Debottam Sinha
QIMR Berghofer Medical Research Institute
25 Papers
45 Citations
Debottam Sinha is an academic researcher from QIMR Berghofer Medical Research Institute. The author has contributed to research in topics: Targeted therapy & Medicine. The author has an hindex of 8, co-authored 21 publications. Previous affiliations of Debottam Sinha include VIT University & Griffith University.
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Papers
Beyond cytokinesis: the emerging roles of CEP55 in tumorigenesis
Jessie Jeffery,Debottam Sinha,Debottam Sinha,Sriganesh Srihari,Murugan Kalimutho,Kum Kum Khanna +5 more
TL;DR: The functions of CEP55 across different effector pathways, and also its roles as a biomarker and driver of tumorigenesis, are discussed in depth in an exhaustive review, thus commemorating a decade of research on CEP 55.
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Mitotic slippage: an old tale with a new twist
TL;DR: The rationale of targeting CEP55 in vivo could prove to be a novel and effective therapeutic strategy for sensitizing cells to microtubule inhibitors and might offer significantly improved patient outcome.
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CEP55 is a determinant of cell fate during perturbed mitosis in breast cancer.
Murugan Kalimutho,Murugan Kalimutho,Debottam Sinha,Debottam Sinha,Jessie Jeffery,Katia Nones,Katia Nones,Sriganesh Srihari,Winnie Fernando,Pascal H.G. Duijf,Claire Vennin,Claire Vennin,Prahlad V. Raninga,Devathri Nanayakkara,Deepak Mittal,Jodi M. Saunus,Jodi M. Saunus,Sunil R. Lakhani,Sunil R. Lakhani,J. Alejandro Lopez,J. Alejandro Lopez,Kevin J. Spring,Kevin J. Spring,Kevin J. Spring,Paul Timpson,Paul Timpson,Brian Gabrielli,Nicola Waddell,Kum Kum Khanna +28 more
TL;DR: High CEP55 levels dictate cell fate during perturbed mitosis, and forced mitotic cell death by blocking MEK1/2‐PLK1 represents a potential therapeutic strategy for MYC‐CEP55‐dependent basal‐like, triple‐negative breast cancers.
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Cep55 overexpression causes male-specific sterility in mice by suppressing Foxo1 nuclear retention through sustained activation of PI3K/Akt signaling.
Debottam Sinha,Murugan Kalimutho,Josephine Bowles,Ai-Leen Chan,D. Jo Merriner,Amanda L. Bain,Jacinta L. Simmons,Raimundo Freire,J. Alejandro Lopez,Robin M. Hobbs,Moira K O'Bryan,Kum Kum Khanna +11 more
TL;DR: Cep55 overexpression causes change in germ cell proportions and manifests as a Sertoli cell only tubule phenotype, similar to that seen in many azoospermic men, and leads to a shift toward the initial maintenance of undifferentiated spermatogonia and ultimately results in progressive germ cell loss.
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Enhanced dependency of KRAS-mutant colorectal cancer cells on RAD51-dependent homologous recombination repair identified from genetic interactions in Saccharomyces cerevisiae
Murugan Kalimutho,Amanda L. Bain,Bipasha Mukherjee,Purba Nag,Devathri Nanayakkara,Sarah K. Harten,Janelle L. Harris,Goutham Subramanian,Debottam Sinha,Senji Shirasawa,Sriganesh Srihari,Sandeep Burma,Kum Kum Khanna +12 more
TL;DR: It is identified that KRAS‐mutated colorectal cancer cells have augmented homologous recombination repair (HRR) signaling by leveraging the largest synthetic lethal genetic interactome in yeast to highlight a possible mechanism by which KRas‐mutant‐dependent cells drive HRR in vitro by upregulating MYC‐RAD51 expression.
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