S
Samaresh Malik
Researcher at Presidency University, Kolkata
Publications - 4
Citations - 44
Samaresh Malik is an academic researcher from Presidency University, Kolkata. The author has contributed to research in topics: Lytic cycle & Ubiquitin. The author has an hindex of 2, co-authored 3 publications receiving 10 citations.
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Journal ArticleDOI
Dysbiosis of Oral Microbiota During Oral Squamous Cell Carcinoma Development.
Purandar Sarkar,Samaresh Malik,Sayantan Laha,Shantanab Das,Soumya Bunk,Jay Gopal Ray,Raghunath Chatterjee,Abhik Saha +7 more
TL;DR: In this paper, the association of bacterial dysbiosis and oral squamous cell carcinoma (OSCC) among the Indian population, malignant lesions and anatomically matched adjacent normal tissues were obtained from fifty well-differentiated OSCC patients and analyzed using 16S rRNA V3-V4 amplicon based sequencing on the MiSeq platform.
Journal ArticleDOI
Proteasomal inhibition triggers viral oncoprotein degradation via autophagy-lysosomal pathway.
Chandrima Gain,Samaresh Malik,Shaoni Bhattacharjee,Arijit Ghosh,Erle S. Robertson,Benu Brata Das,Abhik Saha +6 more
TL;DR: Proteasomal inhibition reduces the colony formation ability of this important viral oncoprotein, induces apoptotic cell death and increases transcriptional activation of both latent and lytic gene expression which further promotes viral reactivation from EBV transformed B-lymphocytes.
Journal ArticleDOI
Differential Microbial Signature Associated With Benign Prostatic Hyperplasia and Prostate Cancer
Purandar Sarkar,Samaresh Malik,Anwesha Banerjee,Chhanda Datta,Dilipkumar Pal,Amlan K. Ghosh,Abhik Saha +6 more
TL;DR: A number of human tumor viruses, including Epstein-Barr virus and hepatitis B virus, along with two high-risk human papillomaviruses - HPV-16 and HPV-18, are significantly associated with the PCa development and strongly correlated with PCa bacterial signature.
Posted ContentDOI
Proteasomal Inhibition Triggers Viral Oncoprotein Degradation via Autophagy-Lysosomal Pathway
Chandrima Gain,Samaresh Malik,Shaoni Bhattacharjee,Arijit Ghosh,Erle S. Robertson,Benu Brata Das,Abhik Saha +6 more
TL;DR: Proteasomal inhibition reduces the colony formation ability of this important viral oncoprotein, increases transcriptional activation of both latent and lytic gene expression and induces viral reactivation from EBV transformed B-lymphocytes, which offers rationale to use proteasome inhibitors as potential therapeutic strategy against multiple EBV associated B-cell lymphomas.