Page 68 - Traité de chimie thérapeutique 6 Médicaments antitumoraux

24 GÉNÉRALITES SUR LES MEDICAMENTS ANTTTUMORAUX

Phospholipides membranaires
i
P~paseA2 Nf·KB JI q Inhibition de 1 'apoptose
• y
Acide arachidonique r\ n
PROLIFÉRATION CELL
Jase=j

Prostaglandines: NÉO-
PG E2 VASCULA RISATION JI 4FE#5ni
4 Aroma tase
PROLIFÉRATION CELL
Testosté<one ~ Estradiot JI
Ex : cancer du sein
(tum eur s hormono-d épendan tes)
Figure 13 : Conséquences liées à la surexpression de COX-2
Les relations précises entre l'isoenzyme COX-2, le récepteur PPAR-y (Peroxisome
Proliferator-Activated Receptorgamma) et le processus prolifératif restent à déterminer.

BIBLIOGRAPHIE

APOPTOSE, SÉNESCENCE
BOUILLET P. et al., The role of the pro-apoptotic Bcl-2 family member bim in physiolo-
gical cell death, Ann. N. Y. Acad. Sei., 2000, 926, 83-89.
CHARETTE S.J., LANDRY J., The interaction of HSP27 with Daxx identifies a potential
regulatory role of HSP27 in fas-induced apoptosis, Ann. N. Y. Acad. Sei., 2000, 926,
126-131.
BLATT N.B., GLICK G.D., Signaling pathways and effector mechanisms pre-program-
med cell death., Bioorg. Med. Chem., 2001, 9, 1371-1384.
SALVESEN G.S., DUCKETT C.S., IAP proteins : blocking the road to death's door, Nature
Rev. (Mol. Cel/. Bio/.), 2002, 3, 401-410.
POELE R.H. et al., DNA damage is able to induce senescence in tumor cells in vitro and
in vivo, Cancer Res., 2002, 62, 1876-1883.
CYCLE CELLULAIRE
DOTTO G.P., p21waf1/Cip1 : more than a break to the cell cycle ? Biochim. Biophys.
Acta, 2000, 1471, M43-M56. .
HARPER J.W., ADAMS P.D., Cyclin-dependent kinases, Chem. Rev., 2001, 101, 2511-
2526.
ORTEGA S. et al., Cyclin D-dependant kinases, INK4 inhibitors and cancer, Biochim.
Biophys. Acta, 2002, 1602, 73-87.