"Hormone-refractory" prostate cancer : a putative new mechanism: the upside-down response to androgens

En aquest article volem revisar la diversitat dels mecanismes moleculars suposadament responsables del creixement independent d'andrògens del càncer de pròstata. Es demostra que alguns càncers de pròstata que escapen de la teràpia endocrinològica estan compostos per cèllules sensibles als andrògens. Ens centraremen els resultats del nostre laboratori i en els d'altres grups de recerca que suggereixen el mateix concepte nou: el comportament del càncer de pròstata refractari als andrògens està associat a una resposta invertida de les cèll. ules als andrògens. Hem observat un alentiment paradoxal en el creixement de diverses línies cell. ulars induït pels andrògens. Aquestes línies cell. ulars provenen de les cèll. ules LNCaP, ja sigui per evolució espontània o per cultiu crònic en un medi sense andrògens. La línia ARCaP (androgen-reverted carcinoma of the prostate) va ser establerta a partir de l'ascitis d'un pacient amb càncer de pròstata avançat. Els tumors que varen créixer a partir d'aquestes cèll. ules reverteixen, encara que transitòriament, en el tractament androgènic. Volem suggerir que la castració podria permetre la proliferació de les cèll. ules que eren paradoxalment alentides pels andrògens i que aquesta reacció invertida als andrògens podria ser el possible mecanisme pel qual el càncer de pròstata deixa de respondre a la teràpia hormonal. Aquests resultats aportarien unes bases racionals per a comprendre el tractament antiandrogènic intermitent.In this paper we survey the diversity of the molecular mechanisms suspected to be responsible for the androgen-independent growth of prostate cancer. It has been shown that some prostate cancers, which escape endocrine therapy, are composed of androgen-sensitive cells. We focus on the results from our laboratory and from a few others that suggest a new concept: that the androgen-refractory behavior of prostate cancer may be associated with an inverted response to androgens by cells. The proliferation of several cell lines was paradoxically slowed by androgens. In the afore-mentioned studies, a series of these cell lines arose from the LNCaP cell line, either spontaneously or after culturing them chronically in androgen-poor culture medium. The ARCaP (androgen-reverted carcinoma of the prostate) was established from the ascites of a patient with advanced prostate cancer. Usually, tumors grown from such cells regress, albeit transiently, under androgen treatment. It has been suggested that castration could allow the proliferation of cells that are paradoxically slowed by androgens and that the inverted response to androgens could possibly be a mechanism, by which prostate cancer escapes from endocrine therapy. These results provide the rationale for intermittent treatment

Etude épidémiologique de la maladie de Kawasaki et lien avec l'épidémie de Yersinia Pseudotuberculosis

TOURS-BU Médecine (372612103) / SudocSudocFranceF

Etude descriptive des lésions de la valve aortique et de l'aorte ascendante dans une population pédiatrique avec valve aortique bicuspide

TOURS-BU Médecine (372612103) / SudocSudocFranceF

Evaluation du diagnostic anténatal des cardiopathies congénitales en Indre-et-Loire de 1995 à 1999

TOURS-BU Médecine (372612103) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Evaluation de la performance et de la qualité du diagnostic anténatal des cardiopathies congénitales en Indre-Et-Loire sur une période de 15 ans

TOURS-BU Médecine (372612103) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Qualité de vie chez les patients porteurs d'une dérivation cavo-pulmonaire totale (étude rétrospective à propos de 34 cas)

TOURS-BU Médecine (372612103) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Tachycardies atriales de l'enfant à coeur sain (à propos de douze cas)

TOURS-BU Médecine (372612103) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Outcome of coronary artery bypass grafting performed in young children

ObjectivesThe long-term patency rate of coronary artery bypass grafting for which arterial grafts are used is known to be high in the pediatric population. However, this issue remains uncertain in children under 3 years of age. Here, we report the outcome in this specific population.MethodsFrom July 1988 to July 2007, 18 children less than 3 years of age (age at operation, 0.1–35 months; median, 4 months) underwent 20 coronary artery bypass graft operations using an arterial graft. Indications for bypass grafting were coronary artery complications related to the arterial switch operation for transposition of the great arteries in 12 patients (coronary obstruction in 8 patients, peroperative coronary anomalies precluding coronary transfer in 4 patients), congenital anomalies of the coronary arteries in 4 patients, and Kawasaki disease in 2 patients.ResultsAfter a mean follow-up of 55 months (range, 1–176 months; median, 41 months), patency of 19 bypass grafts was assessed. One was occluded and 2 have necessitated a percutaneous procedure. Two patients died suddenly (1 with an occluded graft and 1 with a patent graft and hypertrophic myocardiopathy) 3.5 and 4.6 months, respectively, after bypass grafting.ConclusionsCoronary artery bypass grafting should be considered as a possible alternative for coronary revascularization in young children. Although our series shows quite a good patency rate, this procedure remains a technical challenge and requires careful follow-up

"Hormone-refractory" prostate cancer : a putative new mechanism: the upside-down response to androgens

En aquest article volem revisar la diversitat dels mecanismes moleculars suposadament responsables del creixement independent d'andrògens del càncer de pròstata. Es demostra que alguns càncers de pròstata que escapen de la teràpia endocrinològica estan compostos per cèllules sensibles als andrògens. Ens centraremen els resultats del nostre laboratori i en els d'altres grups de recerca que suggereixen el mateix concepte nou: el comportament del càncer de pròstata refractari als andrògens està associat a una resposta invertida de les cèll. ules als andrògens. Hem observat un alentiment paradoxal en el creixement de diverses línies cell. ulars induït pels andrògens. Aquestes línies cell. ulars provenen de les cèll. ules LNCaP, ja sigui per evolució espontània o per cultiu crònic en un medi sense andrògens. La línia ARCaP (androgen-reverted carcinoma of the prostate) va ser establerta a partir de l'ascitis d'un pacient amb càncer de pròstata avançat. Els tumors que varen créixer a partir d'aquestes cèll. ules reverteixen, encara que transitòriament, en el tractament androgènic. Volem suggerir que la castració podria permetre la proliferació de les cèll. ules que eren paradoxalment alentides pels andrògens i que aquesta reacció invertida als andrògens podria ser el possible mecanisme pel qual el càncer de pròstata deixa de respondre a la teràpia hormonal. Aquests resultats aportarien unes bases racionals per a comprendre el tractament antiandrogènic intermitent.In this paper we survey the diversity of the molecular mechanisms suspected to be responsible for the androgen-independent growth of prostate cancer. It has been shown that some prostate cancers, which escape endocrine therapy, are composed of androgen-sensitive cells. We focus on the results from our laboratory and from a few others that suggest a new concept: that the androgen-refractory behavior of prostate cancer may be associated with an inverted response to androgens by cells. The proliferation of several cell lines was paradoxically slowed by androgens. In the afore-mentioned studies, a series of these cell lines arose from the LNCaP cell line, either spontaneously or after culturing them chronically in androgen-poor culture medium. The ARCaP (androgen-reverted carcinoma of the prostate) was established from the ascites of a patient with advanced prostate cancer. Usually, tumors grown from such cells regress, albeit transiently, under androgen treatment. It has been suggested that castration could allow the proliferation of cells that are paradoxically slowed by androgens and that the inverted response to androgens could possibly be a mechanism, by which prostate cancer escapes from endocrine therapy. These results provide the rationale for intermittent treatment