ライフサイエンスコーパス: mitotane

1 n tumor weight in both xenograft models than mitotane.

2 er overall survival with first-line EDP plus mitotane (17.1 month) than with streptozocin plus mitota

3 ane (17.1 month) than with streptozocin plus mitotane (4.7 months).

4 Currently, mitotane, a nonspecific derivative of the pesticide DDT

5 The combination of mitotane and chemotherapy as prescribed in ARAR0332 resu

6 The probabilities of mitotane and chemotherapy feasibility events were 10.5%

7 f patients with stage III or IV treated with mitotane and chemotherapy.

8 erapy is restricted to patients who tolerate mitotane and either experience a clinical response or ar

9 DP plus mitotane than with streptozocin plus mitotane as first-line therapy, with similar rates of to

10 th disseminated or residual disease received mitotane, cisplatin, etoposide, and/or doxorubicin, and

11 Moreover, exposure of cells to mitotane, cisplatin, or radiation rapidly induced pro-cM

12 0.0087 muM for nab-paclitaxel compared with mitotane concentrations of 15.9 muM and 46.4 muM.

13 sensitive to induction of ferroptosis, while mitotane does not induce this iron-dependent mode of reg

14 response rate than those in the streptozocin-mitotane group (23.2% vs. 9.2%, P<0.001) and longer medi

15 sion-free survival was 5.6 months in the EDP-mitotane group and 2.2 months in the streptozocin-mitota

16 Baseline features in the mitotane group and the control group from Italy were sim

17 For first-line therapy, patients in the EDP-mitotane group had a significantly higher response rate

18 o 47 Italian patients after radical surgery (mitotane group), whereas 55 Italian patients and 75 Germ

19 survival was significantly prolonged in the mitotane group, as compared with the two control groups

20 ane group and 2.2 months in the streptozocin-mitotane group.

21 carcinomas (P=0.02) than did patients in the mitotane group.

22 Mitotane has remained the preferred adjuvant treatment a

23 e hypothesize that instead of treatment with mitotane, human adrenocortical carcinomas may be much mo

24 aim was to evaluate the efficacy of adjuvant mitotane in prolonging recurrence-free survival.

25 ected targets were tested in comparison with mitotane in the 2 ACC cell lines (H295R and SW-13) in vi

26 Fas-induced apoptosis, necroptosis, mitotane-induced cell death and growth hormone-releasing

27 optosis (zVAD, emricasan) do not prevent the mitotane-induced cell death but morphologically prevent

28 Whether the use of mitotane is beneficial as an adjuvant treatment has been

29 Mitotane is the only approved therapy for adrenocortical

30 ients, steroidogenesis inhibitors, including mitotane, ketoconazole, metyrapone, and etomidate, shoul

31 participation were required to have a serum mitotane level of less than 2 mg/L.

32 Adjuvant mitotane may prolong recurrence-free survival in patient

33 advanced adrenocortical carcinoma to receive mitotane plus either a combination of etoposide (100 mg

34 ndomized, controlled trials, adjuvant use of mitotane remains controversial, although the authors of

35 effective doses, most clinicians agree that mitotane should be used if the tumor cannot be removed s

36 ival were significantly better with EDP plus mitotane than with streptozocin plus mitotane as first-l

37 tion is obtained when DZNep is combined with mitotane, the gold-standard treatment for ACC.

38 ria included previous pasireotide treatment, mitotane therapy within 6 months, and pituitary irradiat

39 Multivariate analysis indicated that mitotane treatment had a significant advantage for recur

40 Adjuvant mitotane was administered to 47 Italian patients after r

41 served when pharmacologic adrenalectomy with mitotane was done in combination with Ad5IL-12 vector tr

42 Adverse events associated with mitotane were mainly of grade 1 or 2, but temporary dose

43 Patients who had used mitotane within 6 months of study participation were req