Affiliations 

  • 1 Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research-Guwahati, Sila Katamur, Halugurisuk P.O-Changsari, Kamrup, Assam, India-781101
  • 2 Institute of Pharmaceutical Research, GLA University, Mathura, U.P., India
  • 3 Deccan School of Pharmacy, Hyderabad, India
  • 4 Department of Pharmacology and Toxicology, College of Pharmacy, Umm Al-Qura University, Makkah, Saudi Arabia
  • 5 Pharmacology Unit, Jeffrey Cheah School of Medicine and Health Sciences, MONASH University, Malaysia
  • 6 Nirma University, Institute of Pharmacy, Ahmedabad, Gujarat 382481, India; School of Pharmacy, Suresh Gyan Vihar University, Mahal Road, Jagatpura 302017, Jaipur, India
  • 7 School of Pharmacy, Suresh Gyan Vihar University, Mahal Road, Jagatpura 302017, Jaipur, India; Department of Pharmacology, Saveetha Dental College, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai, India; Uttaranchal Institute of Pharmaceutical Sciences, Uttaranchal University, Dehradun, India
PMID: 37522565 DOI: 10.1615/JEnvironPatholToxicolOncol.2023045403

Abstract

According to the World Health Organization (WHO), cancer is the second-highest cause of mortality worldwide, killing nearly 9.6 million people annually. Despite the advances in diagnosis and treatment during the last couple of decades, it remains a serious concern due to the limitations of currently available cancer management strategies. Therefore, alternative strategies are highly required to overcome these glitches. In addition, many etiological factors such as environmental and genetic factors initiate the activation of the Janus kinase (JAK)-signal transducer and activator of the transcription (STAT) pathway. This aberrant activation of the JAK-STAT pathway has been reported in various disease states, including inflammatory conditions, hematologic malignancies, and cancer. For instance, many patients with myeloproliferative neoplasms carry the acquired gain-of-function JAK2 V617F somatic mutation. This knowledge has dramatically improved our understanding of pathogenesis and has facilitated the development of therapeutics capable of suppressing the constitutive activation of the JAK-STAT pathway. Our aim is not to be expansive but to highlight emerging ideas towards preventive therapy in a modern view of JAK-STAT inhibitors. A series of agents with different specificities against different members of the JAK family of proteins is currently undergoing evaluation in clinical trials. Here we give a summary of how JAK-STAT inhibitors function and a detailed review of current clinical drugs for managing cancer as a new therapeutic approach.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.