Copyright © 2026 Authors retain the copyright of this article. This article is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
@article{191613,
author = {Pari Trivedi and Dr. Fariya Khan and Dr. Ashish Ranjan Singh},
title = {Revolutionizing Cancer Research: The Role of AI in Cancer},
journal = {International Journal of Innovative Research in Technology},
year = {2026},
volume = {12},
number = {8},
pages = {7164-7171},
issn = {2349-6002},
url = {https://ijirt.org/article?manuscript=191613},
abstract = {The phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signalling pathway plays a central role in cancer initiation and progression. This pathway regulates essential cellular processes such as cell growth, proliferation, survival, metabolism, angiogenesis, and immune evasion. Aberrant activation of the PI3K/Akt/mTOR pathway leads to uncontrolled cell division, enhanced invasion and metastasis, metabolic reprogramming of cancer cells, and resistance to both chemotherapy and immunotherapy, making it a critical target in oncology research.
Overactivation of this pathway is primarily driven by genetic mutations and post-translational modifications. Common molecular alterations include activating mutations in the PIK3CA gene, loss or inactivation of the tumour suppressor PTEN, amplification or hyperactivation of receptor tyrosine kinases such as EGFR and HER2, and gain-of-function mutations in AKT1, AKT2, and AKT3. These changes collectively promote persistent downstream signalling, enabling tumour cells to evade apoptosis and sustain malignant behaviour. For example, PIK3CA mutations observed in triple-negative breast cancer significantly reduce programmed cell death and contribute to resistance against standard chemotherapeutic agents.
In addition to genetic factors, microRNAs (miRNAs) act as crucial epigenetic regulators of the PI3K/Akt/mTOR pathway by modulating gene expression at the post-transcriptional level. Advances in multiomics approaches, including genomics, transcriptomics, and proteomics, combined with histopathological analysis, have enhanced the understanding of pathway dysregulation. Integrating federated and equitable data-sharing models may further support precision oncology strategies aimed at mitigating cancer progression and improving therapeutic outcomes.},
keywords = {Multiomics, equitable, mitigating, federated, histopathological analysis, oncology.},
month = {January},
}
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