Germline genetic variations at 11q13 and 12p11 locus modulate age at onset for renal cell carcinoma.

Purpose: Few risk factors have been identified for renal cell carcinoma. We performed a validation study in a population with a European background to identify the most significant variants previously identified in association with renal cell carcinoma risk.

Materials And Methods: We performed a case-control validation study after recruiting 463 controls and 463 patients with a histologically confirmed diagnosis of clear cell renal cell carcinoma.

Combination of polymorphisms from genes related to estrogen metabolism and risk of prostate cancers: the hidden face of estrogens.

Purpose: The association between common functional polymorphisms from the CYP17, CYP19, CYP1B1, and COMT genes involved in the estrogen metabolism and the risk of prostate carcinoma was evaluated.

Patients And Methods: The study investigated 1,983 white French men (1,101 patients with prostate cancer and 882 healthy controls) aged between 40 and 98 years. The different alleles and genotypes were analyzed according to case-control status, aggressiveness pattern of the tumors, age at onset, and family history of cancers.

Genetic impact on prostate anatomical variability during ageing: role of CYP17, SRD5A2 and androgen receptor genes polymorphisms.

Objectives: To investigate the role of genetic determinism on individual variability in age-related prostate changes, as defining 'normal' anatomy in prostate gland ageing is a challenge because the variability of changes in prostate morphology increases with age.

Materials And Methods: We assessed the influence of androgen- and oestrogen-regulating genetic polymorphisms on age-related weight and stromal-ratio changes in the prostate, using an anatomical, autopsy-based study. We quantified weight and glandular/stromal ratio in 85 autopsy prostates from men aged > 50 years.

[Impact of obesity on PSA in prostate cancer screening].

Objective: Obesity is associated with changes of serum levels of androgens and oestrogens which could modulate prostate metabolism. The objective of this study was to investigate a possible correlation between the PSA level and the degree of obesity in a candidate population for prostate cancer screening in order to determine whether the PSA level needs to be adapted before performing biopsy.

Material: During a screening campaign in a French district, serum PSA results and body mass index (BMI) were available for 541 men.

Familial prostate cancer cases before and after radical prostatectomy do not show any aggressiveness compared with sporadic cases.

Objectives: To compare the clinical and biologic features at diagnosis between sporadic and familial clinically localized prostate cancer (CaP), and to compare the prognosis of familial with that of sporadic cases after radical prostatectomy in southwestern Europe.

Methods: Eighty-five sporadic (one case of CaP) and 37 familial (two or more CaP cases in the family) patients with clinically localized CaP undergoing radical prostatectomy were compared regarding preoperative (mean age, clinical status, mean prostate-specific antigen level, and mean Gleason score at diagnosis) and postoperative (pT, pN, and pathologic Gleason score) parameters using the Student t test, Fisher's exact test, and the chi-square test. The biochemical relapse-free survival for each group was compared using the Kaplan-Meier method and the log-rank test.

Segregation analysis of prostate cancer in France: evidence for autosomal dominant inheritance and residual brother-brother dependence.

Four segregation analyses concerning prostate cancer (CaP), three conducted in the United States and one in Northern Europe, have shown evidence for a dominant major gene but with different parameter estimates. A recent segregation analysis of Australian pedigrees has found a better fit of a two-locus model than single-locus models. This model included a dominantly inherited increased risk that was greater at younger ages and a recessively inherited or X-linked increased risk that was greater at older ages.

PCAP is the major known prostate cancer predisposing locus in families from south and west Europe.

To date four prostate cancer predisposing loci have been mapped: HPC1 (Hereditary Prostate Cancer 1) on 1q24-25, PCaP (Predisposing for Cancer Prostate) on 1q42.2-43, CAPB (Cancer Prostate and Brain) on 1p36, and HPCX on Xq27-28. We examined evidence for linkage to those loci in 64 families from south and west Europe.

In vivo model mimicking natural history of dog prostate cancer using DPC-1, a new canine prostate carcinoma cell line.

Background: Dog prostate cancer is usually considered to be highly relevant to human prostate cancer. We report the isolation of a new canine prostate cancer epithelial cell line designated DPC-1.

Methods: Primary cultures were established from a canine poorly differentiated prostatic adenocarcinoma.

Early-onset hereditary prostate cancer is not associated with specific clinical and biological features.

Background: Familial prostate cancer (CaP) accounts for 15-20% of all CaP, and hereditary CaP for 5-10% of patients. Few data are available concerning their clinical and biological features.

Methods: We compared diagnostic modalities, age, clinical stage, PSA, and tumor grade at diagnosis in CaP patients according to familial CaP profile: hereditary (HR) (> or =3 CaP), familial nonhereditary (FNH) (= 2 CaP), and sporadic CaP.

Early onset and familial predisposition to prostate cancer significantly enhance the probability for breast cancer in first degree relatives.

Genetic predisposition accounts for >/=10% of all cancer of the prostate (CaP) and is therefore considered a major risk factor, together with age and ethnic origin. Several epidemiological studies have suggested that familial clustering of CaP may be associated with an increased frequency of breast and other cancers among relatives. In order to correlate the incidence of CaP with prevalence of breast and other cancers, we have performed uni- and multi-variate analyses on 691 complete pedigrees including probands, who were consecutive patients with confirmed CaP treated in three French urological departments.

FGF7/KGF triggers cell transformation and invasion on immortalised human prostatic epithelial PNT1A cells.

Fibroblast growth factor 7 (FGF7/KGF) is synthesized exclusively by fibroblasts in normal tissues; it acts as a potent mitogen on epithelial cells, through interaction with the FGF7-specific receptor FGFR2/IIIb. To examine the importance of this growth factor both to prostate physiology and to prostate-cancer progression, we have tested the exogenous effect of FGF7. Thus, by mimicking the paracrine pathway (on proliferation, growth in soft agar and invasion) on the human prostatic epithelial cell line PNT1A positively checked for FGFR2/IIIb expression, FGF7 significantly enhanced cell proliferation at an optimal concentration of 7.