Role of Endocrine-Genotoxic Switchings in Cancer and Other Human Diseases:

Berstein, Lev M.

doi:10.1007/978-0-387-78818-0_3

Cited by 7 publications

(3 citation statements)

References 84 publications

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“…The latter may involve not only estrogens but also peptide factors, for example, activated IGF-1 system. The condition observed upon 'transfer' from the wild-type to a mutant BRCA1 may be designated as endocrine genotoxic liberation (Figure 2), which makes it possible to regard BRCA1 as another modulator of endocrine-genotoxic switchings (EGS) described by this author elsewhere [89,90,91].…”

Section: Summary: Reality Hypotheses and Future Perspectivesmentioning

confidence: 98%

Endocrinology of the Wild and Mutant Brca1 Gene and Types of Hormonal Carcinogenesis

Berstein

2008

Future Oncol.

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Information related to the BRCA1 gene has increasingly become a subject for analysis by endocrinologists. For example, it is hard to dismiss the fact that, in BRCA1 mutation carriers, tumors develop predominantly in such estrogen-dependent organs as the mammary glands and ovaries but not in the endometrium. Another characteristic feature is that although BRCA1 mutants and knock-downs are unable to inhibit the transcriptional activity of estrogen receptor-alpha, in BRCA1 mutation carriers breast cancers are often estrogen receptor-negative and originate from the basal rather than the luminal epithelium. The latter, together with other data, suggests that BRCA1-positive breast neoplasms could be considered to be a consequence of the genotoxic variant of hormonal carcinogenesis (that is, associated with DNA damaging rather then with pure hormonal/physiological properties of hormones or their derivatives). Of indisputable significance are the data demonstrating that knocking down of the BRCA1 gene is accompanied by aromatase overexpression and the abolishment of IGF-1 receptor expression suppression, thus increasing both steroid and insulin signaling. Importantly, the endocrine-genotoxic 'liberation' found upon transfer from the wild-type to the mutant BRCA1 provides grounds to regard BRCA1 as a modulator of endocrine-genotoxic switching (predominantly into a direction of DNA-damaging hormone effects) and also to ask whether this is a property of only this or some other tumor suppressor's.

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Section: Summary: Reality Hypotheses and Future Perspectivesmentioning

confidence: 98%

Endocrinology of the Wild and Mutant Brca1 Gene and Types of Hormonal Carcinogenesis

Berstein

2008

Future Oncol.

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“…После связывания лиганда мембранный рецептор активирует различные сигнальные пути, индуцируя нижестоящие факторы транскрипции [39]. Механизм эстроген-индуцированного канцерогенеза и факторы, усиливающие генотоксический компонент в общем действии эстрогенов, в том числе в случае возрастной патологии [40], очень важны, поскольку могут влиять на тип канцерогенеза и свойства развивающихся гормонозависимых опухолей [41].…”

Section: Lyn и Erα как мишени терапии и причина резистентности к нейunclassified

LYN kinase and estrogen receptor ERα: involvement in carcinogenesis and potential therapeutic target for tumors

2021

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Primary or secondary resistance is an important problem when treating any type of tumor. It is often associated with changes in target genes’ functioning. This raises the question of understanding functional intracellular interactions of genes and proteins in oncological processes and therapeutic resistance occurring. When searching target proteins of targeted therapy, it is necessary to identify biomolecules, participating in cell signaling life, which differ significantly in normal and oncological processes and interact with a large number of pathways. It is also important that these biomolecules are not an artifact of tumor therapy or cell line cultivation, and that it is possible to influence them directly, obtaining complex effect. In addition, it is important to study changes occurring during therapy with the biomolecules, which include proto-oncogene of SRC family kinase LYN and gene of the estrogen receptor α ESR1. All these factors may help to overcome the emerging resistance.Objective – to study the way genes of SRC kinase LYN and estrogen receptor α ESR1 influence oncological processes and occurrence of therapeutic resistance.

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“…In systematic experimental and clinical studies we were able to show that processes resulting in responses to tamoxifen as an agonist and the development of estrogen hypersensitivity of breast cancer cells could potentially be mechanistically linked and involve activation of MAPK signaling and the aromatase system [3]. As to science sensu stricto, my interests were focused (and I believe resulted in the most significant advances) on endocrine-genotoxic switching as a factor that increases the risk of tumor development through the predominant usage of a genotoxic type of hormonal carcinogenesis [4], on the association of different types of macrosomia (including newborn macrosomy) with cancer risk [5,6], on the heterogeneity of obesity and diabetes as a factor that at times may modify predisposition to cancer in an opposing way [7,8], and on the controversial role of antidiabetic biguanides as potential and, in a sense, selective means for cancer prevention and treatment [9,10]. The differences between these duties are significant.…”

Section: Interviewmentioning

confidence: 99%

Cancer Endocrinology Through own Experience: Areas for Further Thought and Development

Berstein¹

2013

Future Oncol.

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Lev Berstein speaks to Natasha Galukande, Assistant Commissioning Editor. Lev Berstein is Chief of Laboratory of Oncoendocrinology at the Petrov Research Institute of Oncology, St Petersburg, Russia. His main scientific interests include mechanisms of hormonal carcinogenesis, studying risk factors of hormone-associated tumors, and new approaches for prevention and treatment of the latter. As a clinician, he is involved in the management of cancer patients needing hormonal therapy or having endocrine pathology. Berstein has received several international distinctions (including an INTAS grant and UICC Translational Cancer Research Fellowship), serves as a Member of Council of the Russian Endocrine Association and is on the editorial boards of several international journals, including Future Oncology, was Guest Editor for a special focus issue of Expert Review of Endocrinology and Metabolism on hormones in breast and prostate cancer, and is a member of the European Association of Cancer Research and The Endocrine Society of the USA. His bibliography includes 11 monographs, 21 chapters and more than 200 papers in peer-reviewed journals. He graduated as a MD from Tartu University in Estonia and completed his PhD and Doctor of Medical Sciences degrees in cancer endocrinology at the NN Petrov Institute in St Petersburg (Russia).

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Role of Endocrine-Genotoxic Switchings in Cancer and Other Human Diseases:

Cited by 7 publications

References 84 publications

Endocrinology of the Wild and Mutant Brca1 Gene and Types of Hormonal Carcinogenesis

Endocrinology of the Wild and Mutant Brca1 Gene and Types of Hormonal Carcinogenesis

LYN kinase and estrogen receptor ERα: involvement in carcinogenesis and potential therapeutic target for tumors

Cancer Endocrinology Through own Experience: Areas for Further Thought and Development

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