Dr. Naresh Sah
'%3e%3cpath%20d='M22.1642%2019.0924C21.7317%2018.068%2021.1041%2017.1375%2020.3163%2016.3527C19.5309%2015.5656%2018.6006%2014.9381%2017.5766%2014.5048C17.5674%2014.5002%2017.5582%2014.4979%2017.5491%2014.4933C18.9774%2013.4616%2019.9059%2011.7811%2019.9059%209.88504C19.9059%206.74408%2017.3611%204.19922%2014.2201%204.19922C11.0792%204.19922%208.53429%206.74408%208.53429%209.88504C8.53429%2011.7811%209.46282%2013.4616%2010.8912%2014.4956C10.882%2014.5002%2010.8728%2014.5025%2010.8636%2014.5071C9.83652%2014.9404%208.91487%2015.5617%208.1239%2016.355C7.33685%2017.1404%206.70933%2018.0707%206.276%2019.0947C5.85031%2020.0972%205.62072%2021.172%205.59967%2022.2609C5.59905%2022.2853%205.60335%2022.3097%205.61229%2022.3325C5.62123%2022.3553%205.63465%2022.376%205.65174%2022.3935C5.66883%2022.4111%205.68926%2022.425%205.71182%2022.4345C5.73437%2022.444%205.7586%2022.4489%205.78308%2022.4489H7.15868C7.25956%2022.4489%207.3398%2022.3686%207.3421%2022.2701C7.38795%2020.5001%208.09868%2018.8425%209.35506%2017.5861C10.655%2016.2862%2012.3814%2015.5709%2014.2201%2015.5709C16.0588%2015.5709%2017.7852%2016.2862%2019.0852%2017.5861C20.3415%2018.8425%2021.0523%2020.5001%2021.0981%2022.2701C21.1004%2022.3709%2021.1807%2022.4489%2021.2815%2022.4489H22.6571C22.6816%2022.4489%2022.7058%2022.444%2022.7284%2022.4345C22.751%2022.425%2022.7714%2022.4111%2022.7885%2022.3935C22.8056%2022.376%2022.819%2022.3553%2022.8279%2022.3325C22.8369%2022.3097%2022.8412%2022.2853%2022.8406%2022.2609C22.8176%2021.165%2022.5907%2020.0989%2022.1642%2019.0924ZM14.2201%2013.8284C13.1678%2013.8284%2012.1773%2013.418%2011.4322%2012.6729C10.6871%2011.9278%2010.2767%2010.9374%2010.2767%209.88504C10.2767%208.83271%2010.6871%207.84227%2011.4322%207.09715C12.1773%206.35204%2013.1678%205.94165%2014.2201%205.94165C15.2724%205.94165%2016.2629%206.35204%2017.008%207.09715C17.7531%207.84227%2018.1635%208.83271%2018.1635%209.88504C18.1635%2010.9374%2017.7531%2011.9278%2017.008%2012.6729C16.2629%2013.418%2015.2724%2013.8284%2014.2201%2013.8284Z'%20fill='%238590A2'/%3e%3c/g%3e%3c/svg%3e)
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Academic Career Length
3Years (2024-Present)
(Calculated once Scilit publication data is synced: current year − year of first publication + 1)
Representative Publications
View All Publications25 January 2025 in Cancer and Metastasis Reviews
Journal Article
SMSarra Mestiri
Sarra MestiriASAna Sami
Ana SamiNaresh SahDEDina Moustafa Abo El-Ella
Dina Moustafa Abo El-EllaSKSabiha Khatoon
Sabiha Khatoon
Shafiul Haque +3
Journal Article
COCharles C. Okechukwu
Charles C. OkechukwuXMXue Ma
Xue MaNaresh SahCMChinnadurai Mani
Chinnadurai ManiKPKomaraiah Palle
Komaraiah Palle
William GmeinerCombination chemotherapy regimens that include fluoropyrimidine (FP) drugs, e.g., 5-fluorouracil (5-FU), are central to the treatment of colorectal cancer liver metastases (CRLMs), a major cause of cancer mortality. We tested a second-generation FP polymer, CF10, in a CC531/WAGRij syngeneic orthotopic rat model of liver metastasis to determine if CF10 improved response relative to 5-FU. CF10 displayed increased potency relative to 5-FU in CC531 rat colorectal cancer cells based on clonogenic assay results and caused increased apoptosis, as shown using a live/dead assay. The increased potency of CF10 to CC531 cells was associated with increased replication stress, as assessed by Western blot for biomarkers of ATR/Chk1 and ATM/Chk2 pathway activation. CF10 dosed to deliver equivalent FP content as an established dose of 5-FU in rats (50 mg/kg) did not cause weight loss in WAGRij rats even when combined with ethynyl uracil (EU), an inhibitor of dihydropyrimidine dehydrogenase, the enzyme primarily responsible for 5-FU degradation in the liver. In contrast, 5-FU caused significant weight loss that was exacerbated in combination with EU. Importantly, CF10 was significantly more effective than 5-FU at inhibiting tumor progression (~90% reduction) in the CC531/WAG/Rij CRLM model. Our results reveal strong potential for CF10 to be used for CRLM treatment.
Journal Article
Naresh SahASAbdul Althaf Shaik
Abdul Althaf ShaikGAGanesh Acharya
Ganesh AcharyaMDManikantha Dunna
Manikantha DunnaASASHOK Silwal
ASHOK SilwalSBSOUNAK BAGCHI
SOUNAK BAGCHI +2
This review article explores the fundamental role of receptor targeting in overcoming drug resistance in cancer therapy, an area of critical concern given the persistently high rates of cancer morbidity and mortality globally. We highlight how receptor biology intersects with the development of therapeutic resistance with a specific focus on anti-angiogenic agents, immune checkpoint inhibitors, and monoclonal antibodies, which directly or indirectly influence receptor pathways. We also explore how other receptor tyrosine kinases can initially suppress tumor growth, yet often lead to resistance, underscoring the need for novel combinatorial approaches that incorporate advanced receptor modulation techniques. Further, the review delves into the mechanisms by which modulation of the tumor microenvironment and immune system via receptor pathways can overcome resistance to traditional immunotherapies. Additionally, emerging technologies in receptor-targeted nanomedicine are also highlighted, showcasing their potential to revolutionize drug delivery and improve therapeutic outcomes by targeting specific receptor interactions. Ultimately, this review calls for a deeper understanding of receptor dynamics to develop more precise interventions, including insights from various healthcare settings that can prevent or circumvent drug resistance, thus enhancing patient outcomes in oncology.
Journal Article
MDManikantha Dunna
Manikantha DunnaSMShivani Munagala
Shivani MunagalaMKMerit Kayastha
Merit KayasthaSPSrinithya Paruchuri
Srinithya ParuchuriSTSona Sara Thomas
Sona Sara ThomasNaresh Sah +2
Receptor dysregulation is a hallmark of cancer and a major driver of tumor initiation, progression, and therapeutic resistance. Among the most clinically relevant receptors are the epidermal growth factor receptor (EGFR), human epidermal growth factor receptor 2 (HER2), estrogen receptor (ER), and androgen receptor (AR), which regulate critical processes including cell proliferation, survival, and metastasis. Genetic alterations, receptor overexpression, and aberrant signaling can lead to persistent activation of these pathways, promoting oncogenic progression. Advances in the understanding of EGFR, HER2, ER, and AR signaling have enabled the development of targeted therapies that have significantly improved clinical outcomes. However, therapeutic resistance, signaling crosstalk, and tumor heterogeneity continue to limit treatment efficacy. This review summarizes the mechanisms underlying the dysregulation of these receptor pathways, their roles in cancer development, and current and emerging therapeutic strategies targeting receptor-driven malignancies. A better understanding of these signaling networks may facilitate the development of more effective biomarkers and precision oncology approaches.
About Me
Dr. Naresh Sah completed his Doctor of Pharmacy (Pharm.D.) with distinction, earning a state-level 2nd Rank from Rajiv Gandhi University of Health Sciences (RGUHS), Bengaluru, India, in 2019. His profound expertise in pharmacotherapeutics has not only enabled him to perform life-saving therapeutic interventions but also to educate 75 physicians on critical pharmacotherapy aspects. Driven by a passion for oncological research, Dr. Sah pursued a Ph.D. at Texas Tech University Health Sciences Center, where he is actively involved in the pioneering development of novel cancer therapeutics.
His research ambitiously targets the genetic and molecular mechanisms underlying aggressive ovarian tumor growth, particularly in African American women, aiming to mitigate racial health disparities in cancer outcomes. Dr. Sah is at the forefront of a Phase I clinical trial for CF10, a promising new nanoscale drug designed to tackle chemoresistance in colorectal. His work emphasizes the intricate crosstalk between oncogenic signals and tumor suppressors, exploring how these interactions contribute to cancer’s therapeutic resistance. Moreover, he investigates innovative approaches to combat renal cell carcinoma, integrating stereotactic body radiation therapy with cutting-edge immunotherapy and targeted treatments.
Dr. Sah has received multiple awards for his research and actively contributes to scientific and academic communities through mentoring and leadership in student organizations.