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8 results on '"Bravo, A.I."'

1. The expression of progesterone receptors coincides with an arrest of DNA synthesis in human breast cancer

Author

Ballare, C., Bravo, A.I., Sorin, I., Guman, N., Schiaffi, J.A., Yomha, R., Bagnati, A., Lema, B., and Mordoh, J.

Subjects
Progesterone -- Receptors, Breast cancer -- Physiological aspects, Hormone receptors -- Physiological aspects, Chemotherapy -- Evaluation, Estrogen -- Receptors, Hormone therapy -- Evaluation, Health
Abstract

Hormonal therapy is effective in only one third of breast cancer patients. Research has demonstrated that the response to hormonal therapy is largely determined by the presence of hormone receptors on the breast cancer cells. In tumor tissue that lacks both estrogen and progesterone receptors, the response rate is about 10 percent. For tumors that are estrogen receptor-positive, but lack the progesterone receptor, the response rate is about 30 percent. When both estrogen and progesterone receptors are present, the response rate jumps to 80 percent. There are too few patients with cells positive for only the progesterone receptor to draw any conclusions about such cells. It is clear, however, that the progesterone receptor is an important determinant of response to hormonal treatment. Varying hypotheses have been put forward to explain the variations of receptor expression and the variations of response to antiestrogen treatment. However, it has been observed clinically that if a patient with estrogen receptor-positive cells relapses after treatment, the cells still express estrogen receptor. The authors suggest that this supports the notion that the original tumor cells lack both receptors, but in the course of tumor growth some cells differentiate to express the estrogen receptor first, and then both progesterone and estrogen receptors. To examine this idea, researchers attempted to correlate the proliferative capacity of breast cancer cells with the expression of hormone receptors. It was found that the cell populations that expressed neither receptor incorporated more radioactive thymidine, indicating a higher rate of DNA synthesis. Cells that possessed the progesterone receptor had a thymidine labelling index of 0.21, while the cells that lacked the progesterone receptor had a thymidine labelling index over four times greater, at 0.94. The indices of cells with and without the estrogen receptor were intermediate at 0.53 and 0.74, respectively. These results indicate that the expression of progesterone receptors is associated with a reduction in DNA synthesis and therefore a reduction in proliferation. The results also suggest that the population of cells expressing the estrogen receptor is different from, but overlaps with, the population of cells expressing the progesterone receptor. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1991

3. Monocyte chemoattractant protein correlates with angiogenesis in metastatic melanoma

Author

Gazzaniga, S., Bravo, A.I., Mordoh, J., and Wainstok, R.

Subjects
Macrophages, Angiogenesis, Melanoma, Monocyte chemoattractant protein-1
Abstract

Biopsies from human metastatic melanomas were analyzed in order to elucidate the relationship between MCP-1/CCL-2 (monocyte chemoattractant protein-1) chemokine expression by tumor cells, angiogenesis and aggressiveness in tumor development. The chemokine was expressed in 100% of the cases, with heterogeneity in the percentage of positive cells within the tumor mass. Tumors presented an important infiltration of macrophages, particularly associated to areas of active angiogenesis. Microvascular development, assessed by immunohistochemistry, correlated with the high percentage of cells expressing MCP-1/CCL-2. There was also significant correlation with vascularization and mitotic index. These results suggest that vascularization could be predictive of more aggressive melanoma metastasis, where the MCP-1/CCL-2 expression would be closely associated to vessel development through macrophages recruitment. Fil:Gazzaniga, S. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.

Published
2006

4. Dendritic Cells Charged with Apoptotic Tumor Cells Induce Long-Lived Protective CD4+ and CD8+ T Cell Immunity against B16 Melanoma

Author

Goldszmid, R.S., Idoyaga, J., Bravo, A.I., Steinman, R., Mordoh, J., and Wainstok, R.

Subjects
melanoma cell, in vitro study, cell migration, dendritic cell, animal experiment, cell stimulation, major histocompatibility antigen class 1, cell maturation, animal cell, cellular immunity, immunogenicity, tumor cell, in vivo study, male, lymphocyte depletion, T lymphocyte, inoculation, controlled study, protein expression, mouse, target cell, cell culture, nonhuman, experiment, animal model, apoptosis, article, tyrosinase related protein 2, CD8 antigen, lymph node, lymphatic drainage, vaccination, antigen recognition, tumor immunity, cytokine release, injection, priority journal, provocation test, cytolysis, antigen expression, gamma interferon, CD4 antigen, coculture, bone marrow cell
Abstract

Dendritic cells (DCs) are potent APCs and attractive vectors for cancer immunotherapy. Using the B16 melanoma, a poorly immunogenic experimental tumor that expresses low levels of MHC class I products, we investigated whether DCs loaded ex vivo with apoptotic tumor cells could elicit combined CD4+ and CD8+ T cell dependent, long term immunity following injection into mice. The bone marrow-derived DCs underwent maturation during overnight coculture with apoptotic melanoma cells. Following injection, DCs migrated to the draining lymph nodes comparably to control DCs at a level corresponding to ∼0.5% of the injected inoculum. Mice vaccinated with tumor-loaded DCs were protected against an intracutaneous challenge with B16, with 80% of the mice remaining tumor-free 12 wk after challenge. CD4+ and CD8+ T cells were efficiently primed in vaccinated animals, as evidenced by IFN-γ secretion after in vitro stimulation with DCs loaded with apoptotic B16 or DCs pulsed with the naturally expressed melanoma Ag, tyrosinase-related protein 2. In addition, B16 melanoma cells were recognized by immune CD8 + T cells in vitro, and cytolytic activity against tyrosinase-related protein 2180-188-pulsed target cells was observed in vivo. When either CD4+ or CD8+ T cells were depleted at the time of challenge, the protection was completely abrogated. Mice receiving a tumor challenge 10 wk after vaccination were also protected, consistent with the induction of tumor-specific memory. Therefore, DCs loaded with cells undergoing apoptotic death can prime melanoma-specific helper and CTLs and provide long term protection against a poorly immunogenic tumor in mice. Fil:Goldszmid, R.S. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Idoyaga, J. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.

Published
2003

6. IL-10 expression by CT26 colon carcinoma cells inhibits their malignant phenotype and induces a T cell-mediated tumor rejection in the context of a systemic Th2 response.

Author

Adris, S.K., Klein, S., Jasnis, M.A., Chuluyan, E., Ledda, M.F., Bravo, A.I., Carbone, C., Chernajovsky, Y., and Podhajcer, O.L.

Subjects
INTERLEUKIN-10, PHENOTYPES, LYMPHOCYTES, GENETIC transformation, LYMPHOID tissue, SPLEEN, CELL migration, CELL growth, IMMUNE response, MICE
Abstract

In spite of the evidence that IL-10 has Th1-immunosuppressive and anti-inflammatory effects, it has been shown that IL-10 may reduce the tumorigenic capacity of certain tumor cell types. In order to characterize the responses elicited by IL-10, we explored the effect of transducing murine CT26 colon carcinoma cells with a recombinant retrovirus expressing mIL-10. IL-10 gene transfer of CT26 cells had no effect on tumor cell growth on plastic surface but inhibited the anchorage-independent growth capacity of tumor cells and their metastatic potential as assessed by their invasive and migration ability. Expression of IL-10 also elicited an antitumor immune response involving both CD4+ and CD8+ T cells. Assessment of the immune status of the animals demonstrated that mice injected with CT26-IL10 cells showed prevalence of a systemic and tumor-specific Th2 response. Spleen cells obtained from these mice showed an increased production of IL-4 and no changes in IFNγ levels, characteristic of a Th2 response. These results demonstrate that IL-10 affects CT26 tumor cell growth by both inhibiting the malignant phenotype and by recruiting and activating a T cell-mediated antitumor response. This T cell response occurs in the context of a shift towards a Th2 response. [ABSTRACT FROM AUTHOR]

Published
1999
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7. Tumor cells engineered to express interleukin-6 exhibit a reduced tumorigenicity depending on the tumor cell model

Author

Ledda, M.F., Adris, S., Bravo, A.I., Bover, L., Carbone, C., Paleolog, E., Mordoh, J., Chernajovsky, Y., and Podhajcer, O.L.

Subjects
Interleukin-6 -- Physiological aspects -- Models -- Research, Carcinogenesis -- Models -- Research, Gene therapy -- Research -- Models -- Physiological aspects, Health, Physiological aspects, Models, Research
Abstract

According to the authors' abstract of an article published in Cellular and Molecular Biology, 'Cytokine gene transfer to tumor cells has been demonstrated to induce tumor rejection in different murine [...]

Published
1996

8. Human leukocyte antigen-E protein is overexpressed in primary human colorectal cancer

Author

Levy E. M., Bianchini M., Von Euw E. M., Barrio M. M., Bravo A. I., Furman D., Domenichini E., Macagno C., Pinsky V., Mordoh J., ZUCCHINI, CINZIA, VALVASSORI, LUISA, Levy E.M., Bianchini M., Von Euw E.M., Barrio M.M., Bravo A.I., Furman D., Domenichini E., Macagno C., Pinsky V., Zucchini C., Valvassori L., and Mordoh J.

Abstract

HLA-E is a non-classical MHC molecule whose expression by tumour cells has been recently reported in several human cancer types. We studied HLA-E expression in colorectal cancer patients, its clinical significance and prognostic value, as well as characterized its expression in colorectal cancer cell lines. We analysed HLA-E expression at the transcript level by qRT-PCR in micro-dissected samples and at the protein level by semiquantitative immunohistochemistry on paraffin-embedded tissue sections from 42 biopsies of colorectal cancer patients. We observed that HLA-E transcript and protein are spontaneously overexpressed in a significant proportion of colorectal tumour biopsies, as compared to normal mucosae. We also found a negative correlation between HLA-E expression and the CD57+ cells infiltrate. Moreover, we analysed HLA-E expression in several colorectal cancer cell lines and demonstrated that IFN-gamma upregulates the expression of membrane HLA-E in vitro. Interestingly, we demonstrated that colorectal cancer cell lines overexpressing HLA-E at the cell surface inhibited NK-mediated cell lysis. Although IFN-gamma regulatory role needs further investigation, we provide evidence suggesting that this cytokine, within the tumour microenvironment, could promote HLA-E translocation to the surface of tumour epithelial cells. Furthermore, we showed that upregulation of HLA-E could be a marker of shorter disease-free survival in Dukes' C patients and we suggest that this molecule renders tumours less susceptible to immune attack.

Published
2008

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