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Jones Parks posted an update 6 months ago
Allogeneic hematopoietic stem cell transplantation (alloHSCT) reduced the relapse risk of IHR patients (3-year RFS alloHSCT 40.0±12.8% vs. chemotherapy 8.6±5.8%, P= 0.010). The prediction model can help identify patients with an unfavorable prognosis and refine risk-adapted therapy for intermediate risk AML patients.Gastric cancer is one of the most common cancers and the leading causes of cancer mortality. However, the molecular mechanisms of gastric cancer malignancy remain unclear. Long noncoding RNAs (lncRNAs) have been well documented in controlling cancer progression. Identification of critical lncRNAs in gastric cancer will provide new sights into the regulation mechanism of gastric cancer. Here, we screened differentially expressed lncRNAs in gastric cancer tissues and matched adjacent tissues and found that lncRNA LIT3527, a 486-nucleotide (nt) sense transcript, was frequently upregulated in gastric cancer tissues. Knockdown of LIT3527 dramatically suppressed proliferation and migration of gastric cancer cells through inducing severe cell death but not affecting cell cycle. Mechanistically, we uncovered that depletion of LIT35227 induced significant cell apoptosis and autophagy through inhibiting AKT/ERK/mTOR signaling pathway. Targeting LIT3527 showed a robust inhibition of lung metastasis of gastric cancer cells. Taken together, these results suggest that LIT3527 is essential for gastric cancer cell survival through maintaining mTOR activity, suggesting that it may be clinically valuable as a therapeutic target for gastric cancer.Pathogenic bacterial strains can alter the normal function of cells and induce different levels of inflammatory responses that are connected to the development of different diseases, such as tuberculosis, diarrhea, cancer etc. selleck Chlamydia trachomatis (C. trachomatis) is an intracellular obligate gram-negative bacterium which has been connected with the cervical cancer etiology. Nevertheless, establishment of causality and the underlying mechanisms of carcinogenesis of cervical cancer associated with C. trachomatis remain unclear. Studies reveal the existence of C. trachomatis in cervical cancer patients. The DNA repair pathways including mismatch repair, nucleotide excision, and base excision are vital in the abatement of accumulated mutations that can direct to the process of carcinogenesis. C. trachomatis recruits DDR proteins away from sites of DNA damage and, in this way, impedes the DDR. Therefore, by disturbing host cell-cycle control, chromatin and DDR repair, C. trachomatis makes a situation favorable for malignant transformation. Inflammation originated due to infection directs over production of reactive oxygen species (ROS) and consequent oxidative DNA damage. This review may aid our current understanding of the etiology of cervical cancer in C. trachomatis-infected patients.The RNA binding protein TRA2A, a member of the transformer 2 homolog family, plays a crucial role in the alternative splicing of pre-mRNA. However, it remains unclear whether TRA2A is involved in non-coding RNA regulation and, if so, what are the functional consequences. By analyzing expression profiling data, we found that TRA2A is highly expressed in esophageal cancer and is associated with disease-free survival and overall survival time. Subsequent gain- and loss-of-function studies demonstrated that TRA2A promotes proliferation and migration of esophageal squamous cell carcinoma and adenocarcinoma cells. RNA immunoprecipitation and RNA pull-down assay indicated that TRA2A can directly bind specific sites on MALAT1 in cells. In addition, ectopic expression or depletion of TRA2A leads to MALAT expression changes accordingly, thus modulates EZH2/β-catenin pathway. Together, these findings elucidated that TRA2A triggers carcinogenesis via MALAT1 mediated EZH2/β-catenin axis in esophageal cancer cells.The discovery of many aberrant expressions of long non-coding RNAs (lncRNAs) in various cancers has focused attention on the effects of lncRNA on cancer cells themselves, including cell proliferation, growth inhibition, cell migration, cell immortality, vascular regeneration and cell viability. But with the increasing role of immunotherapy in cancer therapy, a large number of studies have revealed that the regulatory role of lncRNAs in immunity such as differentiation of immune cells can also influence the development and progression of cancer. In particular, recent publications have suggested that lncRNAs play critical roles in T-lymphocyte activation, proliferation, differentiation, function, apoptosis and metabolism. To elucidate the actual functions of lncRNAs at the molecular level of cancer pathogenesis, we summarize some of the current lncRNA regulatory mechanisms associated with T cell to discuss their effects in cancer in the hope of providing potential cancer therapeutic targets or cancer biomarkers. However, we all know that the differentiation and function of T cells is an extremely complex process that involves the expression and regulation of multiple lncRNAs. As a result, more regulatory mechanisms of lncRNAs need to be further studied.Chemoresistance challenges the clinical treatment of colorectal cancer and requires an urgent solution. Isocitrate dehydrogenase 1 (IDH1) is a key enzyme involved in glucose metabolism that mediates the malignant transformation of tumors. However, the mechanisms by which IDH1 is involved in colorectal cancer cell proliferation and drug resistance induction remain unclear. In this study, we found that IDH1 was highly expressed in human colorectal cancer tissues and could be used to indicate a high-grade tumor. In vitro gene overexpression and knockdown were used to determine whether IDH1 promoted the proliferation of the colorectal cancer cell line HCT8 and resistance to 5-Fluorouracil (5FU). Further studies have shown that the 5FU-resistant cell line, HCT8FU, secreted exosomes that contained a high level of IDH1 protein. The exosomal IDH1 derived from 5FU-resistant cells enhanced the resistance of 5FU-sensitive cells. Metabolic assays revealed that exosomes derived from 5FU-resistant cells promoted a decrease in the level of IDH1-mediated NADPH, which is associated with the development of 5FU resistance in colorectal cancer cells.