Characterization of Four Novel Epithelial Ovarian Cancer Cell Lines

Provencher, Diane; Lounis, H.; Champoux, L.; Tétrault, M.; Manderson, Emily N.; Wang, J. C.; Eydoux, P.; Savoie, R.; Tonin, Patricia N.; Mes‐Masson, Anne‐Marie

doi:10.1290/1071-2690(2000)036<0357:cofneo>2.3.co;2

Cited by 50 publications

(107 citation statements)

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“…7), similar in magnitude to that observed when melanoma cell lines are treated with DAC (37,43,44). When cell lines already express class I MHC molecules at intermediate to high levels, the amount of increase if any, is less than twofold (e.g.…”

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confidence: 71%

Identification and Characterization of Ovarian Carcinoma Peptide Epitopes Recognized by Cylotoxic T Lymphocytes

Hogan¹

2008

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. REPORT DATE PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION REPORT NUMBERUniversity of Virginia Charlottesville, VA 22904 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTES ABSTRACTThe purpose of the research was to identify new ovarian cancer tumor antigens that could be used in the development of an ovarian cancer vaccine. The scope of the work involved identifying peptide antigens recognized by ovarian cancer reactive cytotoxic T lymphocytes (CTL). Eleven ovarian cancer cell lines were characterized for their expression of tumor antigens and MHC molecules This was significant because it provided a resource that could be used for new antigen identification work. CTL were generated against autologous ovarian cancer cells but no evidence was found for the recognition of shared antigens which is significant because this is the type of antigen needed for vaccine development. New methodology was devised for the efficient assessment of the immunogenicity of peptides derived from known protein antigens. This work was significant because it resulted in the identification of two new HLA-A2-restricted antigens derived from TAG-1. It was demonstrated that the treatment of ovarian cancer cells with a demethylating agent is capable of turning on the expression of a large number of cancer/testis antigens and increasing the expression of class I MHC molecules which is significant because known antigens can now be used to target cells that would otherwise escape recognition by CTL. SUBJECT TERMSOvarian carcinoma, immunotherapy, cytotoxic T lymphocytes, epitope, peptide, major histocompatibility complex (MHC)-encoded molecules, class I MHC molecules, HLA INTRODUCTIONThe subject of this research is the identification of ovarian cancer antigens that are recognized by cytotoxic T lymphocytes (CTL). The purpose of the research is to identify ova...

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confidence: 71%

Identification and Characterization of Ovarian Carcinoma Peptide Epitopes Recognized by Cylotoxic T Lymphocytes

Hogan¹

2008

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“…In contrast to RHBDF2, differential expression of CYGB in the EOC cell lines was observed and there was no alteration in gene expression profile in the genetically modified OV-90 derived EOC cell lines. However, it is interesting to note the undetectable levels of CYGB expression in TOV-1946 and OV-1946 EOC cell lines relative to TOV-81D and TOV-2223G, given that these cell lines were all derived from ovarian cancers of the serous histopathological subtype, and that the former exhibit both in vitro and in vivo characteristics associated with tumourigenic potential (36,37). It is possible that the CYGB expression profile is more characteristic of malignant ovarian carcinomas of the serous histopathological subtype as has been observed for other genes differentially expressed in serous ovarian cancer (32).…”

Section: Discussionmentioning

confidence: 97%

“…Cells were cultured in OSE Medium supplemented with 2.5 µg/ml amphotericin B, 50 µg/ ml gentamicin and 15% fetal bovine serum (FBS) as previously described (34). EOC cell lines were derived from a stage IIIc/ grade 1-2 papillary serous adenocarcinoma (TOV-81D), a stage III/grade 3 clear cell carcinoma (TOV-21G), a stage IIIc/ grade 3 endometrioid carcinoma (TOV-112D), the ascites fluid of a stage IIIc/grade 3 adenocarcinoma (OV-90), a stage IIIc/ grade 3 serous carcinoma (TOV-2223G), and both the tumour and the ascites fluid of a stage IIIc/grade 3 serous tumour (TOV-1946 andOV-1946), all from chemotherapy naïve patients, as described (36,37). The non-tumourigenic chromosome 3 transfer radiation hybrids (RH), RH-5, RH-6, and RH-10 cell lines, were derived using a neomycin clone of OV-90 (OV-90 neo r ), and the B78MC166 mouse cell line containing human chromosome 3 as described previously (31).…”

Section: Methodsmentioning

confidence: 99%

“…The non-tumourigenic chromosome 3 transfer radiation hybrids (RH), RH-5, RH-6, and RH-10 cell lines, were derived using a neomycin clone of OV-90 (OV-90 neo r ), and the B78MC166 mouse cell line containing human chromosome 3 as described previously (31). The cell lines were cultured in OSE Medium supplemented with 2.5 µg/ml amphotericin B, 50 µg/ ml gentamicin and 10% FBS as described previously (36,37).…”

Section: Methodsmentioning

confidence: 99%

“…Gene expression analysis of RHBDF2 and CYGB was also investigated by semi-quantitative RT-PCR in EOC cell lines established as long-term passages from chemotherapy naïve ovarian cancer samples in our research group (36,37). The cell lines differ in their in vivo tumourigenic potential, where TOV-81D and TOV-2223G are incapable of forming tumours as xenografts in immunocompromised mice in contrast to OV-90, TOV-21G, TOV-112D, TOV-1946, andOV-1946 (36,37).…”

Section: Defining the 17q25 Tsg Locusmentioning

confidence: 99%

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Chromosome 17q25 genes, RHBDF2 and CYGB, in ovarian cancer

et al. 2012

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Abstract. It has been proposed that the frequent loss of heterozygosity (LOH) of an entire chromosome 17 contig in epithelial ovarian cancers (EOC) is the consequence of the inactivation of multiple tumour suppressor genes on this chromosome. We report the characterization of a 453 Kb 17q25 locus shown previously to exhibit a high frequency of LOH in EOC samples. LOH analysis further defined the minimal region of deletion to a 65 Kb interval flanked by D17S2239 and D17S2244, which contains RHBDF2, CYGB and PRCD as tumour suppressor gene candidates. Tissue specific expression excluded PRCD as a candidate. RHBDF2 was expressed at low levels in the majority of benign and low malignant potential (LMP) tumours, and in a subset of malignant ovarian tumour samples, as compared with primary cultures of normal ovarian surface epithelial cell (NOSE) samples. CYGB was expressed at low levels in the majority of LMP and malignant samples compared with benign and NOSE samples. In contrast to CYGB expression, RHBDF2 was expressed at low or undetectable levels in EOC cell lines exhibiting tumourigenic characteristics and up-regulated in a genetically modified EOC cell line rendered non-tumourigenic. DNA sequence analysis identified variants but no apparent deleterious mutations in either gene. Methylation-specific PCR analysis suggested that promoter methylation of CYGB but not RHBDF2 occurred in 6 of 31 malignant samples. The results combined suggest that RHBDF2 and CYGB may play distinctive roles in ovarian cancer and could be added to the growing roster of chromosome 17 genes implicated in this disease.

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Chromosomes 6 and 18 induce neoplastic suppression in epithelial ovarian cancer cells

Dafou

Ramus

Choi

et al. 2008

Intl Journal of Cancer

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Metaphase comparative genomic hybridisation (CGH) studies indicate that chromosomes 4, 5, 6, 13, 14, 15, and 18 are frequently deleted in primary ovarian cancers (OC). Therefore we used microcell-mediated chromosome transfer (MMCT) to establish the functional effects of transferring normal copies of these chromosomes into two epithelial OC cell lines (TOV112D and TOV21G). The in vitro neoplastic phenotype (measured as anchorage dependent and independent growth and invasion) was compared between recipient OC cell lines and multiple MMCT hybrids. Chromosomes 6 and 18 showed strong evidence of functional, neoplastic suppression for multiple hybrids in both cell lines. We also found evidence in one cancer cell line suggesting that chromosomes 4, 13 and 14 may also cause functional suppression. Array CGH and microsatellite analyses were used to characterise the extent of genomic transfer in chromosome 6 and 18 hybrids. A 36Mb deletion on chromosome 6 in two hybrids from one cell line mapped the candidate region proximal to 6q15 and distal to 6q22.2; and an approximately 10Mb candidate region spanning the centromere on chromosome 18, was identified in two hybrids from the other cell line. These data confirm reported functional effects of chromosome 6 in OC cell lines; but to our knowledge, this is the first time that functional suppression for chromosome 18 has been reported. This suggests that these chromosomes may harbour tumour suppressor like genes. The future identification of these genes may have a significant impact on the understanding and treatment of the disease, the identification of novel therapeutic targets

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Characterization of Four Novel Epithelial Ovarian Cancer Cell Lines

Cited by 50 publications

References 0 publications

Identification and Characterization of Ovarian Carcinoma Peptide Epitopes Recognized by Cylotoxic T Lymphocytes

Identification and Characterization of Ovarian Carcinoma Peptide Epitopes Recognized by Cylotoxic T Lymphocytes

Chromosome 17q25 genes, RHBDF2 and CYGB, in ovarian cancer

Chromosomes 6 and 18 induce neoplastic suppression in epithelial ovarian cancer cells

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