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DNA Damage Responses in Tumors Are Not Proliferative Stimuli, but Rather They Are DNA Repair Actions Requiring Supportive Medical Care

Zsuzsanna Suba

Published 2024 in Cancers

ABSTRACT

Simple Summary This work challenges the traditional principles of cancer therapy: simply targeting and blocking the regulatory pathways of rapidly proliferating tumors is a serious mistake. Since tumor initiation and growth may be attributed to a patient’s genomic instability and damage, genotoxic medications are inappropriate as they cause additional genomic damage in both patients and their cancers. Tumor cells are not enemies to be killed, but rather they are ill human cells which have the remnants of same genome stabilizer pathways like healthy cells. Within tumors, there is a combat for the improvement of their genomic defects. Moreover, tumors ask for help in their kamikaze action by recruiting immune competent cells into their environment. We should learn by watching the genome repairing activities within tumors, in the peritumoral region and in the whole body, and may follow them with supportive care. Successful cancer therapy does not remain a dream to be realized in the far future, but we should set about a cancer cure without delay. Abstract Background: In tumors, somatic mutagenesis presumably drives the DNA damage response (DDR) via altered regulatory pathways, increasing genomic instability and proliferative activity. These considerations led to the standard therapeutic strategy against cancer: the disruption of mutation-activated DNA repair pathways of tumors.Purpose: Justifying that cancer cells are not enemies to be killed, but rather that they are ill human cells which have the remnants of physiologic regulatory pathways. Results: 1. Genomic instability and cancer development may be originated from a flaw in estrogen signaling rather than excessive estrogen signaling; 2. Healthy cells with genomic instability exhibit somatic mutations, helping DNA restitution; 3. Somatic mutations in tumor cells aim for the restoration of DNA damage, rather than further genomic derangement; 4. In tumors, estrogen signaling drives the pathways of DNA stabilization, leading to apoptotic death; 5. In peritumoral cellular infiltration, the genomic damage of the tumor induces inflammatory cytokine secretion and increased estrogen synthesis. In the inflammatory cells, an increased growth factor receptor (GFR) signaling confers the unliganded activation of estrogen receptors (ERs); 6. In breast cancer cells responsive to genotoxic therapy, constitutive mutations help the upregulation of estrogen signaling and consequential apoptosis. In breast tumors non-responsive to genotoxic therapy, the possibilities for ER activation via either liganded or unliganded pathways are exhausted, leading to farther genomic instability and unrestrained proliferation. Conclusions: Understanding the real character and behavior of human tumors at the molecular level suggests that we should learn the genome repairing methods of tumors and follow them by supportive therapy, rather than provoking additional genomic damages.

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