Version 1
: Received: 23 October 2023 / Approved: 23 October 2023 / Online: 23 October 2023 (08:47:58 CEST)
Version 2
: Received: 13 November 2023 / Approved: 13 November 2023 / Online: 13 November 2023 (10:39:49 CET)
How to cite:
Zhang, Y. Cellular Response to an Act of Surviving Drives Tumor Evolution and Tumor Heterogeneity. Preprints2023, 2023101417. https://doi.org/10.20944/preprints202310.1417.v1
Zhang, Y. Cellular Response to an Act of Surviving Drives Tumor Evolution and Tumor Heterogeneity. Preprints 2023, 2023101417. https://doi.org/10.20944/preprints202310.1417.v1
Zhang, Y. Cellular Response to an Act of Surviving Drives Tumor Evolution and Tumor Heterogeneity. Preprints2023, 2023101417. https://doi.org/10.20944/preprints202310.1417.v1
APA Style
Zhang, Y. (2023). Cellular Response to an Act of Surviving Drives Tumor Evolution and Tumor Heterogeneity. Preprints. https://doi.org/10.20944/preprints202310.1417.v1
Chicago/Turabian Style
Zhang, Y. 2023 "Cellular Response to an Act of Surviving Drives Tumor Evolution and Tumor Heterogeneity" Preprints. https://doi.org/10.20944/preprints202310.1417.v1
Abstract
Tumor heterogeneity is a major obstacle to achieving consistent outcomes in cancer therapy. Here, we present a new perspective on tumor heterogeneity. The foundation for understanding tumor heterogeneity lies in recognizing that tumor evolution is a process driven by cells responding to survival challenges, and this cellular response precipitates the development of hallmark cancer capabilities. We posit that tumor heterogeneity arises from cells’ continued development of hallmark cancer capabilities, which ultimately leads to increased molecular chaos. Therapeutic inhibition of the essential genes driving the disease can disrupt tumor evolution, leading to cell death, a phenomenon termed oncogene addiction. Drawing from the same idea that cells respond to survival challenges, we introduce the notion that the increasing primitiveness of cancer during its progress stems from the cellular response to the continuous need for regeneration due to sustained cellular damage. To expand our concept of tumor heterogeneity, we further explore redefining key genes based on heterogeneity levels, and we propose a potential treatment strategy for advanced-stage cancers based on inducing aging-related deterioration. Taken together, the notions explored herein pave the way for novel cancer therapies and the betterment of human health.
Keywords
tumor heterogeneity; cancer progression; oncogene addiction; cancer stem cell
Subject
Biology and Life Sciences, Cell and Developmental Biology
Copyright:
This 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.
