Quivo Tahin

Universidade Estadual de Campinas (UNICAMP)

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R.A Mello

Universidade Estadual de Campinas (UNICAMP)

José Russo

Fox Chase Cancer Center

Silvio Augusto Margarido

Secretaria da Saúde

T.C Cavalcanti

Universidade Estadual de Campinas (UNICAMP)

C.R. Douglas

Universidade Metodista de São Paulo

Irma H. Russo

Fox Chase Cancer Center

Carolyn Slater

Fox Chase Cancer Center

Mohamed H. Lareef

Fox Chase Cancer Center

J. Russo

Agostino Gemelli University Polyclinic

Dana Mihaila

Fox Chase Cancer Center

Cooperative Institutions

Fox Chase Cancer Center

Universidade Estadual de Campinas (UNICAMP)

Universidade de São Paulo

New York University

Prevent Cancer Foundation

Breast Cancer Research Foundation

Temple University Health System

Wayne State University

Cairo University

Hospital de Clínicas da Unicamp

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Role of Ras Oncogene in Human Breast Cancer: An Experimental Approach

Springer eBooks (1992)

J. Russo Gloria M. Calaf Josiah Ochieng I H Russo Quivo Tahin

10.1007/978-1-4615-3494-5_8

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The Fatty Acid Composition of Subcellular Membranes of Rat Liver, Heart, and Brain : Diet‐Induced Modifications

European Journal of Biochemistry (1981)

Quivo Tahin Max Blum Ernesto Carafoli

The influence of diets having different fatty acids composition on the fatty acid content of (the phospholipids) of rat liver mitochondria and microsomes, heart mitochondria, brain mitochondria and microsonies has been analyzed. It has been found that each organelle has its own peculiar composition in fatty acids. This composition may be profoundly influenced by the diet, but to different degrees in different organelles. Those of brain are most resistant. The changes observed are rather rapid, being generally already maximal after three weeks of treatment. The parallel between fatty acid composition of diets, and the changes observed in the organelles, is not strict, and is probably influenced by the metabolic competition among oleic acid, linoleic acid, linolenic acid. Unusual fatty acids like crucic acid. trans ‐oleic acid. and trans ‐linoleic acid can also become incorporated into the membranes of cell organelles.

Organelle

Linolenic acid

10.1111/j.1432-1033.1981.tb06421.x

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Carcinogenicity of estrogens in human breast epithelial cells¹

Apmis (2001)

José Russo Yun Hu Quivo Tahin Dana Mihaila Carolyn Slater

Epidemiological and clinical evidences indicate that breast cancer risk is associated with prolonged ovarian function that results in elevated circulating levels of steroid hormones. Principal among these is estrogen, which is associated with two important risk factors, early onset of menarche and late menopause. However, up to now there is no direct experimental evidence that estrogens are responsible of the initiation of human breast cancer. We postulate that if estrogens are causative agents of this disease, they should elicit in human breast epithelial cells (HBEC) genomic alterations similar to those exhibited by human breast cancers, such as DNA amplification and loss of genetic material representing tumor suppressor genes. These effects could result from binding of the hormone to its nuclear receptors (ER) or from its metabolic activation to reactive metabolites. This hypothesis was tested by treating with the natural estrogen 17β‐estradiol (E 2 ) and the synthetic steroid diethylstilbestrol (DES) MCF‐10F cells, a HBEC line that is negative for ER. Cells treated with the chemical carcinogen benzo (a) pyrene (BP) served as a positive control of cell transformation. BP‐, E 2 ‐, and DES‐treated MCF‐10F cells showed increases in survival efficiency and colony efficiency in agar methocel, and loss of ductulogenic capacity in collagen gel. The largest colonies were formed by BP‐treated cells, becoming progressively smaller in DES‐ and E 2 ‐treated cells. The loss of ductulogenic capacity was maximal in BP‐, and less prominent in E2‐ and DES‐treated cells. Genomic analysis revealed that E 2 ‐ and DES‐treated cells exhibited loss of heterozygosity in chromosomes 3 and 11, at 3p21, 3p21–21.2, 3p21.1–14.2, and 3p14.2–14.1, and at 11q23.3 and 11q23.1–25 regions, respectively. It is noteworthy that these loci are also affected in breast lesions, such as ductal hyperplasia, carcinoma in situ, and invasive carcinoma. Our data are the first ones to demonstrate that estrogens induce in HBEC phenotypic changes indicative of cell transformation and that those changes are associated with significant genomic alterations that might unravel new pathways in the initiation of breast cancer.

10.1111/j.1600-0463.2001.tb00013.x

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Citations (37)

The effect of the thyroidectomy in male rats fed two antagonist lipid diets. Ii. The fatty acid content of lipids of plasma and mitochondria of liver and brain

Arquivos de biologia e tecnologia (1988)

R.A Mello Quivo Tahin T.C Cavalcanti Silvio Augusto Margarido C.R. Douglas

Lipid Accumulation

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Carcinogenicity of estrogens in human breast epithelial cells1

Apmis (2001)

José Russo Yun Hu Quivo Tahin Dana Mihaila Carolyn Slater

Epidemiological and clinical evidences indicate that breast cancer risk is associated with prolonged ovarian function that results in elevated circulating levels of steroid hormones. Principal among these is estrogen, which is associated with two important risk factors, early onset of menarche and late menopause. However, up to now there is no direct experimental evidence that estrogens are responsible of the initiation of human breast cancer. We postulate that if estrogens are causative agents of this disease, they should elicit in human breast epithelial cells (HBEC) genomic alterations similar to those exhibited by human breast cancers, such as DNA amplification and loss of genetic material representing tumor suppressor genes. These effects could result from binding of the hormone to its nuclear receptors (ER) or from its metabolic activation to reactive metabolites. This hypothesis was tested by treating with the natural estrogen 17β‐estradiol (E 2 ) and the synthetic steroid diethylstilbestrol (DES) MCF‐10F cells, a HBEC line that is negative for ER. Cells treated with the chemical carcinogen benzo (a) pyrene (BP) served as a positive control of cell transformation. BP‐, E 2 ‐, and DES‐treated MCF‐10F cells showed increases in survival efficiency and colony efficiency in agar methocel, and loss of ductulogenic capacity in collagen gel. The largest colonies were formed by BP‐treated cells, becoming progressively smaller in DES‐ and E 2 ‐treated cells. The loss of ductulogenic capacity was maximal in BP‐, and less prominent in E2‐ and DES‐treated cells. Genomic analysis revealed that E 2 ‐ and DES‐treated cells exhibited loss of heterozygosity in chromosomes 3 and 11, at 3p21, 3p21‐21.2, 3p21.1–14.2, and 3p14.2–14.1, and at 11q23.3 and 11q23.1–25 regions, respectively. It is noteworthy that these loci are also affected in breast lesions, such as ductal hyperplasia, carcinoma in situ, and invasive carcinoma. Our data are the first ones to demonstrate that estrogens induce in HBEC phenotypic changes indicative of cell transformation and that those changes are associated with significant genomic alterations that might unravel new pathways in the initiation of breast cancer.

10.1111/j.1600-0463.2001.tb05825.x

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DNA content and cell number determination in microdissected samples of breast carcinoma in situ

International Journal of Oncology (2002)

Robert Blumenstein Margarida Figueiredo-Dias Irma H. Russo Quivo Tahin José Russo

Paraffin-embedded tissue (PET) is the specimen of choice for the histopathological diagnosis of cancer. PET has become a valuable resource for correlating cellular phenotype and genotype in microdissected lesions. A definitive improvement in this field has been the development of infra-red laser capture microdissection (LCM), which yields homogeneous populations of cells for DNA extraction and in vitro amplification by polymerase chain reaction (PCR). We report here a photographic and fluorescent technique for determining the number of nuclei and concentration of DNA obtained respectively by laser capture microdissection from paraffin-embedded breast cancer tissue. Breast biopsies containing carcinoma in situ were serially sectioned, mounted on plain glass slides and tumor cells were microdissected using a laser capture microscope. The DNA was extracted in digestion buffer and used directly as a template for PCR. In our protocols, each capture contained 21+/-5.4 nuclei with a DNA concentration of 115+/-5.3 pg. Also, a linear relationship was found between number of captures and DNA content (R2=0.9995). These results represent a novel contribution for a more precise correlation between phenotypic and genotypic diversity in cancer cells studied from microdissected paraffin-embedded tissue.

Laser capture microdissection

Microdissection

Lysis buffer

10.3892/ijo.21.2.447

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Pathways of carcinogenesis and prevention in the human breast

European Journal of Cancer (2002)

J. Russo Hasan M. Lareef Quivo Tahin I H Russo

Etiology

Epidemiology of cancer

10.1016/s0959-8049(02)00276-9

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Estudos sobre a proteolise peptica da ovalbumina

Quivo Tahin

10.47749/t/unicamp.1968.59907

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Hormone receptors and cathepsin D levels in human breast epithelial cells transformed by chemical carcinogens and c-Ha-ras transfection

Breast Cancer Research and Treatment (1994)

Gloria M. Calaf Quivo Tahin María Elena Alvarado Sandino Estrada Thomas R. Cox

clone (Java method)

Neoplastic transformation

Malignant Transformation

10.1007/bf00665678

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Estudos sobre a proteolise peptica da ovalbumina

Quivo Tahin Antonio Cachelli de Mattos Paiva

A composicao de aminoacidos da pepsina caracteriza-se pelo grande numero de residuos dicarboxilicos e de residuos com cadeias laterais apolares, e de raros residuos basicos. Devido a isso, e a presenca de uma fosfoserina, a enzima apresenta ponto isoeletrico menor do que 1,08. A atividade enzimica da pespsina (tanto a proteolitica como a peptidasica, como a esterasica) da-se otimamente em pHs acidos. A proteolise peptica de substratos nativos da-se em pHs otimos mais baixos do que os da proteolise peptica de substratos desnaturados e tambem mais baixos do que os verificados para a hidrolise peptica de peptideos sinteticos ou de esteres sinteticos. Uma das hipoteses para explicar a necessidade dos baixos pHs para a melhor acao catalitica da pepsina baseia-se na possivel atracao eletrostatica entre a enzima, que em meio acido se comportaria como um ânion, e o substrato proteico, que em meio acido se comportaria como um cation (pois geralmente o ponto isoeletrico dos substratos e acima de 4,0). Outra hipotese e a de que o passo limitante da proteolise peptica seria a desnaturacao do substrato, favorecida pelo pH acido. Estudamos neste trabalho o efeito do pH e da temperatura sobre a cinetica da acao da pepsina sobre a ovalbumina nativa ou previamente desnaturada por acido... Observacao: O resumo, na integra, podera ser visualizado no texto completo da tese digital Abstract

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