Unregistered
01-18-2006, 04:02 PM
I was searching "CDKN1A Cyclin d Breast cancer" and this came up a a result.
[CDKN1A was upregulated by an average ratio of 3.2 in rats fed a high DHA v high omega six diet for four months.
I was trying to find how CDKN1A fits in with cyclin D (if at all). Can anybody help.]
The idea that protection can be afforded by administration of oestrogen and prgesterone to stimulate pregnancy is thought provoking indeed.
RB
QUOTE from below
"Because the effect of parity (hormones) is so dramatic and strong in both humans and rodents, it offers an approach to breast cancer prevention that is rational and attainable at the social, sexual, political, and scientific levels. "
http://clincancerres.aacrjournals.org/cgi/content/full/10/1/380S
ABSTRACT
Introduction
Conclusions
Open Discussion
REFERENCES
It has been firmly established in epidemiological studies that early full-term pregnancy affords lifetime protection against the development of breast cancer. This phenomenon can be mimicked in rat and mouse models of mammary cancer in which the hormones estrogen and progesterone are given for 21 days. Carcinogen-induced proliferation is blocked as a consequence of hormone pretreatment. Among several genes implicated by molecular studies to be differentially expressed is the tumor suppressor gene p53. Both immunohistochemical and Western blot studies indicate that p53 protein expression is increased in hormone-pretreated mice and rats. The p53-regulated gene p21Cip1 is also increased concomitantly with p53. To test directly the causative role of p53 in conferring a protective phenotype, we examined the hormone-induced protective effect in BALB/c p53 null mammary epithelium. In the mammary epithelium, the absence of p53 gene expression abrogated the protective effect of prior pregnancy. The tumor incidence curves were superimposable in p53 null mammary epithelium that were treated with 7,12-dimethylbenzanthracene or pregnancy plus 7,12-dimethylbenzanthracene. These results demonstrate that p53 plays a pivotal role in hormone-induced protection and raises the question of the mechanisms by which the steroid hormones, estrogen and progesterone, functionally activate p53.......
Conclusions
Top
ABSTRACT
Introduction
Conclusions
Open Discussion
REFERENCES
The parous mammary gland and the virgin mammary gland represent distinct developmental states of the gland, and information on the signal transduction pathways operative in these different developmental states is scarce. Whereas we know that estrogens and progestins are important in stimulating proliferation and differentiation, the specific receptor subpopulations, secondary messengers, effector loops, and growth factor responses operative in the two mammary cell populations are relatively unknown. It is impossible to effectively interpret the mechanisms underlying the refractory state without understanding the basic biological processes involved in regulation of cell growth and differentiation.
Recent experiments demonstrate the important role of the p53 tumor suppressor gene in the hormone-induced protection. Whereas the downstream effector proteins are partly known (i.e., p21Cip1), the mechanism by which hormones activate p53 function are unknown. Furthermore, it is likely the p53 pathway is only one of several pathways that are important for hormone-mediated protection. Gene expression profile experiments have demonstrated a consistent array of alterations in genes involving a number of growth factor pathways and gene transcription regulatory pathways in the parous mammary gland (8, 9, 10) .
Extensive data have shown the importance of parity as a significant preventive factor. The striking consistency of these data and the profound quantitative differences indicate the strongest need to understand the process at a molecular level. Because the effect of parity (hormones) is so dramatic and strong in both humans and rodents, it offers an approach to breast cancer prevention that is rational and attainable at the social, sexual, political, and scientific levels. The steady high incidence of human breast cancer is extensively documented and essentially unexplained. The economic, medical, and practical benefits of preventive approaches to solving and handling critical and widespread diseases are unarguable. Therefore, the ultimate goal of understanding the molecular mechanisms of hormone-induced protection has great potential for breast cancer prevention. If specific information can be generated on the mechanisms and protocols for hormonal prevention of breast cancer, it is possible that this information can be used to design a prevention protocol applicable for humans.
[CDKN1A was upregulated by an average ratio of 3.2 in rats fed a high DHA v high omega six diet for four months.
I was trying to find how CDKN1A fits in with cyclin D (if at all). Can anybody help.]
The idea that protection can be afforded by administration of oestrogen and prgesterone to stimulate pregnancy is thought provoking indeed.
RB
QUOTE from below
"Because the effect of parity (hormones) is so dramatic and strong in both humans and rodents, it offers an approach to breast cancer prevention that is rational and attainable at the social, sexual, political, and scientific levels. "
http://clincancerres.aacrjournals.org/cgi/content/full/10/1/380S
ABSTRACT
Introduction
Conclusions
Open Discussion
REFERENCES
It has been firmly established in epidemiological studies that early full-term pregnancy affords lifetime protection against the development of breast cancer. This phenomenon can be mimicked in rat and mouse models of mammary cancer in which the hormones estrogen and progesterone are given for 21 days. Carcinogen-induced proliferation is blocked as a consequence of hormone pretreatment. Among several genes implicated by molecular studies to be differentially expressed is the tumor suppressor gene p53. Both immunohistochemical and Western blot studies indicate that p53 protein expression is increased in hormone-pretreated mice and rats. The p53-regulated gene p21Cip1 is also increased concomitantly with p53. To test directly the causative role of p53 in conferring a protective phenotype, we examined the hormone-induced protective effect in BALB/c p53 null mammary epithelium. In the mammary epithelium, the absence of p53 gene expression abrogated the protective effect of prior pregnancy. The tumor incidence curves were superimposable in p53 null mammary epithelium that were treated with 7,12-dimethylbenzanthracene or pregnancy plus 7,12-dimethylbenzanthracene. These results demonstrate that p53 plays a pivotal role in hormone-induced protection and raises the question of the mechanisms by which the steroid hormones, estrogen and progesterone, functionally activate p53.......
Conclusions
Top
ABSTRACT
Introduction
Conclusions
Open Discussion
REFERENCES
The parous mammary gland and the virgin mammary gland represent distinct developmental states of the gland, and information on the signal transduction pathways operative in these different developmental states is scarce. Whereas we know that estrogens and progestins are important in stimulating proliferation and differentiation, the specific receptor subpopulations, secondary messengers, effector loops, and growth factor responses operative in the two mammary cell populations are relatively unknown. It is impossible to effectively interpret the mechanisms underlying the refractory state without understanding the basic biological processes involved in regulation of cell growth and differentiation.
Recent experiments demonstrate the important role of the p53 tumor suppressor gene in the hormone-induced protection. Whereas the downstream effector proteins are partly known (i.e., p21Cip1), the mechanism by which hormones activate p53 function are unknown. Furthermore, it is likely the p53 pathway is only one of several pathways that are important for hormone-mediated protection. Gene expression profile experiments have demonstrated a consistent array of alterations in genes involving a number of growth factor pathways and gene transcription regulatory pathways in the parous mammary gland (8, 9, 10) .
Extensive data have shown the importance of parity as a significant preventive factor. The striking consistency of these data and the profound quantitative differences indicate the strongest need to understand the process at a molecular level. Because the effect of parity (hormones) is so dramatic and strong in both humans and rodents, it offers an approach to breast cancer prevention that is rational and attainable at the social, sexual, political, and scientific levels. The steady high incidence of human breast cancer is extensively documented and essentially unexplained. The economic, medical, and practical benefits of preventive approaches to solving and handling critical and widespread diseases are unarguable. Therefore, the ultimate goal of understanding the molecular mechanisms of hormone-induced protection has great potential for breast cancer prevention. If specific information can be generated on the mechanisms and protocols for hormonal prevention of breast cancer, it is possible that this information can be used to design a prevention protocol applicable for humans.