Prostatic Adenocarcinoma Carcinogenesis and Growth

Moon, Timothy D.; Sloane, Bruce B.

doi:10.1111/j.1532-5415.1989.tb01570.x

Cited by 7 publications

(5 citation statements)

References 97 publications

(99 reference statements)

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“…When estrogen was given concurrently, the tumors developed more rapidly. Finally, in a study in which a group of rats were initially castrated and then treated with 9,10,dimethyl‐1,2 benzanthracene, all the animal subjects developed prostate cancer 3 . These findings suggest a permissive or co‐carcinogen role for androgens but not one of a true carcinogen.…”

Section: Etiologymentioning

confidence: 96%

“…Hormonal Factors While the responsiveness of adenocarcinoma of the prostate to withdrawal of androgens is well known, the role of sex steroids in the disease's carcinogenesis is less clear. In a study of aging male virgin rats, 70% were found to have microscopic foci of prostate cancer 3 . In another study, administration of testosterone to rats markedly increased the incidence of prostatic tumors.…”

Section: Etiologymentioning

confidence: 98%

“…Genetics A family history of prostate cancer increases the risk for other male members of the family. A four‐fold increase in risk has been noted for brothers of patients who had their cancer diagnosed prior to age 65 3 . Chromosomal studies have found abnormalities on chromosome numbers 1, 7, and 10.…”

Section: Etiologymentioning

confidence: 99%

“…Infection Investigators have also studied the possibility that venereal disease and prostatitis may be causative factors for prostate cancer 3 . Herpes simplex II, cytomegalovirus, and reverse transcriptase NC‐type viral particles have been identified from surgical specimens.…”

Section: Etiologymentioning

confidence: 99%

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Prostate Cancer

Moon¹

1992

J American Geriatrics Society

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Clinically, prostate cancer (prostatic adenocarcinoma) is now the most frequently diagnosed cancer in males and the second leading cause of mortality due to cancer in the United States. However, because 75% of histologic prostate cancers remain functionally benign (will not metastasize and kill the patient), mass screening of the male population for the disease has become a hotly debated issue among urologists. The real challenge in the upcoming decade for geriatricians, though, will be to diagnose earlier in their course the prostate cancers which, if not treated, will metastasize and kill the patient and thus allow this subgroup of patients the opportunity to be treated more effectively. This review briefly discusses the etiology of prostate cancer, ways the disease may present, current treatments, depending on disease stage, screening in the diagnosis of prostate cancer, and quality of life issues important to patients confronted with the disease.

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Section: Etiologymentioning

confidence: 96%

Section: Etiologymentioning

confidence: 98%

Section: Etiologymentioning

confidence: 99%

Section: Etiologymentioning

confidence: 99%

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Prostate Cancer

Moon¹

1992

J American Geriatrics Society

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“…26,27 Finasteride, which is used for the treatment of benign prostatic hyperplasia (BPH), inhibits 5␣-reductase, an enzyme that converts testosterone to 5␣-dihydrotestosterone (DHT), the key intraprostatic androgen that promotes prostate cell and organ growth. 26,[28][29][30] Finasteride significantly reduces prostate volume in men with BPH, and it has been approved by the US Food and Drug Administration for treatment of BPH. 31,32 Currently, two trials, described in more detail below, are investigating the chemopreventive potential of tamoxifen and finasteride.…”

Section: Therapeutic Leadsmentioning

confidence: 99%

Chemoprevention

Greenwald

Kelloff

Burch-Whitman

et al. 1995

CA: A Cancer Journal for Clinicians

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The potential for hormonal prevention trials

Ford

Brawley

Perlman

et al. 1994

Cancer

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Breast and prostate cancer are significant causes of morbidity and mortality and are very similar in etiology, epidemiology, and modalities of treatment. Investigational strategies in the prevention of these malignancies also have strong parallels. The National Cancer Institute is sponsoring several large scale clinical trials involving hormonal manipulation and cancer prevention. In the Breast Cancer Prevention Trial, 16,000 women at high risk for breast cancer are being randomized to receive the antiestrogen agent tamoxifen or placebo for 5 years in an effort to determine if breast cancer development can be inhibited. In a similar trial, the Prostate Cancer Prevention Trial, 18,000 men older than 55 years of age will be randomized to receive finasteride, a 5‐alpha‐reductase inhibitor, or placebo to determine if inhibition of dihydrotestosterone synthesis in the prostate over a prolonged period will lead to a decreased incidence of prostate cancer. Both clinical trials offer the possibility of demonstrating that a hormonal intervention can decrease an individual's risk of developing breast or prostate cancer. They also have the potential of providing critical information about cancer risk, etiology, screening, and genetics, as well as quantifying the risks and benefits of specific preventive interventions.

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Prostatic Adenocarcinoma Carcinogenesis and Growth

Cited by 7 publications

References 97 publications

Prostate Cancer

Prostate Cancer

Chemoprevention

The potential for hormonal prevention trials

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