Assuntos
Neoplasias Oculares/complicações , Neoplasias Oculares/secundário , Neoplasias Complexas Mistas/complicações , Neoplasias Complexas Mistas/secundário , Neoplasias Embrionárias de Células Germinativas/complicações , Neoplasias Embrionárias de Células Germinativas/secundário , Descolamento Retiniano/etiologia , Neoplasias Testiculares/patologia , Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos , Biópsia , Carcinoma Embrionário/complicações , Carcinoma Embrionário/secundário , Tumor do Seio Endodérmico/complicações , Tumor do Seio Endodérmico/secundário , Neoplasias Oculares/tratamento farmacológico , Evolução Fatal , Humanos , Neoplasias Pulmonares/secundário , Imageamento por Ressonância Magnética , Masculino , Neoplasias Complexas Mistas/terapia , Neoplasias Embrionárias de Células Germinativas/terapia , Orquiectomia , Seminoma/complicações , Seminoma/secundário , Neoplasias Testiculares/terapia , Tomografia Computadorizada por Raios X , Falha de Tratamento , Adulto JovemRESUMO
Estrogen receptor (ER)(+) progesterone receptor (PR)(-) tumors are a distinct subset of breast cancers characterized by aggressive behavior and tamoxifen resistance in spite of being ER(+). They are categorized as luminal B tumors and have greater genomic instability and a higher proliferation rate. High growth factor (GF) signaling and membranous ER activity contribute to the aggressive behavior of these tumors. The absence of PR is attributable to low serum estrogen, low levels of nuclear ER, and features of molecular crosstalk between GFs and membranous ER. PR expression is also downregulated by expression of mutated epidermal growth factor receptor (EGFRvIII). This subset of patients has greater expression of human epidermal growth factor receptor (HER)-1 and HER-2 and active GF signaling mediated by the phosphoinositide 3-kinase-Akt-mammalian target of rapamycin pathway. Currently, aromatase inhibitors, fulvestrant, and chemotherapy may be the favored treatment approaches for this subset of patients. Overcoming tamoxifen resistance with targeted therapies such as gefitinib is being evaluated and strategies involving short courses of tamoxifen have been postulated for prevention of recurrence of this subtype. Understanding the interplay between molecular endocrinology and tumor biology has provided experimental therapeutic insights, and continued work in this area holds the promise of future advances in prognosis.
