Susmita Ghosh

1 month ago | peerj.com | Clark GT |Susmita Ghosh |JSS Academy |Ganesh Jadhav

1Department of Conservative Dentistry and Endodontics, JSS Dental College and Hospital, JSS Academy of Higher Education and Research, Maysore, Karnataka, India 2Department of Conservative Dentistry and Endodontics, All India Institute of Medical Sciences, Nagpur, Maharashtra, India 3Srinivas Institute of Dental Sciences, Department of Conservative Dentistry and Endodontics, Mangaluru, Karnataka, India 4Department of Restorative Dental Science, King Khalid University, Abha, Aseer, Saudi Arabia...

2 months ago | digitalcommons.library.tmc.edu | Susmita Ghosh

AbstractBackground: KRAS is frequently mutated in the tumors of patients with metastatic colorectal cancer (mCRC) and thus represents a valid target for therapy. However, the strategies of targeting KRAS directly and targeting the downstream effector mitogen-activated protein kinase kinase (MEK) via monotherapies have shown limited efficacy. Thus, there is a strong need for novel, effective combination therapies to improve MEK-inhibitor efficacy in patients with KRAS-mutated mCRC.

2 months ago | digitalcommons.library.tmc.edu | Susmita Ghosh

AbstractMutations in KRAS are found in more than 50% of tumors from patients with metastatic colorectal cancer (mCRC). However, direct targeting of most KRAS mutations is difficult; even the recently developed KRASG12C inhibitors failed to show significant benefit in patients with mCRC. Single agents targeting mitogen-activated protein kinase kinase (MEK), a downstream mediator of RAS, have also been ineffective in colorectal cancer.

Sep 6, 2024 | biorxiv.org | Susmita Ghosh |Fan Fan |Reid T. Powell |Yong D. Park

AbstractBackground: KRAS is frequently mutated in the tumors of patients with metastatic colorectal cancer (mCRC) and thus represents a valid target for therapy. However, the strategies of targeting KRAS directly and targeting the downstream effector mitogen-activated protein kinase kinase (MEK) via monotherapies have shown limited efficacy. Thus, there is a strong need for novel, effective combination therapies to improve MEK-inhibitor efficacy in patients with KRAS-mutated mCRC.

Aug 28, 2024 | digitalcommons.library.tmc.edu | Fan Fan |Susmita Ghosh |Reid T. Powell |Jason Roszik

AbstractMetastatic colorectal cancer (mCRC) is the second leading cause of cancer deaths in the United States. More than 50% of patients with mCRC harbor mutations of the oncogenic driver RAS (KRAS or NRAS). Because directly targeting most mutations of RAS is technically challenging, researchers have concentrated on targeting MEK, a downstream mediator of RAS. However, targeting MEK as single-agent therapy is ineffective in patients with mCRC.