91 research outputs found
SPHINGOSINE KINASE 1 (SPHK1) CONTRIBUTES TO RESISTANCE TO EPIDERMAL GROWTH FACTOR RECEPTOR (EGFR) INHIBITORS IN COLORECTAL CANCER MODELS
Metabolic and anthropometric changes in early breast cancer patients receiving adjuvant therapy
Weight gain and metabolic changes have been related to survival of early breast cancer patients (EBC). ''However, factors influencing metabolism post-diagnosis are not fully understood. We measured anthropometric [body mass index (BMI), body weight, waist and hip circumferences, and waist-to-hip ratio] and metabolic (levels of insulin, glucose, H1Ac, total, HDL, and LDL cholesterol, triglycerides, and the homeostasis model assessment score [HOMA]) parameters in 433 pre- and post-menopausal women with EBC at diagnosis and 3, 6, 9, 12, and 24Â months thereafter. At diagnosis, compared with post-menopausal women, pre-menopausal patients were more likely to be leaner and to have a lower BMI, smaller waist and hip circumferences, and waist-to-hip ratio. They had also lower glucose, HbA1c, and triglyceride levels and a lower HOMA score. Furthermore, they were more likely to have an estrogen- and/or progesterone-positive tumor and a higher proliferating breast cancer. During the first two post-diagnosis years, all women showed a significant increase of weight (+0.72Â kg/year, PÂ <Â 0.001), waist circumference (+1.53Â cm/year, PÂ <Â 0.001), and plasma levels of LDL cholesterol (+5.4Â mg/dl per year, PÂ =Â 0.045) and triglycerides (+10.73Â mg/dl per year, PÂ =Â 0.017). In patients receiving chemotherapy only, there was a significant increase in hip circumference (+3.16Â cm/year, PÂ <Â 0.001) and plasma cholesterol levels (+21.26Â mg/dl per year, PÂ <Â 0.001). We showed that weight, body fat distribution, and lipid profile changed in EBC patients receiving adjuvant therapy. These changes occurred during the first 2 years after diagnosis and were not specifically related to chemotherapy, menopausal status, or initial body weight
Role of DNA repair machinery and p53 in the testicular germ cell cancer: a review
Notwithstanding the peculiar sensitivity to cisplatin-based treatment, resulting in a very high percentage of cures even in advanced stages of the disease, still we do not know the biological mechanisms that make Testicular Germ Cell Tumor (TGCT) "unique" in the oncology scene. p53 and MDM2 seem to play a pivotal role, according to several in vitro observations, but no correlation has been found between their mutational or expression status in tissue samples and patients clinical outcome. Furthermore, other players seem to be on stage: DNA Damage Repair Machinery (DDR) , especially Homologous Recombination (HR) proteins, above all Ataxia Telangiectasia Mutated (ATM), cooperates with p53 in response to DNA damage, activating apoptotic cascade and contributing to cell "fate". Homologous Recombination deficiency has been assumed to be a Germ Cell Tumor characteristic underlying platinum-sensitivity, whereby Poly(ADP-ribose) polymerase (PARP), an enzyme involved in HR DNA repair, is an intriguing target: PARP inhibitors have already entered in clinical practice of other malignancies and trials are recruiting TGCT patients in order to validate their role in this disease. This paper aims to summarize evidence, trying to outline an overview of DDR implications not only in TGCT curability, but also in resistance to chemotherapy
Metabolic and anthropometric changes in early breast cancer patients receiving adjuvant therapy
Epidermal growth factor-receptor activation modulates Src-dependent resistance to lapatinib in breast cancer models
AIRC Regional Grant ; “Breast cancer: preclinical and clinical development of therapeutic strategies targeting molecular mechanisms”.
Pharmacogenetics and Endocrine therapy in postmenopausal early breast cancer patients. Correlation study of gene CYP19 and CYP2D6 polymorphisms with efficacy and Toxicity.
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