RESUMO
Hormone-dependent breast cancer has growth factors that respond positively to the hormones estrogen and progesterone. Thus, adjuvant endocrine therapy causes decreased or undetectable serum levels of these hormones. However, this treatment can have side effects that compromise the sexual health of patients, such as dyspareunia, vaginal dryness and decreased libido. In this scenario, the objective of this work was to document the main outcomes in sexuality in women after treatment for hormonepositive breast cancer. Thus, this is an integrative literature review, in which the following databases were used: U.S. National Library of Medicine (PubMed), Virtual Health Library (BVS), SCOPUS and Scientific Electronic Library Online (SCIELO), using the descriptors: "sexuality", "antineoplastic agents, hormonal" and "breast neoplasms", joined by the Boolean operator "AND". Full articles published in the last 5 years (2017-2022) were included; written in Portuguese or English. Articles dealing with non-hormone-dependent or metastatic breast cancer, or with patients younger than 18 years, or articles that did not answer the research question were excluded. In total, 26 articles were identified, of which 7 comprised the final sample of this review. A total of 3,850 women participated in the included studies. The main sexual dysfunctions found were: dyspareunia, hot flashes, decreased libido, vaginal dryness, breast tenderness, self-image concerns and hair loss. The symptom vaginal dryness was the most prevalent, mentioned in 71.4% of the articles included. In view of the adverse effects listed in this review, there is a need to carry out more studies on this topic, since the diagnosis of this comorbidity brings clinical, psychological, emotional, sociocultural and economic outcomes for the patient. Thus, a multidisciplinary team must assertively address these complaints to improve the overall quality of life of these women (AU)
Assuntos
Humanos , Feminino , Disfunções Sexuais Fisiológicas/induzido quimicamente , Neoplasias da Mama/tratamento farmacológico , Antineoplásicos Hormonais/uso terapêutico , Sexualidade/efeitos dos fármacos , Neoplasias Hormônio-Dependentes/tratamento farmacológicoRESUMO
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.
Assuntos
Animais , Feminino , Camundongos , Adenocarcinoma/tratamento farmacológico , Antimetabólitos Antineoplásicos/farmacologia , Antineoplásicos Hormonais/farmacologia , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Apoptose/efeitos dos fármacos , Neoplasias da Mama/tratamento farmacológico , Estrogênios , Antagonistas de Estrogênios/farmacologia , Inibidores do Crescimento/farmacologia , Neoplasias Hormônio-Dependentes/tratamento farmacológico , Fenilacetatos/farmacologia , /biossíntese , Tamoxifeno/farmacologia , Adenocarcinoma/patologia , Antimetabólitos Antineoplásicos/administração & dosagem , Antineoplásicos Hormonais/administração & dosagem , Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia , Neoplasias da Mama/patologia , Diferenciação Celular/efeitos dos fármacos , Divisão Celular/efeitos dos fármacos , Sinergismo Farmacológico , Genes ras , Camundongos Nus , Transplante de Neoplasias , Neoplasias Hormônio-Dependentes/patologia , /fisiologia , Fenilacetatos/administração & dosagem , /genética , Transfecção , Tamoxifeno/administração & dosagem , Células Tumorais Cultivadas/efeitos dos fármacosRESUMO
The case of a female patient of 35 years of age, with a pedunculated tumor dependent of the vagina, of approximately 25 x 12 x 8 cm, who had a wide resection. The report was consistent with myxoid aggressive angiomyxoma. This is a myxoid mesenchymal neoplasm of slow growth, which mainly appears in deep soft tissues of the pelvic, genital or perineal areas of adult women. It is usually diagnosed after surgical resection by histopathologic examination. Routine evaluation includes: complete physical examination, imaging and pathology report of diagnostic confirmation.
Assuntos
Mixoma/patologia , Neoplasias Hormônio-Dependentes/patologia , Neoplasias Vaginais/patologia , Adulto , Antineoplásicos Hormonais/uso terapêutico , Biomarcadores Tumorais , Terapia Combinada , Diagnóstico por Imagem , Feminino , Hormônio Liberador de Gonadotropina/agonistas , Gosserrelina/uso terapêutico , Humanos , Mixoma/química , Mixoma/diagnóstico , Mixoma/tratamento farmacológico , Mixoma/cirurgia , Invasividade Neoplásica , Proteínas de Neoplasias/análise , Neoplasias Hormônio-Dependentes/química , Neoplasias Hormônio-Dependentes/diagnóstico , Neoplasias Hormônio-Dependentes/tratamento farmacológico , Neoplasias Hormônio-Dependentes/cirurgia , Progesterona , Receptores de Progesterona/análise , Carga Tumoral , Neoplasias Vaginais/química , Neoplasias Vaginais/diagnóstico , Neoplasias Vaginais/tratamento farmacológico , Neoplasias Vaginais/cirurgiaRESUMO
BACKGROUND: male breast cancer is a disease with low incidence, which is further reduced when it comes to bilateral synchronous presentation. There are few published cases in recent years. The aim is to establish guidelines for the management of this disorder that is so rare. CLINICAL CASE: a 75-year-old with tumors in both breasts, which were completely resected with removal of palpable nodes. The histopathological study reported ductal carcinoma. The indicated treatment was adjuvant tamoxifen and radiotherapy. The patient is currently in a disease-free period. CONCLUSIONS: this is a rare disease, whose main treatment is surgery, hence the importance of early diagnosis. Most cases require adjuvant chemotherapy and radiotherapy because they are usually diagnosed at an advanced stage.
antecedentes: el cáncer de mama en el hombre es una enfermedad con baja incidencia, que se reduce aún más cuando es bilateral sincrónica. Existen pocas publicaciones en los últimos años. Objetivo: establecer pautas para el tratamiento de este cáncer, aunque sea infrecuente. Caso clínico: paciente masculino de 75 años de edad, con tumores en ambas mamas, que se le resecaron completamente con exéresis de ganglios palpables. El estudio histopatológico informó que se trataba de un carcinoma ductal infiltrante no especificado. Se indicó tratamiento adyuvante con tamoxifeno y radioterapia; en la actualidad está libre de enfermedad. Conclusiones: el carcinoma mamario bilateral sincrónico en el varón es una enfermedad poco frecuente. Su tratamiento principal es la cirugía, de ahí la importancia del diagnóstico temprano. En la mayoría de los casos se requiere quimioterapia y radioterapia adyuvante porque suelen diagnosticarse en un estadio avanzado.
Assuntos
Neoplasias da Mama Masculina , Carcinoma Ductal de Mama , Neoplasias Primárias Múltiplas , Idoso , Antineoplásicos Hormonais/uso terapêutico , Neoplasias da Mama Masculina/tratamento farmacológico , Neoplasias da Mama Masculina/epidemiologia , Neoplasias da Mama Masculina/patologia , Neoplasias da Mama Masculina/radioterapia , Neoplasias da Mama Masculina/cirurgia , Carcinoma Ductal de Mama/tratamento farmacológico , Carcinoma Ductal de Mama/patologia , Carcinoma Ductal de Mama/radioterapia , Carcinoma Ductal de Mama/cirurgia , Quimioterapia Adjuvante , Terapia Combinada , Moduladores de Receptor Estrogênico/uso terapêutico , Estrogênios , Humanos , Excisão de Linfonodo , Masculino , Mastectomia , Neoplasias Hormônio-Dependentes/tratamento farmacológico , Neoplasias Hormônio-Dependentes/patologia , Neoplasias Hormônio-Dependentes/radioterapia , Neoplasias Hormônio-Dependentes/cirurgia , Neoplasias Primárias Múltiplas/tratamento farmacológico , Neoplasias Primárias Múltiplas/epidemiologia , Neoplasias Primárias Múltiplas/patologia , Neoplasias Primárias Múltiplas/radioterapia , Neoplasias Primárias Múltiplas/cirurgia , Radioterapia Adjuvante , Tamoxifeno/uso terapêuticoRESUMO
BACKGROUND: Hormone receptor-positive advanced breast cancer is an increasing health burden. Although endocrine therapies are recognised as the most beneficial treatments for patients with hormone receptor-positive advanced breast cancer, the optimal sequence of these agents is currently undetermined. METHODS: We reviewed the available data on randomised controlled trials (RCTs) of endocrine therapies in this treatment setting with particular focus on RCTs reported over the last 15 years that were designed based on power calculations on primary end points. RESULTS: In this paper, data are reviewed in postmenopausal patients for the use of tamoxifen, aromatase inhibitors and fulvestrant. We also consider the available data on endocrine crossover studies and endocrine therapy in combination with chemotherapy or growth factor therapies. Treatment options for premenopausal patients and those with estrogen receptor-/human epidermal growth factor receptor 2-positive tumours are also evaluated. CONCLUSION: We present the level of evidence available for each endocrine agent based on its efficacy in advanced breast cancer and a diagram of possible treatment pathways.
Assuntos
Antineoplásicos Hormonais/uso terapêutico , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Neoplasias da Mama/tratamento farmacológico , Neoplasias Hormônio-Dependentes/tratamento farmacológico , Neoplasias da Mama/metabolismo , Neoplasias da Mama/patologia , Feminino , Humanos , Neoplasias Hormônio-Dependentes/metabolismo , Neoplasias Hormônio-Dependentes/patologia , Pós-Menopausa , Ensaios Clínicos Controlados Aleatórios como Assunto , Receptor ErbB-2/metabolismo , Receptores de Estrogênio/metabolismoRESUMO
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.
Assuntos
Animais , Humanos , Masculino , Camundongos , Androgênios , Apoptose , Adenocarcinoma/patologia , Neoplasias Hormônio-Dependentes/patologia , Neoplasias da Próstata/patologia , Adenocarcinoma/tratamento farmacológico , Antineoplásicos Hormonais/farmacologia , Antineoplásicos Hormonais/uso terapêutico , Antineoplásicos/farmacologia , Antineoplásicos/uso terapêutico , Proteínas Reguladoras de Apoptose/fisiologia , Progressão da Doença , Resistencia a Medicamentos Antineoplásicos , Terapia de Alvo Molecular , Proteínas de Neoplasias/genética , Proteínas de Neoplasias/fisiologia , Neoplasias Hormônio-Dependentes/tratamento farmacológico , Células-Tronco Neoplásicas/efeitos dos fármacos , Células-Tronco Neoplásicas/patologia , Neoplasias da Próstata/tratamento farmacológico , Receptores Androgênicos/genética , Receptores Androgênicos/fisiologia , Transdução de SinaisRESUMO
BACKGROUND: Previous studies demonstrated that Letrozole (aromatase inhibitor) and tamoxifen (selective modulator of estrogen receptors) are effective in the treatment of postmenopausal women with locally advanced tumors, stage III and hormone dependent. OBJECTIVE: To present display the complete clinical answer incidence and the complete pathological answer with the use of induction hormonotherapy. METHODS: Put-analysis in 40 patients with breast cancer, to chanalicular infiltrated, eligible were treated in a prospective study, to double blind person, using per os: letrozol, 2.5 mg; tamoxifen, 20 mg, known widely like selective modulator of estrogen receivers; oral route, during 36 consecutive months. Reports at the beginning were taken, subsequent to 3, 6 and 12 months to evaluate the frequency of complete respond. The patients, who did not show answer neoadjuvant therapy, were put under treatment with radiotherapy. The patients who showed good partial pathological respond, or clinical partial respond, went candidates to radical mastectomy. According to the protocol of the study, the patients subsequent to surgery who showed partial pathological respond or complete pathological respond, continued adjuvant handling adyuvant therapy by 2 years consecutive or until the presence of progression of the disease. It was used like statistical method Chi2, with p of Table cloth to evaluate the differences. RESULTS: During a period of 3 years, january of the 2003 to january of the 2005, 2 groups of patients, 40 studied altogether; the age average was of 65,5 years, with a rank of 55 to 75 years with breast cancer, stages: IIA to IIIB. Without complete respond 25% of the group with tamoxifen; 20% with letrozol Those patients happened to radiotherapy. The collateral effects of the use of hormonotherapy with letrozol appeared in a 55% and with the use of tamoxifen in a 60% of the patients with breast cancer (p = 0.5). They did not respond to neoadyuvant therapy (hormonal receptors < to 30%): with letrozol 19% of them and 25% with tamoxifen; reason why they received treatment with radiotherapy. All patients candidates to surgery, were benefitted with the mastectomy handling. CONCLUSIONS: Results although preliminary, suggest that neoadyuvant treatment with hormone-therapy in postmenopausal patients with breast cancer, have good prognosis. Induction therapy, were better tolerated, with greater effectiveness and improved the clinical and objective respond in women with breast cancer in the postmenopausal. Work serves as tool to determine the indication to us of induction hormonotherapy; and identify to those patients with breast cancer, locally advanced in post menopause with better prognosis to be rescued with radical mastectomy. Study needs more background and show the impact of letrozol, as hormonotherapy used in neoadjuvancy, to confirm if relieves period without disease or survives, before mastectomy. In a near future, it shall important to investigate if is useful the radical mastectomy in those postmenopausal patients with complete objective respond, after the use of an aromatase inhibitor.
Assuntos
Antineoplásicos Hormonais/uso terapêutico , Neoplasias da Mama/tratamento farmacológico , Carcinoma Ductal de Mama/tratamento farmacológico , Estrogênios , Terapia Neoadjuvante , Neoplasias Hormônio-Dependentes/tratamento farmacológico , Nitrilas/uso terapêutico , Pós-Menopausa , Progesterona , Moduladores Seletivos de Receptor Estrogênico/uso terapêutico , Tamoxifeno/uso terapêutico , Triazóis/uso terapêutico , Idoso , Neoplasias da Mama/diagnóstico por imagem , Neoplasias da Mama/radioterapia , Neoplasias da Mama/cirurgia , Carcinoma Ductal de Mama/diagnóstico por imagem , Carcinoma Ductal de Mama/radioterapia , Carcinoma Ductal de Mama/cirurgia , Terapia Combinada , Método Duplo-Cego , Feminino , Humanos , Letrozol , Mastectomia Radical , Pessoa de Meia-Idade , Neoplasias Hormônio-Dependentes/diagnóstico por imagem , Neoplasias Hormônio-Dependentes/radioterapia , Neoplasias Hormônio-Dependentes/cirurgia , Cuidados Paliativos , Estudos Prospectivos , Indução de Remissão , Resultado do Tratamento , UltrassonografiaRESUMO
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.
Assuntos
Adenocarcinoma/patologia , Androgênios , Apoptose , Neoplasias Hormônio-Dependentes/patologia , Neoplasias da Próstata/patologia , Adenocarcinoma/tratamento farmacológico , Animais , Antineoplásicos/farmacologia , Antineoplásicos/uso terapêutico , Antineoplásicos Hormonais/farmacologia , Antineoplásicos Hormonais/uso terapêutico , Proteínas Reguladoras de Apoptose/fisiologia , Progressão da Doença , Resistencia a Medicamentos Antineoplásicos , Humanos , Masculino , Camundongos , Terapia de Alvo Molecular , Proteínas de Neoplasias/genética , Proteínas de Neoplasias/fisiologia , Neoplasias Hormônio-Dependentes/tratamento farmacológico , Células-Tronco Neoplásicas/efeitos dos fármacos , Células-Tronco Neoplásicas/patologia , Neoplasias da Próstata/tratamento farmacológico , Receptores Androgênicos/genética , Receptores Androgênicos/fisiologia , Transdução de SinaisRESUMO
Breast cancer growth and dissemination is regulated by estrogen and different growth factor receptor signalling pathways. The increasing knowledge of the biology of breast cancer regarding the interaction of these signalling pathways provides a tool to understand endocrine therapies response and resistance mechanisms. In patients with slowly progressive disease, no visceral involvement, and minimal symptoms, endocrine therapy could be the strategy of choice, even if the tumor has low estrogen receptor expression. Ovarian suppression and tamoxifen are recommended for premenopausal patients whether aromatase inhibitors are the option for postmenopausal ones. Chemotherapy still remains as the right alternative for hormone unresponsive or resistant patients. This is a review focused on the different strategies and combinations of endocrine therapies for metastatic breast cancer patients considering the potential strategies clinically tested to overcome resistance and the different treatments of choice available for each scenario of disseminated disease.
Assuntos
Antineoplásicos Hormonais/uso terapêutico , Inibidores da Aromatase/uso terapêutico , Neoplasias da Mama/tratamento farmacológico , Neoplasias da Mama/patologia , Neoplasias da Mama/secundário , Ensaios Clínicos como Assunto , Feminino , Humanos , Neoplasias Hormônio-Dependentes/tratamento farmacológico , Neoplasias Hormônio-Dependentes/patologia , Receptores de Estrogênio/antagonistas & inibidores , Receptores de Estrogênio/metabolismoRESUMO
Tumor necrosis factor alpha (TNF alpha) enhances proliferation of chemically-induced mammary tumors and of T47D human cell line through not fully understood pathways. Here, we explored the intracellular signaling pathways triggered by TNF alpha, the participation of TNF alpha receptor (TNFR) 1 and TNFR2 and the molecular mechanism leading to breast cancer growth. We demonstrate that TNFalpha induced proliferation of C4HD murine mammary tumor cells and of T47D cells through the activation of p42/p44 MAPK, JNK, PI3-K/Akt pathways and nuclear factor-kappa B (NF-kappa B) transcriptional activation. A TNF alpha-specific mutein selectively binding to TNFR1 induced p42/p44 MAPK, JNK, Akt activation, NF-kappa B transcriptional activation and cell proliferation, just like wild-type TNF alpha, while a mutein selective for TNFR2 induced only p42/p44 MAPK activation. Interestingly, blockage of TNFR1 or TNFR2 with specific antibodies was enough to impair TNF alpha signaling and biological effect. Moreover, in vivo TNF alpha administration supported C4HD tumor growth. We also demonstrated, for the first time, that injection of a selective inhibitor of NF-kappa B activity, Bay 11-7082, resulted in regression of TNF alpha-promoted tumor. Bay 11-7082 blocked TNF alpha capacity to induce cell proliferation and up-regulation of cyclin D1 and of Bcl-xLin vivo and in vitro. Our results reveal evidence for TNF alpha as a breast tumor promoter, and provide novel data for a future therapeutic approach using TNF alpha antagonists and NF-kappa B pharmacological inhibitors in established breast cancer treatment.