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Your search keyword '"Macha, Muzafar A."' showing total 208 results
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208 results on '"Macha, Muzafar A."'

11. Associations between telomere attrition, genetic variants in telomere maintenance genes, and non-small cell lung cancer risk in the Jammu and Kashmir population of North India

Author

Bhat, Gh. Rasool, Jamwal, Rajeshwer Singh, Sethi, Itty, Bhat, Amrita, Shah, Ruchi, Verma, Sonali, Sharma, Minerva, Sadida, Hana Q., Al-Marzooqi, Sara K., Masoodi, Tariq, Mirza, Sameer, Haris, Mohammad, Macha, Muzafar A., Akil, Ammira S. Alshabeeb, Bhat, Ajaz A., and Kumar, Rakesh

Published
2023
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15. Ubiquitin specific peptidase 37 and PCNA interaction promotes osteosarcoma pathogenesis by modulating replication fork progression

Author

Chauhan, Ravi, Gupta, Ashna, Malhotra, Lakshay, Bhat, Ajaz A., Pandita, Raj K., Masoodi, Tariq, Dagar, Gunjan, Sadida, Hana Q., Al-Marzooqi, Sara K., Batra, Atul, Bakhshi, Sameer, Sharma, Mehar Chand, Tanwar, Pranay, Khan, Shah Alam, Samath, Ethayathulla Abdul, Uddin, Shahab, Akil, Ammira S. Al-Shabeeb, Haris, Mohammad, Macha, Muzafar A., Pandita, Tej K., and Singh, Mayank

Published
2023
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23. Cytokine-chemokine network driven metastasis in esophageal cancer; promising avenue for targeted therapy

Author

Bhat, Ajaz A., Nisar, Sabah, Maacha, Selma, Carneiro-Lobo, Tatiana Correa, Akhtar, Sabah, Siveen, Kodappully Sivaraman, Wani, Nissar A., Rizwan, Arshi, Bagga, Puneet, Singh, Mayank, Reddy, Ravinder, Uddin, Shahab, Grivel, Jean-Charles, Chand, Gyan, Frenneaux, Michael P., Siddiqi, Mushtaq A., Bedognetti, Davide, El-Rifai, Wael, Macha, Muzafar A., and Haris, Mohammad

Published
2021
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32. CAR-T-Cell Therapy in Multiple Myeloma: B-Cell Maturation Antigen (BCMA) and Beyond.

Author

Mishra, Abhinava K., Gupta, Ashna, Dagar, Gunjan, Das, Dayasagar, Chakraborty, Abhijit, Haque, Shabirul, Prasad, Chandra Prakash, Singh, Archana, Bhat, Ajaz A., Macha, Muzafar A., Benali, Moez, Saini, Kamal S., Previs, Rebecca Ann, Saini, Deepak, Saha, Dwaipayan, Dutta, Preyangsee, Bhatnagar, Aseem Rai, Darswal, Mrinalini, Shankar, Abhishek, and Singh, Mayank

Subjects
CHIMERIC antigen receptors, MULTIPLE myeloma, CYTOKINE release syndrome, ANTIGENS, LYMPHOCYTE transformation, RADIOTHERAPY, SEZARY syndrome
Abstract

Significant progress has been achieved in the realm of therapeutic interventions for multiple myeloma (MM), leading to transformative shifts in its clinical management. While conventional modalities such as surgery, radiotherapy, and chemotherapy have improved the clinical outcomes, the overarching challenge of effecting a comprehensive cure for patients afflicted with relapsed and refractory MM (RRMM) endures. Notably, adoptive cellular therapy, especially chimeric antigen receptor T-cell (CAR-T) therapy, has exhibited efficacy in patients with refractory or resistant B-cell malignancies and is now also being tested in patients with MM. Within this context, the B-cell maturation antigen (BCMA) has emerged as a promising candidate for CAR-T-cell antigen targeting in MM. Alternative targets include SLAMF7, CD38, CD19, the signaling lymphocyte activation molecule CS1, NKG2D, and CD138. Numerous clinical studies have demonstrated the clinical efficacy of these CAR-T-cell therapies, although longitudinal follow-up reveals some degree of antigenic escape. The widespread implementation of CAR-T-cell therapy is encumbered by several barriers, including antigenic evasion, uneven intratumoral infiltration in solid cancers, cytokine release syndrome, neurotoxicity, logistical implementation, and financial burden. This article provides an overview of CAR-T-cell therapy in MM and the utilization of BCMA as the target antigen, as well as an overview of other potential target moieties. [ABSTRACT FROM AUTHOR]

Published
2023
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49. Mucin (Muc) expression during pancreatic cancer progression in spontaneous mouse model: potential implications for diagnosis and therapy

Author

Rachagani Satyanarayana, Torres María P, Kumar Sushil, Haridas Dhanya, Baine Michael, Macha Muzafar A, Kaur Sukhwinder, Ponnusamy Moorthy P, Dey Parama, Seshacharyulu Parthasarathy, Johansson Sonny L, Jain Maneesh, Wagner Kay-Uwe, and Batra Surinder K

Subjects
Mucins, Inflammatory cytokines, KrasG12D mouse model, Diseases of the blood and blood-forming organs, RC633-647.5, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Pancreatic cancer (PC) is a lethal malignancy primarily driven by activated Kras mutations and characterized by the deregulation of several genes including mucins. Previous studies on mucins have identified their significant role in both benign and malignant human diseases including PC progression and metastasis. However, the initiation of MUC expression during PC remains unknown because of lack of early stage tumor tissues from PC patients. Methods In the present study, we have evaluated stage specific expression patterns of mucins during mouse PC progression in (KrasG12D;Pdx1-Cre (KC)) murine PC model from pancreatic intraepithelial neoplasia (PanIN) to pancreatic ductal adenocarcinoma (PDAC) by immunohistochemistry and quantitative real-time PCR. Results In agreement with previous studies on human PC, we observed a progressive increase in the expression of mucins particularly Muc1, Muc4 and Muc5AC in the pancreas of KC (as early as PanIN I) mice with advancement of PanIN lesions and PDAC both at mRNA and protein levels. Additionally, mucin expression correlated with the increased expression of inflammatory cytokines IFN-γ (p CXCL1 (p CXCL2 (p Conclusions Our study reinforces the potential utility of the KC murine model for determining the functional role of mucins in PC pathogenesis by crossing KC mice with corresponding mucin knockout mice and evaluating mucin based diagnostic and therapeutic approaches for lethal PC.

Published
2012
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50. 14-3-3 zeta is a molecular target in guggulsterone induced apoptosis in Head and Neck cancer cells

Author

Siu KW Michael, Chauhan SS, Matta Ajay, Macha Muzafar A, and Ralhan Ranju

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background The five-year survival rates for head and neck squamous cell carcinoma (HNSCC) patients are less than 50%, and the prognosis has not improved, despite advancements in standard multi-modality therapies. Hence major emphasis is being laid on identification of novel molecular targets and development of multi-targeted therapies. 14-3-3 zeta, a multifunctional phospho-serine/phospho-threonine binding protein, is emerging as an effector of pro-survival signaling by binding to several proteins involved in apoptosis (Bad, FKHRL1 and ASK1) and may serve as an appropriate target for head and neck cancer therapy. Herein, we determined effect of guggulsterone (GS), a farnesoid X receptor antagonist, on 14-3-3 zeta associated molecular pathways for abrogation of apoptosis in head and neck cancer cells. Methods Head and neck cancer cells were treated with guggulsterone (GS). Effect of GS-treatment was evaluated using cell viability (MTT) assay and apoptosis was verified by annexin V, DNA fragmentation and M30 CytoDeath antibody assay. Mechanism of GS-induced apoptosis was determined by western blotting and co-IP assays using specific antibodies. Results Using in vitro models of head and neck cancer, we showed 14-3-3 zeta as a key player regulating apoptosis in GS treated SCC4 cells. Treatment with GS releases BAD from the inhibitory action of 14-3-3 zeta in proliferating HNSCC cells by activating protein phosphatase 2A (PP2A). These events initiate the intrinsic mitochondrial pathway of apoptosis, as revealed by increased levels of cytochrome c in cytoplasmic extracts of GS-treated SCC4 cells. In addition, GS treatment significantly reduced the expression of anti-apoptotic proteins, Bcl-2, xIAP, Mcl1, survivin, cyclin D1 and c-myc, thus committing cells to apoptosis. These events were followed by activation of caspase 9, caspase 8 and caspase 3 leading to cleavage of its downstream target, poly-ADP-ribose phosphate (PARP). Conclusion GS targets 14-3-3 zeta associated cellular pathways for reducing proliferation and inducing apoptosis in head and neck cancer cells, warranting its investigation for use in treatment of head and neck cancer.

Published
2010
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