What is it about?
Genomic instability and cancer development may be originated from the flaw of estrogen signal rather than excessive estrogen signaling. Sensing the DNA damage, tumor cells use their genomic plasticity, helping their own DNA repair and apoptotic death via somatic mutations. Estrogen regulated genes stimulate the anticancer activity of immune competent cells, while motivate apoptotic death in tumor cells in a Janus faced manner.
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Why is it important?
Till now, somatic mutagenesis in tumors was regarded as inducer of cancer driver genes increasing genomic instability and proliferative activity. These considerations led to the standard therapeutic strategy: the disruption of mutation activated DNA repair pathways of tumors. Somatic mutations in tumor cells aim the improvement of DNA damage rather than further genomic derangement. In tumor cells responsive to genotoxic therapy, constitutive mutations help the upregulation of estrogen signal and consequential apoptosis in a Janus faced manner.
Perspectives
The standard therapeutic strategy is the disruption of mutation activated DNA repair pathways of tumors instead of supportive medical care. Understanding the real character and behavior of human tumors at molecular level suggests that we should learn the genome repairing methods of tumors and follow them by supportive medical care rather than provoking additional genomic damages. This work reveals that successful cancer therapy does not remain a dream postponed to the far future but rather we should start boldly on supportive cancer cure without delay.
professor Zsuzsanna Suba
National Institute of Oncology Budapest
Read the Original
This page is a summary of: DNA Damage Responses in Tumors Are Not Proliferative Stimuli but Rather They Are DNA Repair Actions Requiring Supportive Medical Care, March 2024, MDPI AG,
DOI: 10.20944/preprints202403.0456.v1.
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