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1 ective states in humans (FG7142, rimonabant, 13-cis retinoic acid).
2 arrow transplantation (ABMT) with or without 13 cis-retinoic acid.
3 f the type 2 17beta-HSD was not inhibited by 13-cis retinoic acid.
4 and ASCT was performed on day 0, followed by 13-cis-retinoic acid.
5 od stem-cell rescue, local radiotherapy, and 13-cis-retinoic acid.
6                                Isotretinoin (13-cis retinoic acid (13-cis RA)) is the most potent inh
7 e of the risk factors for MGD is exposure to 13-cis retinoic acid (13-cis RA), a metabolite of vitami
8 o determine whether combination therapy with 13-cis-retinoic acid (13-CRA) plus interferon alfa-2a (I
9 tivity in the head and neck and may decrease 13-cis-retinoic acid (13-cRA) toxicity.
10 etinoids, all-trans-retinoic acid (atRA) and 13-cis-retinoic acid (13cisRA), as well as the principal
11 istered as a single agent and in combination 13-cis retinoic acid (13cRA) in children with refractory
12     To conduct a phase III trial of adjuvant 13-cis-retinoic acid (13cRA) plus interferon alfa (IFN-a
13 tudy was to test interferon alfa (IFNalpha), 13-cis-retinoic acid (13cRA), and cisplatin biochemother
14 es treatment with the retinoid isotretinoin (13-cis retinoic acid; 13cRA), which is used in the post-
15 ative fluorescence technique, that Accutane (13-cis-retinoic acid), a drug used in the treatment of a
16      We compared these effects with those of 13-cis-retinoic acid, a chemoprevention agent, and with
17 ng the following search terms: isotretinoin, 13-cis-retinoic acid, Accutane, retinoids, acitretin, su
18 ta-apo-12'-carotenal, beta-apo-8'-carotenal, 13-cis-retinoic acid, all-trans-retinoic acid, beta-caro
19   At high concentrations, the combination of 13-cis-retinoic acid and each of the five other drugs re
20 site, achieving mixed clinical results (with 13-cis-retinoic acid and etretinate) in superficial blad
21 at C-4 of all-trans-retinoic acid (ATRA) and 13-cis-retinoic acid, and modification of terminal carbo
22                      All-trans-, 9-cis-, and 13-cis-retinoic acid, and the synthetic retinoid Ch55, i
23 f other hydroxylase in response to 9-cis and 13-cis retinoic acid application to adult human skin in
24 ame preparations were unable to use 9-cis or 13-cis retinoic acid as substrate for the hydroxylation
25  chemotherapy, and subsequent treatment with 13-cis-retinoic acid (cis-RA).
26 d the combination of phenylbutyrate (PB) and 13-cis retinoic acid (CRA) as a differentiation and anti
27                       Temozolomide (TMZ) and 13-cis-retinoic acid (cRA) have shown activity in prior
28                           A phase I trial of 13-cis-retinoic acid (CRA), IFNalpha, and paclitaxel (TA
29              It was found that all-trans and 13-cis retinoic acids exerted modest, dose-dependent eff
30 receive no further therapy or treatment with 13-cis-retinoic acid for six months.
31 3-0.150 microM); sulindac sulfide, NDGA, and 13-cis-retinoic acid had intermediate potency (IC50 = 4-
32                                We found that 13-cis retinoic acid induced, in a concentration-depende
33  in SG homogenates; and (iv) to determine if 13-cis retinoic acid inhibits 17beta-HSD activity.
34 bination of low-dose MK886, ciglitazone, and 13-cis-retinoic acid interacted at least in a superaddit
35  produced by isomerization of both 9-cis and 13-cis retinoic acids is the likely inducer of the 4-hyd
36                                Isotretinoin (13-cis retinoic acid) is frequently prescribed for sever
37  of the follicle, or (ii) in the presence of 13-cis-retinoic acid, is due to the reduced expression o
38                                              13 cis Retinoic acid (isotretinoin) is a retinoid with p
39 alone, and whether subsequent treatment with 13-cis-retinoic acid (isotretinoin) further improves eve
40                                         Oral 13-cis-retinoic acid maintenance therapy was administere
41                                 Therapy with 13-cis retinoic acid or low-dose chemotherapy can induce
42        Subsequently, they were randomized to 13-cis-retinoic acid or no further treatment.
43 e have evaluated whether IFN-alpha-2a and/or 13-cis-retinoic acid (RA) enhance radiation cytotoxicity
44 ctive component of the acne drug Accutane is 13-cis-retinoic acid (RA), and it is highly teratogenic
45 nd, and NDGA with paclitaxel, cisplatin, and 13-cis-retinoic acid, regardless of drug-resistance phen
46 everal of these agents (including tamoxifen, 13-cis-retinoic acid, retinyl palmitate, and an acyclic
47                        Neither all-trans nor 13-cis retinoic acids s affected cell size as assessed b
48  of other inhibitors such as fenretinide and 13-cis-retinoic acid showed multiple advantages of Ret-N
49  lower levels of all-trans retinoic acid and 13-cis retinoic acid than control subjects but similar 9
50 he 130 patients who were assigned to receive 13-cis-retinoic acid than among the 128 patients assigne
51 tion of 0.1% all-trans, 0.1% 9-cis, and 0.1% 13-cis retinoic acid to human skin for 2 d resulted in i
52                    The inability of 9-cis or 13-cis retinoic acid to induce their own hydroxylation a
53                  In addition, treatment with 13-cis-retinoic acid was beneficial for patients without
54                         Maintenance doses of 13-cis-retinoic acid were then administered until tumor