_jproteome_5c00088 crossref_primary_10_1093_jnci_djy071 crossref_primary_10_1371_journal_pone_0118927 crossref_primary_10_1002_cam4_6729 crossref_primary_10_1038_bjc_2017_195 crossref_primary_10_1097_MD_0000000000001695 crossref_primary_10_1016_j_jsbmb_2014_02_010 crossref_primary_10_1038_s41598_017_05519_2 crossref_primary_10_1186_s13048_014_0095_1 crossref_primary_10_1177_1933719116648212 crossref_primary_10_1002_btm2_10131 crossref_primary_10_1038_onc_2017_11 crossref_primary_10_1002_ijc_34354 crossref_primary_10_1186_s12929_020_00638_x crossref_primary_10_1080_07391102_2024_2335290 crossref_primary_10_1016_j_neo_2022_100866 crossref_primary_10_1016_j_tranon_2024_102130 crossref_primary_10_1158_0008_5472_CAN_17_1671 crossref_primary_10_1371_journal_pmed_1002893 crossref_primary_10_3892_ol_2016_5493 crossref_primary_10_1245_s10434_020_08208_z crossref_primary_10_1016_j_bbrc_2023_09_065 crossref_primary_10_1038_s41598_019_51697_6 crossref_primary_10_1002_cjp2_4 crossref_primary_10_29254_2077_4214_2021_4_162_291_296 crossref_primary_10_1186_s12906_018_2241_6 crossref_primary_10_1186_s13045_020_00971_6 crossref_primary_10_1111_tog_12258 crossref_primary_10_1080_14737159_2016_1259069 crossref_primary_10_5301_tj_5000623 crossref_primary_10_1186_s13000_023_01317_9 crossref_primary_10_1016_j_labinv_2024_102059 crossref_primary_10_1097_PGP_0000000000000440 crossref_primary_10_1007_s10517_021_05062_1 crossref_primary_10_1186_s12880_025_01865_0 crossref_primary_10_1016_j_cca_2015_03_047 crossref_primary_10_1007_s10565_024_09938_6 crossref_primary_10_1038_s41467_019_13116_2 crossref_primary_10_1155_2019_2867372 crossref_primary_10_1097_PGP_0000000000000604 crossref_primary_10_3390_biom5043438 crossref_primary_10_3390_cancers15041141 crossref_primary_10_1016_j_ebiom_2022_104001 crossref_primary_10_1016_j_ygyno_2024_05_010 |
| ContentType | Journal Article |
| DBID | CGR CUY CVF ECM EIF NPM 7X8 |
| DOI | 10.1093/annonc/mdt463 |
| DatabaseName | Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic |
| DatabaseTitle | MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE MEDLINE - Academic |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: 7X8 name: MEDLINE - Academic url: https://search.proquest.com/medline sourceTypes: Aggregation Database |
| DeliveryMethod | no_fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 1569-8041 |
| ExternalDocumentID | 24265397 |
| Genre | Research Support, U.S. Gov't, Non-P.H.S Journal Article Review |
| GroupedDBID | --- -E4 .2P .86 .I3 .XZ .ZR 08P 0R~ 0U7 1TH 23M 2WC 4.4 482 48X 53G 5GY 5VS 5WA 6.Y 6J9 70D AAEDW AAGQS AAJKP AAJQQ AAKAS AAKUH AALRI AAMVS AAOGV AAPNW AAUQX AAXUO ABEUO ABIXL ABJNI ABKDP ABLJU ABNGD ABNKS ABOCM ABQLI ABQTQ ABSAR ABSMQ ABZBJ ACGFO ACGFS ACPQN ACPRK ACUFI ACUTO ADBBV ADEYI ADHKW ADHZD ADJQC ADOCK ADRIX ADRTK ADVLN ADYVW ADZCM ADZXQ AEGPL AEGXH AEHUL AEJOX AEKPW AEKSI AEMDU AENEX AENZO AEPUE AEWNT AFETI AFIYH AFJKZ AFOFC AFSHK AFXEN AGINJ AGKEF AGKRT AGSYK AHMBA AHXPO AIAGR AIJHB AITUG AKRWK ALMA_UNASSIGNED_HOLDINGS ALUQC AMRAJ APIBT APWMN AQKUS ASPBG ATTQO AVWKF AXUDD AZFZN BAWUL BAYMD BGNMA BHONS BTRTY BVRKM BZKNY C1A CAG CDBKE CGR CKLRP COF CS3 CUY CVF CZ4 DAKXR DIK DILTD DL5 D~K E3Z EBS ECM EE~ EIF EJD EX3 F9B FDB FEDTE GJXCC GX1 H13 H5~ HAR HVGLF HW0 HZ~ I09 IH2 IHE IOX J21 KAQDR KDC KOM KOP KQ8 KSI KSN LAK M-Z M41 M49 M4Y MBLQV MHKGH N9A NCXOZ NGC NOYVH NPM NTWIH NU0 NVLIB O9- OAWHX ODMLO OJQWA OK1 OVD P2P P6G PAFKI PB- PEELM PQQKQ Q1. Q5Y QBD R44 RD5 RNI ROL ROX ROZ RPX RW1 RXO RZC RZE RZF RZO SDH TCURE TEORI TJX TMA TR2 U2A W8F WOQ WOW X7H YAYTL YFH YKOAZ ZKX ZXP ~91 7X8 ACVFH ADCNI AEUPX AFPUW AIGII AKBMS AKYEP EFKBS |
| ID | FETCH-LOGICAL-c398t-61dc8650fefbdca87de118dc483e29f43191b00a4a7feb3a2911a8be55c4582d2 |
| IEDL.DBID | 7X8 |
| ISICitedReferencesCount | 251 |
| ISICitedReferencesURI | http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000327511500002&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| ISSN | 1569-8041 |
| IngestDate | Sat Sep 27 20:17:29 EDT 2025 Wed Feb 19 02:32:20 EST 2025 |
| IsDoiOpenAccess | false |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Language | English |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c398t-61dc8650fefbdca87de118dc483e29f43191b00a4a7feb3a2911a8be55c4582d2 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 |
| OpenAccessLink | http://www.annalsofoncology.org/article/S0923753419373855/pdf |
| PMID | 24265397 |
| PQID | 1465861960 |
| PQPubID | 23479 |
| ParticipantIDs | proquest_miscellaneous_1465861960 pubmed_primary_24265397 |
| PublicationCentury | 2000 |
| PublicationDate | 2013-12-01 |
| PublicationDateYYYYMMDD | 2013-12-01 |
| PublicationDate_xml | – month: 12 year: 2013 text: 2013-12-01 day: 01 |
| PublicationDecade | 2010 |
| PublicationPlace | England |
| PublicationPlace_xml | – name: England |
| PublicationTitle | Annals of oncology |
| PublicationTitleAlternate | Ann Oncol |
| PublicationYear | 2013 |
| SSID | ssj0006929 |
| Score | 2.5643065 |
| SecondaryResourceType | review_article |
| Snippet | A new paradigm for the pathogenesis of ovarian cancer has recently been proposed which helps to explain persistent problems in describing the development and... |
| SourceID | proquest pubmed |
| SourceType | Aggregation Database Index Database |
| StartPage | x16 |
| SubjectTerms | Carcinoma - classification Carcinoma - epidemiology Carcinoma - genetics Carcinoma - pathology Clinical Trials as Topic Female Humans Neoplasm Grading Ovarian Neoplasms - classification Ovarian Neoplasms - epidemiology Ovarian Neoplasms - genetics Ovarian Neoplasms - pathology Quality of Life Treatment Outcome |
| Title | Origin and molecular pathogenesis of ovarian high-grade serous carcinoma |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/24265397 https://www.proquest.com/docview/1465861960 |
| Volume | 24 Suppl 10 |
| WOSCitedRecordID | wos000327511500002&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| hasFullText | |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1LSwMxEA5qRbz4ftQXEbwGd7OPJCcRsfTS2oNCb0s2j9KDm9qt_f3ObLf0JAhecguEYWbyfZnwfYQ8xKVwXgrP4lxwlnoXsVJnilmlvXLSW859YzYhhkM5HqtR--BWt98q1z2xadQ2GHwjf4SKziSg_Tx6mn0xdI3C6WprobFNOglAGcxqMd6oheeqcSkDiqIY6uy0GptA4tHkJVQGWP8iRQXQ39Blc8v0Dv97viNy0OJL-rxKiGOy5aoTsjdoJ-inpP_WOGFRXVn6ubbGpehLHCbY9qY1DZ6GJVBoXVEUM2aTubaOQqqG75oa9B6qwqc-Ix-91_eXPmvdFJhJlFwAR7RGAh7zzpfWaCmsA3JhTSoTx5UHIKFiqEGdauGBYWsObVDL0mWZwdma5edkB2LmLgnNjM29iLxOojRNfCyNkagjlpSOa2Vsl9yvY1RAtuIIQlcODllsotQlF6tAF7OVrEaBYCEDeHT1h93XZJ-jL0Xzr-SGdDzUqrslu2a5mNbzuyYNYB2OBj8O6L-C |
| linkProvider | ProQuest |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Origin+and+molecular+pathogenesis+of+ovarian+high-grade+serous+carcinoma&rft.jtitle=Annals+of+oncology&rft.au=Kurman%2C+R+J&rft.date=2013-12-01&rft.issn=1569-8041&rft.eissn=1569-8041&rft.volume=24+Suppl+10&rft.spage=x16&rft_id=info:doi/10.1093%2Fannonc%2Fmdt463&rft.externalDBID=NO_FULL_TEXT |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1569-8041&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1569-8041&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1569-8041&client=summon |