Immunosuppressive plasma cells impede T-cell-dependent immunogenic chemotherapy.
San Diego, United States. In Nature, 07 Jun 2015
Our previous studies revealed that B cells recruited by the chemokine CXCL13 into prostate cancer tumours promote the progression of castrate-resistant prostate cancer by producing lymphotoxin, which activates an IκB kinase α (IKKα)-BMI1 module in prostate cancer stem cells.
Cancer stem cells in oesophageal squamous cell carcinoma: Identification, prognostic and treatment perspectives.
Gold Coast, Australia. In Crit Rev Oncol Hematol, 16 May 2015
It has also been demonstrated that stem cell markers like ALDH1, HIWI, Oct3/4, ABCG2, SOX2, SALL4, BMI-1, NANOG, CD133 and podoplanin are associated with patient's prognosis, pathological stages, cancer recurrence and therapy resistance.
Anticancer Effect of AntiMalarial Artemisinin Compounds.
Dibrugarh, India. In Ann Med Health Sci Res, Mar 2015
Artemisinins seem to regulate key factors such as nuclear factor-kappa B, survivin, NOXA, hypoxia-inducible factor-1α, and BMI-1, involving multiple pathways that may affect drug response, drug interactions, drug resistance, and associated parameters upon normal cells.
Clinical Implications of Intestinal Stem Cell Markers in Colorectal Cancer.
Denmark. In Clin Colorectal Cancer, Jan 2015
This review provides an overview of the intestinal stem cell markers leucine-rich repeat-containing G-protein-coupled receptor 5 (LGR5), B cell-specific Moloney murine leukemia virus insertion site 1 (BMI1), Musashi1 (MSI1), and sex-determining region y-box 9 (SOX9) and their implications in human CRC.
FAL1ing inside an amplicon.
Pamplona, Spain. In Cancer Cell, Oct 2014
FAL1 acts as an oncogene by stabilizing BMI1, which results in the repression of CDKN1A expression.
Novel therapeutic targets for pancreatic cancer.
Hong Kong, Hong Kong. In World J Gastroenterol, Sep 2014
In order to give a better understanding of the current findings and to seek the direction in future pancreatic cancer research; in this review we will focus on targets suppressing tumour metastatsis and progression, KRAS activated downstream effectors, the relationship of Notch signaling and Nodal/Activin signaling with pancreatic cancer cells, the current findings of non-coding RNAs in inhibiting pancreatic cancer cell proliferation, brief discussion in transcription remodeling by epigenetic modifiers (e.g., HDAC, BMI1, EZH2) and the plausible therapeutic applications of cancer stem cell and hyaluronan in tumour environment.