The journal Cell Biology: Research & Therapy (CBRT) promotes rigorous research that makes a significant contribution in advancing knowledge in the fields of cell and molecular biology.
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Distribution of Characteristic Mutations in Native Ductal Adenocarcinoma of the Pancreas and Pancreatic Cancer Cell Lines
Although oncological treatment of pancreatic adenocarcinoma (PDAC) has improved within the last few years, PDAC continues to have a very low 5- year survival rate. Basic research is needed to improve and develop new therapeutic strategies. Pancreatic tumour cell lines (CLs) are a prerequisite for such basic research. However, the isolation of CLs is challenging. Outgrowth of cells is only achieved in a small proportion of tumour samples, although the reason for this poor growth remains unknown.
Chemotherapy Increases Aggressiveness of Prostate Cancer via Epithelial Mesenchymal Transition
Although chemotherapy has been used as a major therapeutic weapon against advanced prostate cancer, overcoming drug resistance is still a major challenge. Cancer has been known to diminish therapeutic effect by several molecular mechanisms– increasing efflux by recruiting cell membrane pumps and limiting drug diffusion by constructing leaky vasculature. Moreover, recent studies suggest that long-term treatment with chemotherapy may have detrimental effects for patients presenting with solid tumors. Specifically, prostate cancer epithelial cells develop resistance to chemotherapy and may convert into mesenchymal cells. This switching process, known as Epithelial to Mesenchymal Transition (EMT), is a critical precursor in prostate cancer invasion and metastasis.
NGF and APP Interplay: Focus on YENPTY Motif of Amyloid Precursor Protein and Y682 Residue
Cholinergic deficits originated from NGF metabolism disruption, represent one of the early changes in Alzheimer’s disease, where abnormal deposition of β-amyloid peptide (Aβ) and phosphorylated Tau define the neuropathological hallmarks of the disorder. A failure in NGF maturation can promote pro-apoptotic pathway activation, through p75 receptor; while lack of NGF signalling can generate an atypical TrkA receptor phosphorylation resulting in neuronal cell death and Aβ toxicity. These evidences suggest a complex interaction between TrkA, p75, and Aβ, whose exact cellular mechanisms remain still elusive. Here, we provide a general overview on the current knowledge on NGF and APP interplay, focusing on the events that mediate NGF signalling impairment, and, mostly, on the role of APP Tyrosine 682 phosphorylation whose absence in APPY682G mice impairs APP/TrkA interaction and leads to cholinergicneurodegeneration.
The human skeletal system is a dynamic system that plays vital roles in the sustenance of life. Bone loss is a phenomenon that occurs in humans both in short and in long term spaceflights. The phenotype can be also reproduced on the ground in human and animals and also modeled in cell-based analogs. With limited missions in space, experimental studies in these analogs have provided much of our understanding of bone loss.