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921.
Transcriptional Biomarkers in Oral Cancer: An Integrative Analysis and the Cancer Genome Atlas Validation
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Kinjal D PatelHemangini H VoraPrabhudas S Patel 《Asian Pacific journal of cancer prevention》2021,22(2):371-380
Objective: An impervious mortality rate in oral cancer (OC) to a certain extent explains the exigencies of precise biomarkers. Therefore, the study was intended to identify OC candidate biomarkers using samples of healthy normal tissues (N=335), adjacent normal tissues (N=93) and OC tissues (N=533) from online microarray data. Methods: Differentially expressed genes (DEGs) were recognised through GeneSpring software (Fold change >4.0 and ‘p’ value 相似文献
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Zyanya Reyes-Castillo José Francisco Muñoz-Valle Mara A. Llamas-Covarrubias 《Autoimmunity reviews》2018,17(2):94-102
Rheumatoid arthritis (RA) is the most common rheumatic autoimmune disease worldwide, which causes progressive joint damage and can lead to functional disability. Despite prominent advances in RA diagnosis and treatment during the last 20 years, there is still a need for novel biomarkers that aid in diagnosis and prognosis of this heterogeneous disease. Citrullination is a key post-translational modification implicated on anti-citrullinated protein/peptide antibodies (ACPA) production in RA, catalyzed by human peptidylarginine deiminases (PADs). Among these enzymes, PAD4 has been recognized as an important player in RA pathogenesis and the enzyme itself is a target of autoantibodies (anti-PAD4) in a subgroup of RA patients. Accumulating evidence suggests that anti-PAD4 autoantibodies may be useful as a severity biomarker in RA and recent studies have also shed light on the functional significance of these autoantibodies. This review summarizes the evidence on anti-PAD4 autoantibodies in RA, and addresses its usefulness for disease diagnosis and prognosis. Novel immunological aspects of anti-PAD4 antibodies and their relevance to RA pathogenesis are also discussed. 相似文献
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Joaquin Mateo Heather H. Cheng Himisha Beltran David Dolling Wen Xu Colin C. Pritchard Helen Mossop Pasquale Rescigno Raquel Perez-Lopez Verena Sailer Michael Kolinsky Ada Balasopoulou Claudia Bertan David M. Nanus Scott T. Tagawa Heather Thorne Bruce Montgomery Suzanne Carreira Johann S. de Bono 《European urology》2018,73(5):687-693
Background
Germline DNA damage repair gene mutation (gDDRm) is found in >10% of metastatic prostate cancer (mPC). Their prognostic and predictive impact relating to standard therapies is unclear.Objective
To determine whether gDDRm status impacts benefit from established therapies in mPC.Design, setting, and participants
This is a retrospective, international, observational study. Medical records were reviewed for 390 mPC patients with known gDDRm status. All 372 patients from Royal Marsden (UK), Weill-Cornell (NY), and University of Washington (WA) were previously included in a prevalence study (Pritchard, NEJM 2016); the remaining 18 were gBRCA1/2m carriers, from the kConFab consortium, Australia.Outcome measurements and statistical analysis
Response rate (RR), progression-free survival (PFS), and overall survival (OS) data were collected. To account for potential differences between cohorts, a mixed-effect model (Weibull distribution) with random intercept per cohort was used.Results and limitations
The gDDRm status was known for all 390 patients (60 carriers of gDDRm [gDDRm+], including 37 gBRCA2m, and 330 cases not found to carry gDDRm [gDDRm–]); 74% and 69% were treated with docetaxel and abiraterone/enzalutamide, respectively, and 36% received PARP inhibitors (PARPi) and/or platinum. Median OS from castration resistance was similar among groups (3.2 vs 3.0 yr, p = 0.73). Median docetaxel PFS for gDDRm+ (6.8 mo) was not significantly different from that for gDDRm– (5.1 mo), and RRs were similar (gDDRm+ = 61%; gDDRm– = 54%). There were no significant differences in median PFS and RR on first-line abiraterone/enzalutamide (gDDRm+ = 8.3 mo, gDDRm– = 8.3 mo; gDDRm+ = 46%, gDDRm– = 56%). Interaction test for PARPi/platinum and gDDRm+ resulted in an OS adjusted hazard ratio of 0.59 (95% confidence interval 0.28–1.25; p = 0.17). Results are limited by the retrospective nature of the analysis.Conclusions
mPC patients with gDDRm appeared to benefit from standard therapies similarly to the overall population; prospective studies are ongoing to investigate the impact of PARPi/platinum.Patient summary
Patients with inherited DNA repair mutations benefit from standard therapies similarly to other metastatic prostate cancer patients. 相似文献926.
ObjectivesThis study aimed to characterize mammospheres from hormonal receptor (HR) positive and triple-negative breast cancer (TNBC), hypothesizing a differential profile of CSC and differentiation markers, and a stemness enrichment when successive sphere forming-protocols are performed.MethodsBreast cancer cells MCF-7 and HCC1806 were submitted to sphere-forming protocols. The first sphere generation (MS1) was cultured in adherent conditions (G1). This procedure was repeated and generations of mammospheres (MS1, MS2, and MS3) and sphere-derived cells in adherent conditions (G1, G2, and G3) were obtained. The mammosphere forming capacity, self-renewal, area and doubling time were evaluated. Flow cytometry regarding CD133, CD24, and CD44 and western-blot regarding aldehyde dehydrogenase (ALDH), hormonal receptors and P53 expression was performed.ResultsBreast cancer cell lines harboured the capacity to form spheres, which originated derived adherent populations. The sphere-forming capacity was enhanced in HCC1806-MS3 compared to MS1. Self-renewal was higher in MCF-7 mammospheres, which also had an increased area. The putative CSC markers CD133 showed tendency to be enhanced in mammospheres but the CD44+/CD24-/low phenotype was not identified. The expression of ALDH was greater in mammospheres from MCF-7 and HCC1806 than in the respectively derived adherent cells. The expression of oestrogen receptor (ER)-α, progesterone receptor (PR) and P53 decreased in MCF-7 spheres. ER-β expression was lower in mammospheres from both cell lines compared with parental and derived adherent populations.ConclusionsLoss of HR and P53 expression in HR-positive mammospheres evidences the minor population of CSC which shares characteristics with the TNBC phenotype. 相似文献
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Vyacheslav Ryabov Aleksandra Gombozhapova Yuliya Rogovskaya Julia Kzhyshkowska Mariya Rebenkova Rostislav Karpov 《Immunobiology》2018,223(4-5):413-421
Myocardial infarction (MI) remains the leading cause of mortality and morbidity throughout the world. Macrophages are key innate immune cells that play a significant role in transition from the inflammatory to the regenerative phase during wound healing following MI. The scavenger receptor stabilin-1 is one of the most interesting macrophage biomarkers. This receptor contributes to wound healing, angiogenesis, and tissue remodeling. We suggested a research protocol using macrophage biomarkers to study the cellular basis of cardiac remodeling and healing in patients with acute MI. The purpose of the research was to translate experimental knowledge regarding macrophage subsets and their biomarkers in post-infarction myocardial regeneration into results observed in clinical settings. The study included 41 patients with fatal MI type 1. All patients were divided into four groups according to the timeline of MI histopathology. In addition to routine histopathological analysis, macrophage infiltration was assessed by immunohistochemistry. We used CD68 as a marker for the cells of the macrophage lineage and stabilin-1 as an M2-like macrophage biomarker. The number of CD68+ and stabilin-1+ macrophages in the infarct area increased and peaked in the regenerative phase and did not decrease in the late stage of MI. In the peri-infarct area, the number of CD68+ macrophages increased in the inflammatory phase, peaked during the reparative phase, and did not decrease in the late phase, while the number of stabilin-1+ macrophages increased in the regenerative phase and remained unchanged. Additionally, in the reparative phase, we observed increase in the number of CD68+ and stabilin-1+ macrophages in the non-infarct area. The research protocol suggested allowed us to translate experimental knowledge regarding macrophage subsets and their biomarkers in post-infarction myocardial regeneration into clinical data. Taken together, these results demonstrated biphasic cardiac macrophage response following acute MI somewhat similar to that in a murine model. The increase in stabilin-1+ macrophage infiltration noticed in the myocardium during the regenerative phase and the strong positive correlation between the number of these cells and timeline of MI histopathology enabled us to propose stabilin-1 as a diagnostic macrophage biomarker in myocardium wound healing in patients with acute MI. 相似文献
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