Boys in white: um clássico da pesquisa qualitativa completa cinquenta anos / Boys in white: a classic of qualitative research turns 50

O artigo analisa o livro Boys in white: student culture in medical school, de Howard S. Becker, Blanche Geer, Everett C. Hughes e Anselm Strauss, considerado um dos modelos de pesquisa qualitativa em sociologia. A análise aborda as trajetórias dos autores, do livro, da pesquisa qualitativa e dos estudantes de medicina, enfatizando sua importância nas origens da sociologia médica e da sociologia da educação médica. Na trajetória dos autores são apresentados aspectos biobibliográficos; na da pesquisa qualitativa, o modo como essa metodologia de investigação atravessa a construção do trabalho de campo; e na dos estudantes, sua forma de atravessar os primeiros anos da escola médica e construir sua própria “cultura do estudante”.

This article analyzes Boys in white: student culture in medical schoolby Howard S. Becker, Blanche Geer, Everett C. Hughes and Anselm Strauss, considered a model of qualitative research in sociology. The analysis investigates the trajectories of the authors, the book, qualitative analysis, and the medical students, emphasizing their importance in the origins of medical sociology and the sociology of medical education. In the trajectory of the authors, bibliographical information is given. The trajectory of qualitative research focuses on how this methodology influences the construction of the field. The investigation of the students’ trajectory shows how they progress through their first years at medical school to build their own student culture.

Differential toxicological endpoints of di(2-ethylhexyl) phthalate (DEHP) exposure in MCF-7 and MDA-MB-231 cell lines: Possible estrogen receptor α (ERα) independent modulations.

Wide spread use of Di-(2-ethylhexyl) phthalate (DEHP) has made it a ubiquitous contaminant in today’s environment, responsible for possible carcinogenic and endocrine disrupting effects. In the present investigation an integrative toxico-proteomic approach was made to study the estrogenic potential of DEHP. In vitro experiments carried out with DEHP (0.1-100 μM) induced proliferations (E-screen assay) in human estrogen receptors-α (ERα) positive MCF-7 and ERα negative MDA-MB-231 breast cancer cells irrespective of their ERα status. Further, DEHP suppressed tamoxifen (a potent anti-breast cancer drug) induced apoptosis in both cell types as shown by flowcytometric cell cycle analysis. Label-free quantitative proteomics analysis of the cell secretome of both the cell lines indicated a wide array of stress related, structural and receptor binding proteins that were affected due to DEHP exposure. The secretome of DEHP treated MCF-7 cells revealed the down regulation of lactotransferrin, an ERα responsive iron transport protein. The results indicated that toxicological effects of DEHP did not follow an ERα signaling pathway. However, the differential effects in MCF-7 and MDA-MB-231 cell lines indicate that ERα might have an indirect modulating effect on DEHP induced toxicity.

Cáncer de próstata y apoptosis / Prostate Cancer and Apoptosis

El cáncer de próstata presenta una progresión andrógeno-dependiente mediada por el receptor de andrógeno (AR), por lo que el bloqueo androgénico es la terapia estándar para su tratamiento en estado avanzado. Sin embargo, a pesar de una sensibilidad inicial, estos cánceres usualmente evolucionan hacia un estado hormono-resistente. Esta resistencia puede ser debida a una amplificación del gen AR, a sus mutaciones y al aumento en la expresión de proteínas co-activadoras. Igualmente, el receptor AR puede permanecer activo, independientemente de la fijación del ligando por fosforilación de factores de crecimiento y de citosinas. Adicionalmente, hay otras posibles vías independientes del receptor AR, como lo ejemplifica la adquisición del fenotipo neuroendocrino. En esta revisión se examinan tanto los mecanismos moleculares involucrados en la progresión del cáncer de próstata así como la forma en que sus células evaden la apoptosis.

Prostate cancer presents an androgen-dependent growth mediated by the androgen receptor (AR). Androgen pathway blockage is the standard therapy for the treatment of prostate cancer at an advanced stage. In spite of an initial sensitivity, prostate cancer usually becomes refractory to hormone treatment. This resistance can be due to the amplification of the AR gene, AR mutations and the increase in co-activator protein expression. Likewise, growth factors and cytokines can induce AR phosphorylation, independently of ligand fixation. Moreover, there are other AR-independent pathways, such as the acquisition of the neuroendocrine phenotype. In this review, we examine the molecular mechanisms that are involved in the progression of prostate cancer, as well as the ways its cells evade apoptosis.

Predisposición genética para el cáncer de mama: genes BRCA1 y BRCA2 / Genetic predisposition for breast cancer: BRCA1 and BRCA2 genes

El descubrimiento de los genes BRCA1 y BRCA2 ha llevado a la introducción de pruebas genéticas cada vez más sofisticadas para medir el riesgo de cáncer de mama de origen hereditario, entre otras cosas. En el presente artículo exploramos los criterios a seguir para realizar pruebas para estos genes, así como las implicaciones en el tratamiento para los pacientes en caso de identificarlos.

The discovery of genes BRCA1 and BRCA2 has led to the introduction of genetic tests more complex every time for the evaluation ofthehereditarycancerrisk,amongothers.In the present paper we explore the criteria to decide when to run the testing for the genes, as well as the implications for the treatment of patients who are identified with them.

Inducción de adenocarcinomas mamarios por progestagenos en ratones BALB/c. Progresión del tumor hormono-dependiente al autónomo / Progestin-induced mammary adenocarcinomas in BALB/c mice. Progression from hormone-dependent to autonomous tumors

We have developed an experimental model in which the administration of progestins induces mammary tumors in female virgin BALB/c mice. In this paper we review the morphological and biological features of progestin-induced tumors, such as estrogen receptor (ER) and progesterone receptor (PR) patterns of expression, hormone dependence and epidermal growth factor receptors (EGF-R) we also examine our data concerning the systemic effects of medroxyprogesterone acetate (MPA) as regards its stimulating EGF synthesis in salivary glands and its subsequent increase in serum. This growth factor seems to play an important role in the induction of mammary tumors. Direct MPA proliferative effects mediated by PR were demonstrated using primary cultures of progestin-dependent (PD) mammary tumors. Antiprogestins inhibited cell growth beyond control values, suggesting that PR are involved in cell proliferation even in the absence of the ligand. Progesterone-independent (PI) tumors expressing high levels of PR and ER are also inhibited by estrogen or antiprogestin treatment, suggesting that PR are involved in the control of autonomous tumor growth. Estrogen-resistant variants may be selected which may revert to an estrogen-sensitive phenotype after several transplants in untreated mice. The similarities between the tumors obtained with this model and human breast cancer as regards morphological features, evolution and the regulation of growth control converts this model into a useful tool to explore the mechanisms related with acquisition of hormone independence and autonomous tumor growth.

Estrogenic effects on growth and vitamin D3 receptor levels in human breast cancer cells

Estrogen is essential for growth and development of 30 per cent of malignant breast tumors and concentration of estrogen receptor (ER) is an indicator of hormone dependence. The effects of estradiol-l7beta (E2) on growth promotion and vitamin D (VDR) and progesterone (PR) receptor modulation were evaluated in hormone-dependent (MCF-7, T47D) and -independent (MDA-MB-231) breast carcinoma cells lines. 10(-7)M E2 stimulated the proliferation of MCF-7 and T47D cells the extent of which was correlated to ER content, being sensitive to growth inhibition of 10(-6) M tamoxifen. No effect on growth and PR levels was observed in E2 treated MDA-MB-231 cells. A statistically significant 10(-7)M E(2-)mediated induction of VDR was verified in T47D cells which was abolished by 10(-6)M tamoxifen, revealing an ER-mediated mechanism. 10(-6)M tamoxifen treatment alone upregulated VDR levels in T47D cells, suggesting that this drug may utilize a distinct pathway (ER-independent) for stimulation of VDR content, by a mechanism, now in progress, to be elucidated. These results, taken together, suggest the importance of VDR level assessment as new a prognostic indicator in breast carcinoma.