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Titolo:
Dietary 4-HPR suppresses the development of bone metastasis in vivo in a mouse model of prostate cancer progression
Autore:
Shaker, MR; Yang, G; Timme, TL; Park, SH; Kadmon, D; Ren, CZ; Ji, XR; Lee, HM; Sehgal, I; Anzano, M; Sporn, MB; Thompson, TC;
Indirizzi:
Baylor Coll Med, Scott Dept Urol, Houston, TX 77030 USA Baylor Coll Med Houston TX USA 77030 ott Dept Urol, Houston, TX 77030 USA Baylor Coll Med, Dept Cell Biol, Houston, TX 77030 USA Baylor Coll Med Houston TX USA 77030 ept Cell Biol, Houston, TX 77030 USA Baylor Coll Med, Dept Radiotherapy, Houston, TX 77030 USA Baylor Coll MedHouston TX USA 77030 Radiotherapy, Houston, TX 77030 USA NCI, Lab Cell Regulat & Carcinogenesis, Bethesda, MD 20892 USA NCI Bethesda MD USA 20892 egulat & Carcinogenesis, Bethesda, MD 20892 USA Dartmouth Coll, Hitchcock Med Ctr, Dartmouth Med Sch, Dept Pharmacol, Hanover, NH 03756 USA Dartmouth Coll Hanover NH USA 03756 Dept Pharmacol, Hanover, NH 03756 USA Vet Affairs Med Ctr, Houston, TX 77030 USA Vet Affairs Med Ctr Houston TXUSA 77030 s Med Ctr, Houston, TX 77030 USA
Titolo Testata:
CLINICAL & EXPERIMENTAL METASTASIS
fascicolo: 5, volume: 18, anno: 2001,
pagine: 429 - 438
SICI:
0262-0898(2001)18:5<429:D4STDO>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
LOBUND-WISTAR RATS; CARCINOGENESIS; PREVENTION; SYSTEM; ACID;
Keywords:
bone metastasis; chemoprevention; prostate cancer; retinoids;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
22
Recensione:
Indirizzi per estratti:
Indirizzo: Thompson, TC Baylor Coll Med, Scott Dept Urol, 6560 Fannin,Suite 2100, Houston, TX 77030 USA Baylor Coll Med 6560 Fannin,Suite 2100 Houston TX USA 77030 A
Citazione:
M.R. Shaker et al., "Dietary 4-HPR suppresses the development of bone metastasis in vivo in a mouse model of prostate cancer progression", CLIN EXP M, 18(5), 2001, pp. 429-438

Abstract

The effects of the synthetic retinoid N-(4-hydroxyphenyl) retinamide (4-HPR) on prostate cancer metastasis in vivo were evaluated in the mouse prostate reconstitution (MPR) model. MPRs were produced by infection of either heterozygous (+/-) or nullizygous (-/-) p53-mutant fetal prostatic epithelialcells with the recombinant retrovirus Zipras/myc 9. Previous studies have documented that loss of p53 function potentiates metastasis in this model system. MPRs were grafted into homozygous (+/+) p53 male mice, fed a 4-HPR containing diet or a control diet and maintained until the status of tumor progression dictated sacrifice. Under these experimental conditions, treatment with 4-HPR did not have a significant effect on primary tumor wet weightfor either p53 +/- or p53 -/- MPRs. For, p53 +/- MPRs the animals fed the 4-HPR diet had a slight improvement in survival and a significant reductionin the number of mesenteric metastases (P=0.0477, t-test). Notably, in p53+/- MPRs the incidence of metastasis to lumbar spine and sternum was 92% in the control animals compared to 54% in the 4-HPR treated animals (P = 0.035, chi (2)-test). In p53 -/- MPRs there was a trend toward a reduction in the number of soft tissue metastases to lung and liver in the 4-HPR group relative to the control diet group and a statistically significant reductionin the incidence of metastasis to bone was demonstrated in that 50% of control animals versus 30% of 4-HPR treated p53 -/- animals harbored bone metastases (P = 0 < 0.05, chi (2)-test). Cell lines were established from portions of the primary tumor and from selected metastatic deposits in each experimental group. Clonal analysis, by retroviral integration pattern, indicated increased clonal diversity in both the primary tumors and metastasis-derived cell lines from 4-HPR treated animals relative to the control animals. In vitro treatment with 4-HPR did not reveal discriminating differences between cell lines derived from primary tumors and bone metastases or controland treatment groups in regard to growth arrest or apoptotic responses. Overall these studies indicate limited anti-tumor and anti-metastatic activity in this highly aggressive in vivo mouse model of prostate cancer, yet 4-HPR treatment significantly suppressed the development of bone metastases inp53 +/- and p53 -/- MPRs revealing a novel and potentially clinically useful activity of this retinoid.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/01/20 alle ore 20:07:00