The DOI matches its Crossref record.
Gene Expression Profiles Associated with Response to Chemotherapy in Epithelial Ovarian Cancers
Published version of a preprint
Abstract
Purpose: The goal of this study was to determine whether distinct gene expression profiles are associated with intrinsic and/or acquired chemoresistance in epithelial ovarian carcinoma. Experimental Design: Gene expression profiles were generated from 21 primary chemosensitive tumors and 24 primary chemoresistant tumors using cDNA-based microarrays. Gene expression profiles of both groups of primary tumors were then compared with those of 15 ovarian carcinomas obtained following platinum-based chemotherapy (“postchemotherapy” tumors). A theme discovery tool was used to identify functional categories of genes involved in drug resistance. Results: Comparison of primary chemosensitive and chemoresistant tumors revealed differential expression of 85 genes (P < 0.001). Comparison of gene expression profiles of primary chemosensitive tumors and postchemotherapy tumors revealed more robust differences with 760 genes differentiating the two groups (P < 0.001). In contrast, only 230 genes were differentially expressed between primary chemoresistant and postchemotherapy groups (P < 0.001). Common to both gene lists were 178 genes representing transcripts differentially expressed between postchemotherapy tumors and all primary tumors irrespective of intrinsic chemosensitivity. The gene expression profile of postchemotherapy tumors compared with that of primary tumors revealed statistically significant overrepresentation of genes encoding extracellular matrix–related proteins. Conclusions: These data show that gene expression profiling can discriminate primary chemoresistant from primary chemosensitive ovarian cancers. Gene expression profiles were also identified that correlate with states of intrinsic and acquired chemoresistance and that represent targets for future investigation and potential therapeutic interventions.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Advances in molecular omics strategies have revealed significant genetic and molecular heterogeneity of OvCa that could influence prognostic and chemotherapeutic response.
“Advances in molecular “omics” strategies have revealed the significant genetic and molecular heterogeneity of OvCa that could influence the prognostic and chemotherapeutic response of patients5–9.”
Citations
Cites
No references could be resolved yet.
Research works printed but not linked: 47
- Chi DS, Sabbatini P. Advanced ovarian cancer. Curr Treat Options Oncol 2000;1:139–46. · DOI
- Salom E, Almeida Z, Mirhashemi R. Management of recurrent ovarian cancer: evidence-based decisions. Curr Opin Oncol 2002;14:519–27. · DOI
- McGuire WP, Markman M. Primary ovarian cancer chemotherapy: current standards of care. Br J Cancer 2003;89:S3–8. · DOI
- Markman M, Hoskins W. Responses to salvage chemotherapy in ovarian cancer: a critical need for precise definitions of the treated population [editorial]. J Clin Oncol 1992;10:513–4. · DOI
- Alberts DS. Treatment of refractory and recurrent ovarian cancer. Semin Oncol 1999;26:8–14.
- Spriggs D. Optimal sequencing in the treatment of recurrent ovarian cancer. Gynecol Oncol 2003;90:S39–44. · DOI
- Johnson SW, Ozols RF, Hamilton TC. Mechanisms of drug resistance in ovarian cancer. Cancer 1993;71:644–9. · DOI
- Aebi S, Kurdihaidar B, Gordon R, et al. Loss of DNA mismatch repair in acquired resistance to cisplatin. Cancer Res 1996;56:3087–90.
- Coukos G, Rubin SC. Chemotherapy resistance in ovarian cancer: new molecular perspectives. Obstet Gynecol 1998;91:783–92. · DOI
- Vasey PA. Resistance to chemotherapy in advanced ovarian cancer: mechanisms and current strategies. Br J Cancer 2003;89:S23–8. · DOI
- Agarwal R, Kaye SB. Ovarian cancer: strategies for overcoming resistance to chemotherapy. Nat Rev Cancer 2003;3:502–16. · DOI
- Skipper HE. Kinetics of mammary tumor cell growth and implications for therapy. Cancer 1971;28:1479–99. · DOI
- Norton L, Simon R, Brereton HD, Bogden AE. Predicting the course of Gompertzian growth. Nature 1976;264:542–5. · DOI
- Van Gelder RN, von Zastrow ME, Yool A, Dement WC, Barchas JD, Eberwine JH. Amplified RNA synthesized from limited quantities of heterogeneous cDNA. Proc Natl Acad Sci U S A 1990;87:1663–7. · DOI
- Hosack DA, Dennis G, Sherman BT, Lane HC, Lempicki RA. Identifying biological themes within lists of genes with EASE. Genome Biol 2003;4:R70. · DOI
- Losch A, Schindl M, Kohlberger P, et al. Cathepsin D in ovarian cancer: prognostic value and correlation with p53 expression and microvessel density. Gynecol Oncol 2004;92:545–52. · DOI
- Ioachim E, Tsanou E, Briasoulis E, et al. Clinicopathological study of the expression of hsp27, pS2, cathepsin D and metallothionein in primary invasive breast cancer. Breast 2003;12:111–9. · DOI
- Glondu M, Liaudet-Coopman E, Derocq D, Platet N, Rochefort H, Garcia M. Down-regulation of cathepsin-D expression by antisense gene transfer inhibits tumor growth and experimental lung metastasis of human breast cancer cells. Oncogene 2002;21:5127–34. · DOI
- Ioachim E, Charchanti A, Stavropoulos N, Athanassiou E, Bafa M, Agnantis NJ. Expression of cathepsin D in urothelial carcinoma of the urinary bladder: an immunohistochemical study including correlations with extracellular matrix components, CD44, p53, Rb, c-erbB-2 and the proliferation indices. Anticancer Res 2002;22:3383–8.
- Mok SC, Wong KK, Chan RK, et al. Molecular cloning of differentially expressed genes in human epithelial ovarian cancer. Gynecol Oncol 1994;52:247–52. · DOI · Paper page
- Wiechen K, Diatchenko L, Agoulnik A, et al. Caveolin-1 is down-regulated in human ovarian carcinoma and acts as a candidate tumor suppressor gene. Am J Pathol 2001;159:1635–43. · DOI
- Manzano RG, Montuenga LM, Dayton M, et al. CL100 expression is down-regulated in advanced epithelial ovarian cancer and its re-expression decreases its malignant potential. Oncogene 2002;21:4435–7. · DOI
- van der Zee AG, Hollema H, de Jong S, et al. P-glycoprotein expression and DNA topoisomerase I and II activity in benign tumors of the ovary and in malignant tumors of the ovary, before and after platinum/cyclophosphamide chemotherapy. Cancer Res 1991;51:5915–20.
- Jazaeri AA, Yee CJ, Sotiriou C, Brantley KR, Boyd J, Liu ET. Gene expression profiles of BRCA1-linked, BRCA2-linked, and sporadic ovarian cancers. J Natl Cancer Inst 2002;94:990–1000. · DOI
- Tiniakos DG, Yu H, Liapis H. Osteopontin expression in ovarian carcinomas and tumors of low malignant potential (LMP). Hum Pathol 1998;29:1250–4. · DOI
- Kim JH, Skates SJ, Uede T, et al. Osteopontin as a potential diagnostic biomarker for ovarian cancer. J Am Med Assoc 2002;287:1671–9. · DOI
- Zhang P, Liegeois NJ, Wong C, et al. Altered cell differentiation and proliferation in mice lacking p57KIP2 indicates a role in Beckwith-Wiedemann syndrome. Nature 1997;387:151–8. · DOI
- Luque A, Carpizo DR, Iruela-Arispe ML. ADAMTS1/METH1 inhibits endothelial cell proliferation by direct binding and sequestration of VEGF165. J Biol Chem 2003;278:23656–65. · DOI
- Babic AM, Kireeva ML, Kolesnikova TV, Lau LF. CYR61, a product of a growth factor-inducible immediate early gene, promotes angiogenesis and tumor growth. Proc Natl Acad Sci U S A 1998;95:6355–60. · DOI · Paper page
- Wittig R, Nessling M, Will RD, et al. Candidate genes for cross-resistance against DNA-damaging drugs. Cancer Res 2002;62:6698–705.
- Goldie JH, Coldman AJ. A mathematic model for relating the drug sensitivity of tumors to their spontaneous mutation rate. Cancer Treat Rep 1979;63:1727–33.
- Ferrandina G, Scambia G, Fagotti A, et al. Immunoradiometric and immunohistochemical analysis of cathepsin D in ovarian cancer: lack of association with clinical outcome. Br J Cancer 1998;78:1645–52. · DOI
- Scambia G, Panici PB, Ferrandina G, et al. Clinical significance of cathepsin D in primary ovarian cancer. Eur J Cancer 1994;30A:935–40. · DOI
- Baekelandt M, Holm R, Trope CG, Nesland JM, Kristensen GB. The significance of metastasis-related factors cathepsin-D and nm23 in advanced ovarian cancer. Ann Oncol 1999;10:1335–41. · DOI
- Wu GS, Saftig P, Peters C, El-Deiry WS. Potential role for cathepsin D in p53-dependent tumor suppression and chemosensitivity. Oncogene 1998;16:2177–83. · DOI
- Brustmann H. Apoptotic bodies as a morphological feature in serous ovarian carcinoma: correlation with nuclear grade, Ki-67 and mitotic indices. Pathol Res Pract 2002;198:85–90. · DOI
- Sherman-Baust CA, Weeraratna AT, Rangel LB, et al. Remodeling of the extracellular matrix through overexpression of collagen VI contributes to cisplatin resistance in ovarian cancer cells. Cancer Cell 2003;3:377–86. · DOI
- Bradshaw AD, Sage EH. SPARC, a matricellular protein that functions in cellular differentiation and tissue response to injury. J Clin Invest 2001;107:1047–54. · DOI
- Korn EL, McShane LM, Troendle JF, Rosenwald A, Simon R. Identifying pre-post chemotherapy differences in gene expression in breast tumours: a statistical method appropriate for this aim. Br J Cancer 2002;83:1093–6. · DOI
- Mok SC, Chan WY, Wong KK, Muto MG, Berkowitz RS. SPARC, an extracellular matrix protein with tumor-suppressing activity in human ovarian epithelial cells. Oncogene 1996;12:1895–901.
- Yiu GK, Chan WY, Ng SW, et al. SPARC (secreted protein acidic and rich in cysteine) induces apoptosis in ovarian cancer cells. Am J Pathol 2001;159:609–22. · DOI
- Dhanesuan N, Sharp JA, Blick T, Price JT, Thompson EW. Doxycycline-inducible expression of SPARC/osteonectin/BM40 in MDA-MB-231 human breast cancer cells results in growth inhibition. Breast Cancer Res Treat 2002;75:73–85. · DOI
- Gilles C, Bassuk JA, Pulyaeva H, Sage EH, Foidart JM, Thompson EW. SPARC/osteonectin induces matrix metalloproteinase 2 activation in human breast cancer cell lines. Cancer Res 1998;58:5529–36.
- Fujita T, Shiba H, Sakata M, Uchida Y, Nakamura S, Kurihara H. SPARC stimulates the synthesis of OPG/OCIF, MMP-2 and DNA in human periodontal ligament cells. J Oral Pathol Med 2002;31:345–52. · DOI
- Claeskens A, Ongenae N, Neefs JM, et al. Hevin is down-regulated in many cancers and is a negative regulator of cell growth and proliferation. Br J Cancer 2000;82:1123–30. · DOI
- Chen X, Whitney EM, Gao SY, Yang VW. Transcriptional profiling of Kruppel-like factor 4 reveals a function in cell cycle regulation and epithelial differentiation. J Mol Biol 2003;326:665–77. · DOI
- McCluggage WG, Lyness RW, Atkinson RJ, et al. Morphological effects of chemotherapy on ovarian carcinoma. J Clin Pathol 2002;55:27–31. · DOI
Cited by
Sorted by citations
HDAC4-Regulated STAT1 Activation Mediates Platinum Resistance in Ovarian Cancer
Stronach, E. A., Alfraidi, A., Rama, N., Datler, C., Studd, J. B., Agarwal, R., Guney, T. G., Gourley, C., Hennessy, B. T., Mills, G. B., et al. (2011) · Cancer Research · doi:10.1158/0008-5472.can-10-4111 · Cited by 176
Sun, J., Bao, S., Xu, D., Zhang, Y., Su, J., Liu, J., Hao, D., & Zhou, M. (2019) · Cell Death & Disease · doi:10.1038/s41419-019-1874-9 · Cited by 23
Metadata
- Authors
- Jazaeri, A. A., Awtrey, C. S., Chandramouli, G. V. R., Chuang, Y. E., Khan, J., Sotiriou, C., Aprelikova, O., Yee, C. J., Zorn, K. K., Birrer, M. J., Barrett, J. C., & Boyd, J.
- Affiliations
- 1Laboratory of Biosystems and Cancer and
- 4Gynecology and Breast Research Laboratory, Department of Surgery, and
- Center for Cancer Research (US)
- National Cancer Institute (US)
- Memorial Sloan Kettering Cancer Center (US)
- ORCID
- Venue
- Clinical Cancer Research
- Published
- 2005-09-01
- Volume
- 11
- Issue
- 17
- Pages
- 6300-6310
- ISSN
- 1078-0432 (ISSN-L)
- 1557-3265
- OpenAlex
- W2109449896
- Cited by
- 192
- References
- 0
- Citations by year
- 2025: 1 · 2024: 7 · 2023: 12 · 2022: 4 · 2021: 6 · 2020: 4 · 2019: 4 · 2018: 7 · 2017: 4 · 2016: 10 · 2015: 14 · 2014: 9 · 2013: 12 · 2012: 19
- FWCI
- 14.77
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Clinical Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) (submittedVersion)
- Funders
- National Cancer Institute (U01CA088175, U01CA88175)
- Topics
- Health Sciences › Medicine › Oncology › Ovarian cancer diagnosis and treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gene expression and cancer classification
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Breast Cancer Treatment Studies
- Keywords
- epithelial ovarian cancer, chemoresistance, gene expression profiling, acquired chemoresistance, platinum-based chemotherapy, extracellular matrix genes, differential gene expression
- MeSH terms
- Adult, Aged, Aged, 80 and over, Antineoplastic Agents, Female, Humans, Immunoenzyme Techniques, Middle Aged, Neoplasm Proteins, Neoplasm Staging, Ovarian Neoplasms, RNA, Neoplasm, Biomarkers, Tumor, Gene Expression Regulation, Neoplastic, Carcinoma, Endometrioid, Cystadenocarcinoma, Serous, Reverse Transcriptase Polymerase Chain Reaction, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review