US
(888) 440-0954
Home  |   Resources

<< Back

Publications | Posters | White Papers | QC Reports

Malini Manoharan, Nitin Mandloi, Sushri Priyadarshini, Ashwini Patil, Rohit Gupta, Laxman Iyer, Ravi Gupta and Amitabha Chaudhuri

A large number of tumor intrinsic and extrinsic factors determine long-term survival in human cancers. In this study, we stratified 9120 tumors from 33 cancers with respect to their immune cell content and identified immunogenomic features associated with long-term survival. Our analysis demonstrates that tumors infiltrated by CD8+ T cells expressing higher levels of activation marker (PD1hi) along with TCR signaling genes and cytolytic T cell markers (IL2hi/TNF-αhi/IFN-γhi/GZMA-Bhi) extend survival, whereas survival benefit was absent for tumors infiltrated by anergic and hyperexhausted CD8hi T cells characterized by high expression of CTLA-4, TIM3, LAG3, and genes linked to PI3K signaling pathway. The computational approach of using robust and highly specific gene expression signatures to deconvolute the tumor microenvironment has important clinical applications, such as selecting patients who will benefit from checkpoint inhibitor treatment.

Sajesh Puthenpurackal Krishnankutty, Megha Muraleedharan, Rajadurai Chinnasamy Perumal, Saju Michael, Jubina Benny, Bipin Balan, Pramod Kumar, Jishnu Manazhi, Bangaruswamy Dhinoth Kumar, Sam Santhosh, George Thomas, Ravi Gupta and Arun Zachariah

The oral cavities of snakes are replete with various types of bacterial flora. Culture-dependent studies suggest that some of the bacterial species are responsible for secondary bacterial infection associated with snakebite. A complete profile of the ophidian oral bacterial community has been unreported until now. Therefore, in the present study, we determined the complete bacterial compositions in the oral cavity of some snakes from India.

Snigdha Majumder, Rakshit Shah, Jisha Elias, Malini Manoharan, Priyanka Shah, Anjali Kumari, Papia Chakraborty, Vasumathi Kode, Yogesh Mistry, Karunakaran Coral, Bharti Mittal, Sakthivel Murugan SM, Lakshmi Mahadevan, Ravi Gupta, Amitabha Chaudhuri & Arati Khanna-Gupta

Lynch Syndrome (LS) is an inherited heterozygous autosomal dominant disorder which predisposes affected individuals to the risk of developing colorectal cancer (CRC) as well as to endometrial carcinomas, tumours of the stomach, small intestines, ureter, brain, pelvis and prostate among others1. It is the most common hereditary CRC syndrome accounting for 2–5% of all CRCs. In the developed world, the estimated disease frequency ranges from 1:370 to 1:20002 but no prevalence details have been officially reported from developing nations to date. In India, while the overall incidence of CRC is comparatively lower than in the west, a large percentage of patients develop CRC before the age of 45 with a higher proportion (10–15%) of LS-CRC cases3.

Sam Santhosh, Hiranjith G.H., Michael Nemzek and Amitabha Chaudhuri

Currently approved checkpoint inhibitors are antibodies that block the function of three key proteins expressed on the surface of T cells: CTLA-4, PD-1 and PD-L1. Under normal conditions, these proteins function as brakes to prevent immune-related toxicity from arising because of persistent T cell activity. Cancer hijacks this essential function   of immune homeostasis to protect itself from immune- mediated elimination [1, 2]. By expressing high levels of PD- L1, tumor cells engage PD-1 receptors on T cells, suppressing  their anti-tumor activity and escaping T cell-mediated killing. By blocking PD-1 and PD-L1 signaling, the checkpoint inhibitors remove the brakes on T cells imposed by the tumor and enhance their anti-tumor activity

Sam Santhosh, Hiranjith G.H., Michael Nemzek and Amitabha Chaudhuri

Currently approved checkpoint inhibitors are antibodies that block the function of three key proteins expressed on the surface of T cells: CTLA-4, PD-1 and PD-L1.

Under normal conditions, these proteins function as brakes to prevent immune-related toxicity from arising because of persistent T cell activity. Cancer hijacks this essential function of immune homeostasis to protect itself from immune-mediated elimination [1, 2]. By expressing high levels of PD-L1, tumor cells engage PD-1 receptors on T cells, suppressing their anti-tumor activity and escaping T cell-mediated killing. By blocking PD-1 and PD-L1 signaling, the checkpoint inhibitors remove the brakes on T cells imposed by the tumor and enhance their anti-tumor activity [3].

*
 
*
*