International Journal of Cancer Therapeutics

Cancer versus anticancer factors: A review of these factors, health impacts, and awareness

Uttam Chowdhury, Shreya Chowdhury

Dr. Uttam Chowdhury, Ph.D., is a renowned researcher in the field of arsenics. He worked in the Department of Molecular and Cellular Biology at the University of Arizona, USA (2003-2010) as an Assistant Research Professor/Researcher/Co-PI with a renowned Toxicologist named Prof. H. Vas Aposhian. With a Ph.D. in Science from SOES (School of Environmental Science), Jadavpur University, India, under the supervision of Dr. Dipankar Chakraborti, one of the world-famous scientists on the field of arsenic research, Dr. Chowdhury has made significant contributions to the field of environmental science on arsenic research. His scholarly output includes over 90 research articles in peer-reviewed journals, book chapters, conference papers and abstracts, with publications in prestigious journals such as Nature. Uttam Chowdhury's enormous scientific merit is demonstrated through 6810 citations (25 publications cited more than 50 times and one publication cited more than 1320 times), 39931 reads, 3354 research interest score, and an h-index of 34 till today, January 31, 2024 (Source: ResearchGate and Google Scholar). One of his publications has been reported as entitled “Arsenic in Asia-Water at Its Worst” on the “Science Selections” in the EHP journal (May 2000, Volume 108, Number 5, Page A 224) by Karen Breslin. This topic was also selected and used as the cover page of this journal (EHP, May 2000, Volume 108, Number 5).

Imatinib Miracle Medicine; for the Treatment of Ph+ Chronic Myeloid Leukemia (CML)

Pranav Adithya Navath, Suryakiran Navath

Chronic Myeloid Leukemia poses a significant health threat, with the Ph+ subtype being particularly challenging to manage. The discovery of the BCR-ABL1 fusion gene as a driver mutation in Ph+ CML paved the way for targeted therapies. Imatinib, as a tyrosine kinase inhibitor, has shown remarkable efficacy in inhibiting the activity of the BCR-ABL1 protein, disrupting the signaling pathways responsible for the uncontrolled proliferation of myeloid cells.1-5Chronic Myeloid Leukemia (CML) poses a formidable challenge in the realm of hematological malignancies. Distinguished by the presence of the Philadelphia chromosome (Ph+), this subtype of leukemia is notorious for its relentless progression and resistance to conventional therapies. However, the emergence of imatinib, a tyrosine kinase inhibitor, has heralded a new era in the management of Ph+ CML, earning the accolade of a "miracle medicine."

The journey to this groundbreaking therapy begins with the unraveling of the molecular intricacies underlying CML. The identification of the BCR-ABL1 fusion gene as the driving force behind Ph+ CML opened the door to targeted interventions. Imatinib, with its ability to selectively inhibit the BCR-ABL1 tyrosine kinase, disrupts the aberrant signaling cascade responsible for the uncontrolled proliferation of myeloid cells.6-10This introduction sets the stage for a comprehensive exploration of imatinib's role as a transformative treatment for Ph+ CML. It delves into the mechanism of action, highlighting the specificity of imatinib in targeting the molecular aberrations driving CML progression. Furthermore, the introduction outlines the clinical landscape, summarizing key trials that substantiate imatinib's status as a "miracle medicine" by achieving unprecedented responses and reshaping the prognosis of Ph+ CML patients.11-15

Advances in the Treatment of Ph+ Chronic Myeloid Leukemia: A Comprehensive Study

Pranav Adithya Navath, Suryakiran Navath

Chronic Myeloid Leukemia is a hematological malignancy that arises from the abnormal proliferation of myeloid cells. The hallmark of CML is the presence of the Philadelphia chromosome, leading to the constitutively active BCR-ABL1 tyrosine kinase. The advent of targeted therapy, particularly tyrosine kinase inhibitors, has dramatically improved the prognosis and quality of life for patients with Ph+ CML.1-5Chronic Myeloid Leukemia (CML), a myeloproliferative disorder characterized by the presence of the Philadelphia chromosome (Ph+), has long stood as a formidable challenge in the realm of hematologic malignancies. The dawn of the molecular era brought about a paradigm shift in the understanding and management of CML, with the discovery of tyrosine kinase inhibitors (TKIs) heralding a new era of targeted therapy.6-9

Synthesis of 4-amino-N-(4-((3-nitroacridin-9-yl)amino) phenyl)butane-1- sulfonamide (Acridine): A Novel Tyrosine Kinase Inhibitor Targeting Oncogenic Pathways

Pranav Adithya Navath, Suryakiran Navath

The dysregulation of tyrosine kinase activity is a hallmark of various cancers, making tyrosine kinase inhibitors promising candidates for targeted cancer therapy. Acridine, designed with a nitroacridine scaffold, presents a novel pharmacophore for potential inhibition of tyrosine kinase pathways. This manuscript details the synthesis of Acridine, outlining the key steps and characterizing the compound's structural features.1-5The dysregulation of tyrosine kinase signaling pathways plays a pivotal role in the pathogenesis and progression of various cancers. Consequently, the development of small-molecule tyrosine kinase inhibitors has emerged as a promising strategy for targeted cancer therapy. In this context, the synthesis of Acridine, a novel compound featuring a 3-nitroacridin-9-yl moiety, is undertaken with the aim of designing a potent tyrosine kinase inhibitor that can selectively modulate oncogenic pathways.6,7

The dysregulation of tyrosine kinase activity is a hallmark of various cancers, making tyrosine kinase inhibitors promising candidates for targeted cancer therapy. Acridine, designed with a nitroacridine scaffold, presents a novel pharmacophore for potential inhibition of tyrosine kinase pathways. This manuscript details the synthesis of Acridine, outlining the key steps and characterizing the compound's structural features.1-5The dysregulation of tyrosine kinase signaling pathways plays a pivotal role in the pathogenesis and progression of various cancers. Consequently, the development of small-molecule tyrosine kinase inhibitors has emerged as a promising strategy for targeted cancer therapy. In this context, the synthesis of Acridine, a novel compound featuring a 3-nitroacridin-9-yl moiety, is undertaken with the aim of designing a potent tyrosine kinase inhibitor that can selectively modulate oncogenic pathways.6,7

Synthesis and structural evaluation of (5-(6-(Furan-2-ylmethylamino)-9H-purin-9- yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl Dihydrogen Phosphate as a Redox Drug Discovery Targeting Human Skin Cancer 

Pranav Adithya Navath, Suryakiran Navath

Human skin cancer remains a significant health concern, necessitating the exploration of novel therapeutic agents. In this study, we report the synthesis of (5-(6-(Furan-2-ylmethylamino)-9H-purin-9-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl Dihydrogen Phosphate, a purine derivative designed as a redox drug for targeting skin cancer cells. Skin cancer is a prevalent and often debilitating disease that poses a significant public health challenge worldwide. The increasing incidence of skin cancer, coupled with limited effective therapeutic options, underscores the urgent need for the development of novel and targeted treatments. In recent years, redox-active compounds have gained attention as promising candidates for anticancer drug discovery due to their ability to modulate cellular redox processes and induce selective cytotoxicity in cancer cells.1-5