Assembly of MHC class I molecules in ex vivo carcinoma cells induced by IFN-γ or by a binding peptide

Wang, P.; Vánky, Farkas; Végh, Zsuzsa; Persson, Ulla; Hising, Ch.; Klein, Eva

doi:10.1016/0008-8749(92)90291-v

Cited by 5 publications

(4 citation statements)

References 21 publications

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“…Because the tumor-specific cytotoxicity exhibited by CTLs is dependent on the presentation of peptides on the cell surface bound to MHC on tumor cells, it follows that absent or reduced expression of MHC antigens may interfere with CTL recognition. It has been shown that the expression of MHC class I or MHC class II surface antigens may be reduced on various solid tumors, including breast [72][73][74][75][76], colon [74][75][76], melanoma [77], genitourinary [74,78], and ovarian carcinoma [79][80][81][82]. It is evident, moreover, that downregulation of MHC alleles may not be restricted to specific alleles, such as HLA-A2, and that all MHC alleles may be frequently involved [81,82].…”

Section: Lymphokine Activated Killer Cells and Tumor Infiltrating Lymphocytesmentioning

confidence: 99%

“…It has been shown that the expression of MHC class I or MHC class II surface antigens may be reduced on various solid tumors, including breast [72][73][74][75][76], colon [74][75][76], melanoma [77], genitourinary [74,78], and ovarian carcinoma [79][80][81][82]. It is evident, moreover, that downregulation of MHC alleles may not be restricted to specific alleles, such as HLA-A2, and that all MHC alleles may be frequently involved [81,82].…”

Section: Lymphokine Activated Killer Cells and Tumor Infiltrating Lymphocytesmentioning

confidence: 99%

“…In vitro and in vivo priming of EOe cells with interferon-/, Induction or increased expression of MHC can be accomplished by treatment of tumor cells with cytokines that induce the expression of the MHC molecules [81,82,[103][104][105]. IFN-y alone [103] or IFN-y with TNF-a [81] increase the expression of MHC class I and II molecules on ovarian tumor cells in vitro.…”

Section: %mentioning

confidence: 99%

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Immunotherapy for peritoneal ovarian carcinoma metastasis using ex vivo expanded tumor infiltrating lymphocytes

Freedman¹,

Platsoucas²

1996

Cancer Treatment and Research

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Background to the standard treatment of ovarian cancer Cancer of the ovary is responsible for the highest proportion of the mortality in patients with gynecologic malignancies. The overall survival for these patients at 5 years is 39% [1]. Epithelial ovarian carcinoma (EOC) represents 90% of the histologies and is thus the most frequent histologic group. Primary peritoneal carcinoma, also called extraovarian mullerian carcinoma, has the same pattern of tumor spread and sensitivity to chemotherapy as EOC, although the ovaries arc not primarily involved in the pathologic process. Other malignancies that originate from the ovaries include those of germ cell and stromal cell origin. These are considered separately and have a different clinical presentation and a different response to treatment.The standard first-line treatment of EOC or peritoneal carcinomatosis includes an initial exploratory laparotomy. Abdominal surgery is performed to accomplish certain objectives: (1) to establish a histopathologic diagnosis, (2) to obtain intraoperative staging of the tumor, and (3) to achieve the maximum feasible removal of the tumor. Currently, surgical staging follows the 1985 recommendations of the Federation Internationale Gynecologie Obstetrique (FIGO). Surgical treatment is followed in most cases by platinum-based chemotherapy utilizing either carboplatinum or cisplatinum in combination with cyclophosphamide. Platinum-based chemotherapy is the treatment of choice in patients who have stage II-IV disease, which represents 90% of all patients with EOC. No single adjuvant treatment approach has been established for patients whose disease appears to be confined to the ovaries, although many of these patients will ultimately relapse, even after receiving chemotherapy. Combination chemotherapy regimens that include cisplatin or carboplatin produce overall response rates that are in the range of 60-80% [2,3]. The majority of these patients will ultimately progress, or will relapse after a complete pathologic response due to either primary or acquired drug resistance [4]. Recent phase II data have shown high response rates with taxoids, for example, taxol or taxotere [5,6], although there are few complete responses and treatment with these drugs may be both toxic and costly. In consideration of the overall low frequency

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Section: Lymphokine Activated Killer Cells and Tumor Infiltrating Lymphocytesmentioning

confidence: 99%

Section: Lymphokine Activated Killer Cells and Tumor Infiltrating Lymphocytesmentioning

confidence: 99%

Section: %mentioning

confidence: 99%

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Immunotherapy for peritoneal ovarian carcinoma metastasis using ex vivo expanded tumor infiltrating lymphocytes

Freedman¹,

Platsoucas²

1996

Cancer Treatment and Research

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“…in 8 tumors selective losses of one or more HLA allele products were detected biochemically (IEF) while in the 2 other cases class-I antigens were not detectable by indirect immunofluorescence with W6132 MAb ( Table I). One of these 2 tumors was further analysed and a defect in heavy-and light-chain assembly was demonstrated (Wang et a/., 1992).…”

Section: Proliferative Response In Autologous Mltcsmentioning

confidence: 99%

HLA‐B5‐restricted auto‐tumor‐specific cytotoxic T cells generated in mixed lymphocyte‐tumor‐cell culture

Wang

Végh

Vánky

et al. 1992

Intl Journal of Cancer

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T-cell-enriched lymphocyte populations derived from the malignant exudate of a patient with ovarian carcinoma were exposed to autologous tumor cells in the mixed lymphocyte-tumor-cell culture (MLTC) and propagated for 42 days. Proliferation of lymphocytes depended on exposures to autologous tumor cells and on the presence of IL-2. After 7 days, the MLTC-lymphocytes lysed K562 and the autologous tumor cells. The latter effect was not inhibited by monoclonal antibodies (MAbs) reactive with MHC class-I antigens or with CD3. After 7 restimulations, the culture was enriched in CD8+ cells (92%) and showed selective lytic activity against the autologous tumor. This function was inhibited by the alpha-class I or alpha-CD3 MAbs, and also by antibodies reactive with the HLA B locus or B5 allele products. The antibodies reactive with HLA A molecules had no such effect. It seems therefore that the function of the CTLs was restricted by HLA B5. Analysis of the TCR beta genes indicated clonal T-cell expansion in this culture. This MLTC was 1 of 21 initiated with 11 blood- and 10 tumor-derived lymphocyte (TIL) populations prepared from the malignant effusions of ovarian carcinoma patients. None of these ex-vivo lymphocytes lysed autologous tumor cells. In 17 MLTCs the lymphocytes did not proliferate, and in 3 cultures the proliferation was maintained only for 2-3 weeks. In 3 of 4 cultures auto-tumor cytotoxicity was induced.

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Generation of tumor cell lysate-loaded dendritic cells preprogrammed for IL-12 production and augmented T cell response

Végh¹,

Mazumder²

2003

Cancer Immunol Immunother

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Assembly of MHC class I molecules in ex vivo carcinoma cells induced by IFN-γ or by a binding peptide

Cited by 5 publications

References 21 publications

Immunotherapy for peritoneal ovarian carcinoma metastasis using ex vivo expanded tumor infiltrating lymphocytes

Immunotherapy for peritoneal ovarian carcinoma metastasis using ex vivo expanded tumor infiltrating lymphocytes

HLA‐B5‐restricted auto‐tumor‐specific cytotoxic T cells generated in mixed lymphocyte‐tumor‐cell culture

Generation of tumor cell lysate-loaded dendritic cells preprogrammed for IL-12 production and augmented T cell response

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