Berntsenzhang6555

To investigate the ability of tumor stiffness, tumor blood flow, and Ki-67 expression alone or in combination in predicting the pathological response to neoadjuvant chemotherapy (NACT) in breast cancer.

This prospective cohort study included 145 breast cancer patients treated with NACT. Tumor stiffness (maximum stiffness (Emax), mean stiffness (Emean)), blood score (BS), and their relative changes, were evaluated before (t0), during (t1-t5), and at the end of NACT (t6) by shear-wave elastography and optical imaging. Ki-67 expression was quantitatively evaluated by immunohistochemistry using core biopsy specimens obtained before NACT. Pathological responses were evaluated by residual cancer burden. The ability of tumor stiffness, BS, Ki-67, and predRCB-which combined ΔEmean (t2) (the relative changes in Emean after the second NACT cycle), BS2 (BS after the second NACT cycle), and Ki-67-in predicting tumor responses was compared using receiver operating characteristic curves and the Z-test.

Tumor stiffnesOvarian cancer (OC) is characterized by a high mortality rate due to the late diagnosis and the elevated metastatic potential. Autophagy, a lysosomal-driven catabolic process, contributes to the macromolecular turnover, cell homeostasis, and survival, and as such, it represents a pathway targetable for anti-cancer therapies. It is now recognized that the vascularization and the cellular composition of the tumor microenvironment influence the development and progression of OC by controlling the availability of nutrients, oxygen, growth factors, and inflammatory and immune-regulatory soluble factors that ultimately impinge on autophagy regulation in cancer cells. An increasing body of evidence indicates that OC carcinogenesis is associated, at least in the early stages, to insufficient autophagy. On the other hand, when the tumor is already established, autophagy activation provides a survival advantage to the cancer cells that face metabolic stress and protects from the macromolecules and organelles damages induced by chemo- and radiotherapy. Additionally, upregulation of autophagy may lead cancer cells to a non-proliferative dormant state that protects the cells from toxic injuries while preserving their stem-like properties. Further to complicate the picture, autophagy is deregulated also in stromal cells. Thus, changes in the tumor microenvironment reflect on the metabolic crosstalk between cancer and stromal cells impacting on their autophagy levels and, consequently, on cancer progression. Here, we present a brief overview of the role of autophagy in OC hallmarks, including tumor dormancy, chemoresistance, metastasis, and cell metabolism, with an emphasis on the bidirectional metabolic crosstalk between cancer cells and stromal cells in shaping the OC microenvironment.Worldwide, cervical cancer was the fourth leading cause of cancer death among women, while in Mexico was the second cause (5.28%). Cancer patients receiving chemotherapy and radiotherapy have a high risk of malnutrition secondary to the disease and treatment, affects the patient's overall, with adverse effects on gastrointestinal symptoms. These use affects the medical therapy. The aim of the present study was to evaluate the benefits on individualized nutritional therapy on decrease weight loss and gastrointestinal adverse effects and to consider these outcomes in pharmacology research, especially in repurposing drugs. We conducted a longitudinal design with two comparation groups with medical diagnosis of cervical cancer and received radiotherapy weekly, 1) the intervention group (nutritional intervention and counseling -INC-) with 20 participants and 2) control group (retrospective cohort -CG-) with 9 participants. Weekly body composition, dietary intake, adverse effects (gastrointestinal symptoms), glucose, hemoglobin, and blood pressure were analyzed during 4 to 5 weeks. Both groups had weight loss weekly (p = 0.013 and p = 0.043 respectively) but the CG vs INC presented loss fat-free mass ≥500g in 67 and of 37% respectively. By the end of the intervention a 25% of the INC group had 0.05). The number needed to treat was 4 (95% CI, 2 to 13). The nutritional intervention and counseling weekly during radiotherapy in cervical cancer to maintain/improve muscle mass, hemoglobin, and dietary intake above 70% of the recommendations for INC group compared to the evidence. Adequate nutritional status was maintained and decrease the rate of complications, mainly gastrointestinal symptoms, in INC group. The efficacy of drug repurposing can improve through individualized nutritional therapy for preventing adverse effects of radiotherapy in patients with cervical cancer.The prevalence and incidence of cancers has risen over the last decade. this website Available treatments have improved outcomes, yet mortality and morbidity remain high, creating an urgent demand for personalized and new therapy targets. Interferon induced transmembrane protein (IFITM3) is highly expressed in cancers and is a marker of poor prognosis. In this review, we discuss recent advances in IFITM3 biology, the regulatory pathways, and its function within cancer as part of immunity and maintaining stemness. Overexpression of IFITM3 is likely an indirect effect of ongoing inflammation, immune and cancer epithelial-to-mesenchymal (EMT) related pathways i.e., interferons, TGF-β, WNT/β-catenin, etc. However, IFITM3 also influences tumorigenic phenotypes, such as cell proliferation, migration and invasion. Furthermore, IFITM3 plays a key role in cancer growth and maintenance. Silencing of IFITM3 reduces these phenotypes. Therefore, targeting of IFITM3 will likely have implications for potential cancer therapies.Adoptive T cell therapy (ACT) is highly effective in the treatment of hematologic malignancies, but shows limited success in solid tumors. Inactivation of T cells in the tumor milieu is a major hurdle to a wider application of ACT. Cytotoxicity is the most relevant activity for tumor eradication. Here, we document that cytotoxic T cells (CTL) in lactic acidosis exhibited strongly reduced tumor cell killing, which could be compensated partly by increasing the CTL to tumor cell ratio. Lactic acid intervened at multiple steps of the killing process. Lactic acid repressed the number of CTL that performed lytic granule exocytosis (degranulation) in tumor cell co-culture, and, additionally impaired the quality of the response, as judged by the reduced intensity of degranulation and lower secretion of cytotoxins (perforin, granzyme B, granzyme A). CTL in lactic acid switched to a low bioenergetic profile with an inability to metabolize glucose efficiently. They responded to anti-CD3 stimulation poorly with less extracellular acidification rate (ECAR).