Publications by authors named "Kamala Bhatt"

Article Synopsis
  • - Diverse cellular stresses activate heat shock factor 1 (HSF1), which helps manage protein stability and has broader roles in promoting cancer, but its effects on immune cells in tumors are not well understood.
  • - Research using a model of HSF1 activation shows that heightened HSF1 activity in natural killer (NK) cells negatively affects their ability to kill tumors and produce cytokines for immune response.
  • - HSF1 directly influences the expression of important factors for NK cell function, suggesting that understanding its role could improve therapies using NK cells to fight cancer and lead to better treatment combinations.
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Cellular transformation is accompanied by extensive rewiring of many biological processes leading to augmented levels of distinct types of cellular stress, including proteotoxic stress. Cancer cells critically depend on stress-relief pathways for their survival. However, the mechanisms underlying the transcriptional initiation and maintenance of the oncogenic stress response remain elusive.

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Although the BCL6 transcriptional repressor is frequently expressed in human follicular lymphomas (FL), its biological role in this disease remains unknown. Herein, we comprehensively identify the set of gene promoters directly targeted by BCL6 in primary human FLs. We noted that BCL6 binds and represses and NOTCH pathway genes.

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​Heat-shock factor 1 (​HSF1) orchestrates the heat-shock response in eukaryotes. Although this pathway has evolved to help cells adapt in the presence of challenging conditions, it is co-opted in cancer to support malignancy. However, the mechanisms that regulate ​HSF1 and thus cellular stress response are poorly understood.

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