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Mantle Cell Lymphoma: A North Indian Tertiary Care Centre Experience
Das, Chandan Krushna,Gogia, Ajay,Kumar, Lalit,Sharma, Atul,Sharma, Mehar Chand,Mallick, Saumya Ranjan Asian Pacific Journal of Cancer Prevention 2016 Asian Pacific journal of cancer prevention Vol.17 No.10
Background: Mantle cell lymphoma (MCL) is an aggressive non-Hodgkin's lymphoma, with a pathognomonic chromosomal translocation t (11;14). Prognosis is uniformly dismal but there is a paucity of information on MCL from India. Materials and methods: We retrospectively analysed clinicopathological information on all treated patients with MCL at our centre. STATA 14.0 was used for analysis. Survival was assessed by Kaplan-Meier analysis and the Cox's proportional hazards method. Statistical significance was defined as a P value of < 0.05. Results: Fifty-one patients with MCL were reviewed. The median age at presentation was 57.0 years. Extranodal involvement was seen in 39.0 (74.0%) while bone marrow positivity at presentation was found in 27.0 (54.0%). Initial treatment was chemotherapy with or without rituximab. Patients receiving rituximab-based therapy (n = 24) had 5-year progression-free survival (PFS) of 21.0 (88.0%), compared with 14.0 (61.0%) for those not receiving rituximab (n = 23, P = 0.036). Twenty-three patients were alive with a median follow-up of 20.7 months (range 2.5-89.2). PFS at 1 and 2 years was 51.0% and 27.0%, and overall survival (OS) 78.0% and 72.0%, respectively. Use of more than 2.0 lines of therapy, use of bendamustine-rituximab, and high TLC (>10,000.0/cu.mm) significantly affected PFS. Conclusions: In our experience, MCL patients from north India have an early age at presentation. When treated with regimens including rituximab results in an improved response rate and PFS. This study provided comprehensive insights into the treatment of MCL in a developing country.
Verma, Shiv Prakash,Sisoudiya, Saumya,Das, Parimal Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.18
Purpose: Anti-cancer activity evaluation of aqueous extract of CRUEL (herbomineral formulation) capsules on renal cell carcinoma cell lines, and exploration of mechanisms of cell death. Materials and Methods: To detect the cytotoxic dose concentration in renal cell carcinoma (RCC) cells, MTT assays were performed and morphological changes after treatment were observed by inverted microscopy. Drug effects against RCC cell lines were assessed with reference to cell cycle distribution (flow cytometry), anti-metastatic potential (wound healing assay) and autophagy(RT-PCR). Results: CRUEL showed anti-proliferative effects against RCC tumor cell lines with an IC50 value of ${\approx}4mg/mL$ in vitro., while inducing cell cycle arrest at S-phase of cell cycle and inhibiting wound healing. LC3 was found to be up-regulated after drug treatment in RT-PCR resulting in an autophagy mode of cell death. Conclusions: This study provides the experimental validation for antitumor activity of CRUEL.
miR-31a-5p promotes postnatal cardiomyocyte proliferation by targeting RhoBTB1
Junjie Xiao,Hui Liu,Dragos Cretoiu,Daniela Oana Toader,Nicolae Suciu,Jing Shi,Shutong Shen,Yihua Bei,Joost PG Sluijter,Saumya Das,Xiangqing Kong,Xinli Li 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-
A limited number of microRNAs (miRNAs, miRs) have been reported to control postnatal cardiomyocyte proliferation, but their strong regulatory effects suggest a possible therapeutic approach to stimulate regenerative capacity in the diseased myocardium. This study aimed to investigate the miRNAs responsible for postnatal cardiomyocyte proliferation and their downstream targets. Here, we compared miRNA profiles in cardiomyocytes between postnatal day 0 (P0) and day 10 (P10) using miRNA arrays, and found that 21 miRNAs were upregulated at P10, whereas 11 were downregulated. Among them, miR-31a-5p was identified as being able to promote cardiomyocyte proliferation as determined by proliferating cell nuclear antigen (PCNA) expression, double immunofluorescent labeling for α-actinin and 5-ethynyl-2-deoxyuridine (EdU) or Ki-67, and cell number counting, whereas miR-31a-5p inhibition could reduce their levels. RhoBTB1 was identified as a target gene of miR-31a-5p, mediating the regulatory effect of miR-31a-5p in cardiomyocyte proliferation. Importantly, neonatal rats injected with a miR-31a-5p antagomir at day 0 for three consecutive days exhibited reduced expression of markers of cardiomyocyte proliferation including PCNA expression and double immunofluorescent labeling for α-actinin and EdU, Ki-67 or phospho-histone-H3. In conclusion, miR-31a-5p controls postnatal cardiomyocyte proliferation by targeting RhoBTB1, and increasing miR-31a-5p level might be a novel therapeutic strategy for enhancing cardiac reparative processes.