Epithelial ovarian cancer: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
Line 7: Line 7:
==== The origin of mucinous tumors of gastrointestinal type and transitional cell (Brenner) tumors: Still a mystery to solve ====
==== The origin of mucinous tumors of gastrointestinal type and transitional cell (Brenner) tumors: Still a mystery to solve ====
* Mucinous and the transitional tumors of ovaries are two of the least common types of the epithelial ovarian tumors. In fact, most of the mucinous tumors in ovaries are secondary and primary tumors only form about 3% of all epithelial ovarian cancers. Mucinous epithelium in mucinous tumors of ovaries resemble more to intestinal mucinous epithelium rather than that of endocervix as was previously argued. Transitional cell tumors, on the other hand, are closer to bladder epithelium in histological studies.<ref name="pmid18317228">{{cite journal |vauthors=Kurman RJ, Shih IeM |title=Pathogenesis of ovarian cancer: lessons from morphology and molecular biology and their clinical implications |journal=Int. J. Gynecol. Pathol. |volume=27 |issue=2 |pages=151–60 |date=April 2008 |pmid=18317228 |pmc=2794425 |doi=10.1097/PGP.0b013e318161e4f5 |url=}}</ref><ref name="pmid21683865">{{cite journal |vauthors=Kurman RJ, Shih IeM |title=Molecular pathogenesis and extraovarian origin of epithelial ovarian cancer--shifting the paradigm |journal=Hum. Pathol. |volume=42 |issue=7 |pages=918–31 |date=July 2011 |pmid=21683865 |pmc=3148026 |doi=10.1016/j.humpath.2011.03.003 |url=}}</ref><ref name="pmid19038766">{{cite journal |vauthors=Dubeau L |title=The cell of origin of ovarian epithelial tumours |journal=Lancet Oncol. |volume=9 |issue=12 |pages=1191–7 |date=December 2008 |pmid=19038766 |pmc=4176875 |doi=10.1016/S1470-2045(08)70308-5 |url=}}</ref><ref name="pmid10366144">{{cite journal |vauthors=Riopel MA, Ronnett BM, Kurman RJ |title=Evaluation of diagnostic criteria and behavior of ovarian intestinal-type mucinous tumors: atypical proliferative (borderline) tumors and intraepithelial, microinvasive, invasive, and metastatic carcinomas |journal=Am. J. Surg. Pathol. |volume=23 |issue=6 |pages=617–35 |date=June 1999 |pmid=10366144 |doi= |url=}}</ref><ref name="pmid17527072">{{cite journal |vauthors=Vang R, Gown AM, Zhao C, Barry TS, Isacson C, Richardson MS, Ronnett BM |title=Ovarian mucinous tumors associated with mature cystic teratomas: morphologic and immunohistochemical analysis identifies a subset of potential teratomatous origin that shares features of lower gastrointestinal tract mucinous tumors more commonly encountered as secondary tumors in the ovary |journal=Am. J. Surg. Pathol. |volume=31 |issue=6 |pages=854–69 |date=June 2007 |pmid=17527072 |doi=10.1097/PAS.0b013e31802efb45 |url=}}</ref>
* Mucinous and the transitional tumors of ovaries are two of the least common types of the epithelial ovarian tumors. In fact, most of the mucinous tumors in ovaries are secondary and primary tumors only form about 3% of all epithelial ovarian cancers. Mucinous epithelium in mucinous tumors of ovaries resemble more to intestinal mucinous epithelium rather than that of endocervix as was previously argued. Transitional cell tumors, on the other hand, are closer to bladder epithelium in histological studies.<ref name="pmid18317228">{{cite journal |vauthors=Kurman RJ, Shih IeM |title=Pathogenesis of ovarian cancer: lessons from morphology and molecular biology and their clinical implications |journal=Int. J. Gynecol. Pathol. |volume=27 |issue=2 |pages=151–60 |date=April 2008 |pmid=18317228 |pmc=2794425 |doi=10.1097/PGP.0b013e318161e4f5 |url=}}</ref><ref name="pmid21683865">{{cite journal |vauthors=Kurman RJ, Shih IeM |title=Molecular pathogenesis and extraovarian origin of epithelial ovarian cancer--shifting the paradigm |journal=Hum. Pathol. |volume=42 |issue=7 |pages=918–31 |date=July 2011 |pmid=21683865 |pmc=3148026 |doi=10.1016/j.humpath.2011.03.003 |url=}}</ref><ref name="pmid19038766">{{cite journal |vauthors=Dubeau L |title=The cell of origin of ovarian epithelial tumours |journal=Lancet Oncol. |volume=9 |issue=12 |pages=1191–7 |date=December 2008 |pmid=19038766 |pmc=4176875 |doi=10.1016/S1470-2045(08)70308-5 |url=}}</ref><ref name="pmid10366144">{{cite journal |vauthors=Riopel MA, Ronnett BM, Kurman RJ |title=Evaluation of diagnostic criteria and behavior of ovarian intestinal-type mucinous tumors: atypical proliferative (borderline) tumors and intraepithelial, microinvasive, invasive, and metastatic carcinomas |journal=Am. J. Surg. Pathol. |volume=23 |issue=6 |pages=617–35 |date=June 1999 |pmid=10366144 |doi= |url=}}</ref><ref name="pmid17527072">{{cite journal |vauthors=Vang R, Gown AM, Zhao C, Barry TS, Isacson C, Richardson MS, Ronnett BM |title=Ovarian mucinous tumors associated with mature cystic teratomas: morphologic and immunohistochemical analysis identifies a subset of potential teratomatous origin that shares features of lower gastrointestinal tract mucinous tumors more commonly encountered as secondary tumors in the ovary |journal=Am. J. Surg. Pathol. |volume=31 |issue=6 |pages=854–69 |date=June 2007 |pmid=17527072 |doi=10.1097/PAS.0b013e31802efb45 |url=}}</ref>
* Another study demonstrated the presence of Brenner tumor foci in mucinous cystadenoma in almost one fifth of the cases. Alternatively the association of mucinous tumors with Walthard cell nests, which are composed of transitional-type epithelium, also indicates the connection between mucinous and transitional tumors.<ref name="pmid18317228">{{cite journal |vauthors=Kurman RJ, Shih IeM |title=Pathogenesis of ovarian cancer: lessons from morphology and molecular biology and their clinical implications |journal=Int. J. Gynecol. Pathol. |volume=27 |issue=2 |pages=151–60 |date=April 2008 |pmid=18317228 |pmc=2794425 |doi=10.1097/PGP.0b013e318161e4f5 |url=}}</ref><ref name="pmid21683865">{{cite journal |vauthors=Kurman RJ, Shih IeM |title=Molecular pathogenesis and extraovarian origin of epithelial ovarian cancer--shifting the paradigm |journal=Hum. Pathol. |volume=42 |issue=7 |pages=918–31 |date=July 2011 |pmid=21683865 |pmc=3148026 |doi=10.1016/j.humpath.2011.03.003 |url=}}</ref><ref name="pmid19038766">{{cite journal |vauthors=Dubeau L |title=The cell of origin of ovarian epithelial tumours |journal=Lancet Oncol. |volume=9 |issue=12 |pages=1191–7 |date=December 2008 |pmid=19038766 |pmc=4176875 |doi=10.1016/S1470-2045(08)70308-5 |url=}}</ref>
* Another study demonstrated the presence of Brenner tumor foci in mucinous cystadenoma in almost one fifth of the cases. Alternatively the association of mucinous tumors with Walthard cell nests, which are composed of transitional-type epithelium, also indicates the connection between mucinous and transitional tumors.<ref name="pmid18317228">{{cite journal |vauthors=Kurman RJ, Shih IeM |title=Pathogenesis of ovarian cancer: lessons from morphology and molecular biology and their clinical implications |journal=Int. J. Gynecol. Pathol. |volume=27 |issue=2 |pages=151–60 |date=April 2008 |pmid=18317228 |pmc=2794425 |doi=10.1097/PGP.0b013e318161e4f5 |url=}}</ref><ref name="pmid21683865">{{cite journal |vauthors=Kurman RJ, Shih IeM |title=Molecular pathogenesis and extraovarian origin of epithelial ovarian cancer--shifting the paradigm |journal=Hum. Pathol. |volume=42 |issue=7 |pages=918–31 |date=July 2011 |pmid=21683865 |pmc=3148026 |doi=10.1016/j.humpath.2011.03.003 |url=}}</ref><ref name="pmid19038766">{{cite journal |vauthors=Dubeau L |title=The cell of origin of ovarian epithelial tumours |journal=Lancet Oncol. |volume=9 |issue=12 |pages=1191–7 |date=December 2008 |pmid=19038766 |pmc=4176875 |doi=10.1016/S1470-2045(08)70308-5 |url=}}</ref><ref name="pmid17527072">{{cite journal |vauthors=Vang R, Gown AM, Zhao C, Barry TS, Isacson C, Richardson MS, Ronnett BM |title=Ovarian mucinous tumors associated with mature cystic teratomas: morphologic and immunohistochemical analysis identifies a subset of potential teratomatous origin that shares features of lower gastrointestinal tract mucinous tumors more commonly encountered as secondary tumors in the ovary |journal=Am. J. Surg. Pathol. |volume=31 |issue=6 |pages=854–69 |date=June 2007 |pmid=17527072 |doi=10.1097/PAS.0b013e31802efb45 |url=}}</ref>
*  
*  
*[[File:ARIDA loss and PIK3CA activation in clear cell cancer of ovaries.png|center|frame|'''<big>ARIDA loss and PIK3CA activation in clear cell cancer of ovaries.</big>'''<ref name="pmid256256252">{{cite journal |vauthors=Chandler RL, Damrauer JS, Raab JR, Schisler JC, Wilkerson MD, Didion JP, Starmer J, Serber D, Yee D, Xiong J, Darr DB, Pardo-Manuel  de Villena F, Kim WY, Magnuson T |title=Coexistent ARID1A-PIK3CA mutations promote ovarian clear-cell tumorigenesis through pro-tumorigenic inflammatory cytokine signalling |journal=Nat Commun |volume=6 |issue= |pages=6118 |date=January 2015 |pmid=25625625 |pmc=4308813 |doi=10.1038/ncomms7118 |url=}}</ref>(A)  ARID1A and PIK3CA alterations plot against TCGA datasets. Significance of association between ARID1A and PIK3CA mutations were determined using Fisher’s exact test. (B) Determination of CRE-deleted (''Arid1aΔ'') allele in samples of tumor DNA. (C) RT-PCR was used to detect ARID1A loss or ''(Gt)Rosa26Pik3ca<sup>*H1047R</sup>'' transcripts.  (D and E) Expression of ARID1A in normal ovaries (E) Expression of ARID1A in the normal ovarian surface epithelium (arrowhead). (F) ARID1A expression is not observed in the tumors. (H, I) Highest expression of P-AKT S473 in surface epithelium of ovaries in normal ovaries (E, arrowhead) and are greatly increased in ovarian tumors (F, arrowhead). Asterisk in ''E'' denotes an oocyte. (J,K) Morbid ''Arid1a<sup>fl/fl</sup>;(Gt)Rosa26Pik3ca<sup>*H1047R</sup>'' mouse at sacrifice with hemorrhagic ascites (inset), primary ovarian tumor of moderate size, and bilateral tumor metastases (arrowheads). (L,M) Morbid ''Arid1a<sup>fl/fl</sup>;(Gt)Rosa26Pik3ca<sup>*H1047R</sup>'' mouse at sacrifice with hemorrhagic ascites (inset), large primary ovarian tumor, and no visible metastases. The mice shown in ''J-M'' were sacrificed at 7 and 9 weeks post-AdCRE, respectively, because of visible ascitic fluid burden. (N,O) ''Arid1a<sup>fl/+</sup>;(Gt)Rosa26Pik3ca<sup>*H1047R</sup>'' mice at 11-weeks post-AdCRE showing no evidence for tumor formation. In ''K'' and ''M'', dashed circles indicate primary ovarian tumor on injected ovary. In ''N'', arrows denote the AdCRE injected ovary. In ''K'', ''M'', and ''O'', asterisks denote the uninjected, control ovary.]]
*[[File:ARIDA loss and PIK3CA activation in clear cell cancer of ovaries.png|center|frame|'''<big>ARIDA loss and PIK3CA activation in clear cell cancer of ovaries.</big>'''<ref name="pmid256256252">{{cite journal |vauthors=Chandler RL, Damrauer JS, Raab JR, Schisler JC, Wilkerson MD, Didion JP, Starmer J, Serber D, Yee D, Xiong J, Darr DB, Pardo-Manuel  de Villena F, Kim WY, Magnuson T |title=Coexistent ARID1A-PIK3CA mutations promote ovarian clear-cell tumorigenesis through pro-tumorigenic inflammatory cytokine signalling |journal=Nat Commun |volume=6 |issue= |pages=6118 |date=January 2015 |pmid=25625625 |pmc=4308813 |doi=10.1038/ncomms7118 |url=}}</ref>(A)  ARID1A and PIK3CA alterations plot against TCGA datasets. Significance of association between ARID1A and PIK3CA mutations were determined using Fisher’s exact test. (B) Determination of CRE-deleted (''Arid1aΔ'') allele in samples of tumor DNA. (C) RT-PCR was used to detect ARID1A loss or ''(Gt)Rosa26Pik3ca<sup>*H1047R</sup>'' transcripts.  (D and E) Expression of ARID1A in normal ovaries (E) Expression of ARID1A in the normal ovarian surface epithelium (arrowhead). (F) ARID1A expression is not observed in the tumors. (H, I) Highest expression of P-AKT S473 in surface epithelium of ovaries in normal ovaries (E, arrowhead) and are greatly increased in ovarian tumors (F, arrowhead). Asterisk in ''E'' denotes an oocyte. (J,K) Morbid ''Arid1a<sup>fl/fl</sup>;(Gt)Rosa26Pik3ca<sup>*H1047R</sup>'' mouse at sacrifice with hemorrhagic ascites (inset), primary ovarian tumor of moderate size, and bilateral tumor metastases (arrowheads). (L,M) Morbid ''Arid1a<sup>fl/fl</sup>;(Gt)Rosa26Pik3ca<sup>*H1047R</sup>'' mouse at sacrifice with hemorrhagic ascites (inset), large primary ovarian tumor, and no visible metastases. The mice shown in ''J-M'' were sacrificed at 7 and 9 weeks post-AdCRE, respectively, because of visible ascitic fluid burden. (N,O) ''Arid1a<sup>fl/+</sup>;(Gt)Rosa26Pik3ca<sup>*H1047R</sup>'' mice at 11-weeks post-AdCRE showing no evidence for tumor formation. In ''K'' and ''M'', dashed circles indicate primary ovarian tumor on injected ovary. In ''N'', arrows denote the AdCRE injected ovary. In ''K'', ''M'', and ''O'', asterisks denote the uninjected, control ovary.]]

Revision as of 16:36, 25 February 2019


Template:Epithelial ovarian cancer Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Hannan Javed, M.D.[2]


The origin of mucinous tumors of gastrointestinal type and transitional cell (Brenner) tumors: Still a mystery to solve

  • Mucinous and the transitional tumors of ovaries are two of the least common types of the epithelial ovarian tumors. In fact, most of the mucinous tumors in ovaries are secondary and primary tumors only form about 3% of all epithelial ovarian cancers. Mucinous epithelium in mucinous tumors of ovaries resemble more to intestinal mucinous epithelium rather than that of endocervix as was previously argued. Transitional cell tumors, on the other hand, are closer to bladder epithelium in histological studies.[1][2][3][4][5]
  • Another study demonstrated the presence of Brenner tumor foci in mucinous cystadenoma in almost one fifth of the cases. Alternatively the association of mucinous tumors with Walthard cell nests, which are composed of transitional-type epithelium, also indicates the connection between mucinous and transitional tumors.[1][2][3][5]
  • ARIDA loss and PIK3CA activation in clear cell cancer of ovaries.[6](A)  ARID1A and PIK3CA alterations plot against TCGA datasets. Significance of association between ARID1A and PIK3CA mutations were determined using Fisher’s exact test. (B) Determination of CRE-deleted (Arid1aΔ) allele in samples of tumor DNA. (C) RT-PCR was used to detect ARID1A loss or (Gt)Rosa26Pik3ca*H1047R transcripts.  (D and E) Expression of ARID1A in normal ovaries (E) Expression of ARID1A in the normal ovarian surface epithelium (arrowhead). (F) ARID1A expression is not observed in the tumors. (H, I) Highest expression of P-AKT S473 in surface epithelium of ovaries in normal ovaries (E, arrowhead) and are greatly increased in ovarian tumors (F, arrowhead). Asterisk in E denotes an oocyte. (J,K) Morbid Arid1afl/fl;(Gt)Rosa26Pik3ca*H1047R mouse at sacrifice with hemorrhagic ascites (inset), primary ovarian tumor of moderate size, and bilateral tumor metastases (arrowheads). (L,M) Morbid Arid1afl/fl;(Gt)Rosa26Pik3ca*H1047R mouse at sacrifice with hemorrhagic ascites (inset), large primary ovarian tumor, and no visible metastases. The mice shown in J-M were sacrificed at 7 and 9 weeks post-AdCRE, respectively, because of visible ascitic fluid burden. (N,O) Arid1afl/+;(Gt)Rosa26Pik3ca*H1047R mice at 11-weeks post-AdCRE showing no evidence for tumor formation. In K and M, dashed circles indicate primary ovarian tumor on injected ovary. In N, arrows denote the AdCRE injected ovary. In K, M, and O, asterisks denote the uninjected, control ovary.

References

  1. ↑ 1.0 1.1 Kurman RJ, Shih I (April 2008). "Pathogenesis of ovarian cancer: lessons from morphology and molecular biology and their clinical implications". Int. J. Gynecol. Pathol. 27 (2): 151–60. doi:10.1097/PGP.0b013e318161e4f5. PMC 2794425. PMID 18317228. Vancouver style error: initials (help)
  2. ↑ 2.0 2.1 Kurman RJ, Shih I (July 2011). "Molecular pathogenesis and extraovarian origin of epithelial ovarian cancer--shifting the paradigm". Hum. Pathol. 42 (7): 918–31. doi:10.1016/j.humpath.2011.03.003. PMC 3148026. PMID 21683865. Vancouver style error: initials (help)
  3. ↑ 3.0 3.1 Dubeau L (December 2008). "The cell of origin of ovarian epithelial tumours". Lancet Oncol. 9 (12): 1191–7. doi:10.1016/S1470-2045(08)70308-5. PMC 4176875. PMID 19038766.
  4. ↑ Riopel MA, Ronnett BM, Kurman RJ (June 1999). "Evaluation of diagnostic criteria and behavior of ovarian intestinal-type mucinous tumors: atypical proliferative (borderline) tumors and intraepithelial, microinvasive, invasive, and metastatic carcinomas". Am. J. Surg. Pathol. 23 (6): 617–35. PMID 10366144.
  5. ↑ 5.0 5.1 Vang R, Gown AM, Zhao C, Barry TS, Isacson C, Richardson MS, Ronnett BM (June 2007). "Ovarian mucinous tumors associated with mature cystic teratomas: morphologic and immunohistochemical analysis identifies a subset of potential teratomatous origin that shares features of lower gastrointestinal tract mucinous tumors more commonly encountered as secondary tumors in the ovary". Am. J. Surg. Pathol. 31 (6): 854–69. doi:10.1097/PAS.0b013e31802efb45. PMID 17527072.
  6. ↑ Chandler RL, Damrauer JS, Raab JR, Schisler JC, Wilkerson MD, Didion JP, Starmer J, Serber D, Yee D, Xiong J, Darr DB, Pardo-Manuel de Villena F, Kim WY, Magnuson T (January 2015). "Coexistent ARID1A-PIK3CA mutations promote ovarian clear-cell tumorigenesis through pro-tumorigenic inflammatory cytokine signalling". Nat Commun. 6: 6118. doi:10.1038/ncomms7118. PMC 4308813. PMID 25625625.
Retrieved from "https://www.wikidoc.org/index.php?title=Epithelial_ovarian_cancer&oldid=1553984"