Bidirectional crosstalk between estrogen signaling pathways and DNA repair machinery

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Citation (Scopus)

Abstract

Until now, the fight against cancer has included the use of various cytotoxic compounds and therapeutic irradiation aiming to inhibit the uncontrolled cell proliferation and to kill rapidly growing malignancies. These inadequate treatment measures are not capable of differentiation between malignant cells and physiologic structures. The therapeutic results are serious toxic effects even in healthy tissues with either rapid or moderate proliferative activity, while the tumor suppressing capacity is usually transient and unpredictable. The continuous pharmaceutical development of cytotoxic anticancer agents and the advances in radiotherapy techniques could not achieve appropriate results in the improvement of cancer-related mortality. Malignant tumor cells are integrative parts of the whole body; they are not “wicked” enemies, but rather human cells embarrassed by the partial or near total loss of the highest intranuclear control machinery, which safeguarded their somatic and reproductive functions. There is a wide range of malignant tumors from highly differentiated to completely undifferentiated phenotypes. Consequently, the higher the differentiation of a malignancy, the stronger is the partial preservation, or even defensive overexpression of certain DNA repairing activities in tumor cells. The revelation of various DNA damages and biochemical disturbances in tumor cells suggests that the repair of DNA damage and genomic stabilization would be the key to cancer treatment instead of the aggressive destruction of tumors. Genome stabilizer natural compounds are capable of distinction between tumor cells and defensive cellular reactions in the microenvironment of tumors. Recovery of the same intranuclear repair machinery leads to dichotomous pathways, causing apoptotic death for tumor cells whilst strengthening functional activity and beneficial mediator synthesis of defensive healthy cells.

Original languageEnglish
Title of host publicationAdvances in Carcinogenesis Research
PublisherNova Science Publishers, Inc.
Pages1-28
Number of pages28
ISBN (Electronic)9781536104455
ISBN (Print)9781634858496
Publication statusPublished - Jan 1 2016

Fingerprint

DNA Repair
Estrogens
Neoplasms
DNA Damage
Tumor Microenvironment
Poisons
Cytotoxins
Therapeutics
Human Body
Antineoplastic Agents
Cell Death
Radiotherapy
Cell Proliferation
Genome
Phenotype

Keywords

  • Antiestrogen use
  • Cancer prevention
  • Estrogen signaling
  • Genome stabilization
  • Hormonal equilibrium

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Suba, Z. (2016). Bidirectional crosstalk between estrogen signaling pathways and DNA repair machinery. In Advances in Carcinogenesis Research (pp. 1-28). Nova Science Publishers, Inc..

Bidirectional crosstalk between estrogen signaling pathways and DNA repair machinery. / Suba, Z.

Advances in Carcinogenesis Research. Nova Science Publishers, Inc., 2016. p. 1-28.

Research output: Chapter in Book/Report/Conference proceedingChapter

Suba, Z 2016, Bidirectional crosstalk between estrogen signaling pathways and DNA repair machinery. in Advances in Carcinogenesis Research. Nova Science Publishers, Inc., pp. 1-28.
Suba Z. Bidirectional crosstalk between estrogen signaling pathways and DNA repair machinery. In Advances in Carcinogenesis Research. Nova Science Publishers, Inc. 2016. p. 1-28
Suba, Z. / Bidirectional crosstalk between estrogen signaling pathways and DNA repair machinery. Advances in Carcinogenesis Research. Nova Science Publishers, Inc., 2016. pp. 1-28
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