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Titolo:
A new trend of breast cancer research in the genome era (Review)
Autore:
Kodama, M; Kodama, T;
Indirizzi:
Kodama Res Inst Prevent Med, Chikusa Ku, Nagoya, Aichi 4640005, Japan Kodama Res Inst Prevent Med Nagoya Aichi Japan 4640005 chi 4640005, Japan
Titolo Testata:
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
fascicolo: 3, volume: 8, anno: 2001,
pagine: 291 - 302
SICI:
1107-3756(200109)8:3<291:ANTOBC>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
TERM TISSUE-CULTURE; ESTROGEN WINDOW HYPOTHESIS; 2-STEP PHENOMENON; PROSTATE-CANCER; RISK; GENESIS; JAPAN; CARCINOGENESIS; AGE; DEHYDROEPIANDROSTERONE;
Keywords:
etiology of breast cancer; genome analysis system; multisteroidal-versus monosteroidal-carcinogenesis hypotheses; dualism of tamoxifen action; dualism of breast cancer; ovulation failure; Cushing syndrome; relative infertility; central obesity;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
65
Recensione:
Indirizzi per estratti:
Indirizzo: Kodama, M Kodama Res Inst Prevent Med, Chikusa Ku, 50-5 Chiyogaoka, Nagoya, Aichi 4640005, Japan Kodama Res Inst Prevent Med 50-5 Chiyogaoka Nagoya Aichi Japan 4640005
Citazione:
M. Kodama e T. Kodama, "A new trend of breast cancer research in the genome era (Review)", INT J MOL M, 8(3), 2001, pp. 291-302

Abstract

The decipherment of the human genome, as accomplished recently in USA and in Europe, now enables us to search for the cause of a disease at the levels of the whole spectrum of gene expressions (mRNAs) of the human genome. A set of investigations came to the world in AD 2000 to show that: a) A totalof 50 genes of the estrogen receptor positive (ER+) human breast cancer cell line MCF-7 in their gene expressions were found to undergo stimulation from a physiological concentration of 17 beta -estradiol. b) Comparison of estrogen-responsiveness among a number of estrogen-responsive genes, among cancer cell lines of both the breast and endometrium with and without activeER, and among cell lines of normal tissues revealed that association between the presence of active ER and estrogen-responsive genes is quantitative rather than qualitative including some exceptions, and that none of the estrogen-responsive genes tested was classified as of breast cancer specific. For this review, we collected information from our and other laboratories to investigate problems that remain to be disputed. Five items of discussionare given as follows: a) The dose of a steroid used for the production of an experimental tumor was fixed not to a physiological concentration but toa pharmacological concentration. In the case of estradiol, the latter was higher than the former by over 3 orders. The mitotic activity of MCF-7 underwent stimulation from the former but distinct suppression from the latter.b) A massive dose of a single steroid, when given at a good time of the host age, could produce a tumor of any kind. The timing of treatment rather than the nature of a steroid was found critical. c) Experience with the morphological development of Drosophila suggests the possibility that deficiency rather than amplification of gene expression in the infant age of Drosophila is responsible for the induction of morphological changes in an adult fly. Likewise, deficiencies of some escort steroids rather than overflow of estradiol may have more chance of occurrence in the genesis of spontaneous breast cancer, as suggested by many researchers including us. The plasma concentration of estradiol was found to be normal in patients with cancers ofboth the breast and endometrium. Future studies of breast cancer as well as other cancers should be directed to the multisteroidal carcinogenesis hypothesis rather than the monosteroidal carcinogenesis hypothesis. d) The necessity of recruiting an appropriate case-control data set and the difficulty of data interpretation were emphasized in the search for good biomarkers of breast cancer. e) Case-control studies of tamoxifen use was found usefulfor the prevention and clinical control of breast cancer of non-hereditarytype but not for the breast cancer of hereditary type. Both decreased riskof breast cancer and increased risk of endometrial cancer were detected inthe same population of tamoxifen use. The observed dualism of both human breast cancer and tamoxifen action can be taken as evidence to support the multi-steroidal carcinogenesis hypothesis rather than the mono-steroidal carcinogenesis hypothesis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 14/07/20 alle ore 13:01:28