ライフサイエンスコーパス: antiestrogen therapy

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1 inhibition by p21 and p27, and resistance to antiestrogen therapy.

2 following cisplatin, ionizing radiation, and antiestrogen therapy.

3 hormone deprivation and become resistant to antiestrogen therapy.

4 cers that rely on estrogen for their growth, antiestrogen therapy.

5 s, particularly those that are refractory to antiestrogen therapy.

6 y than non-navigated participants to receive antiestrogen therapy.

7 ophagy to determine cell fate in response to antiestrogen therapy.

8 survival, tumor recurrence, and response to antiestrogen therapies.

9 though ER-positive tumors usually respond to antiestrogen therapies, 30% of them do not.

10 negative, with ERalpha+ tumors responding to antiestrogen therapy and having a better prognosis.

11 nespimycin (a heat shock protein inhibitor), antiestrogen therapies, and an antibody-drug conjugate (

12 ned Cox regression analysis identified prior antiestrogen therapy as a significant factor in the HER2

13 y significant higher likelihood of receiving antiestrogen therapy compared with non-navigated control

14 the prevalence of BMD abnormalities, whether antiestrogen therapy decreased BMD, and if treatment wit

15 YStat5 was associated with increased risk of antiestrogen therapy failure as measured by univariate C

16 of active Stat5 in tumors is associated with antiestrogen therapy failure in patients.

17 erienced disease progression while receiving antiestrogen therapy for advanced disease.

18 Current antiestrogen therapy for breast cancer is limited by the

19 elapse within 12 months of stopping adjuvant antiestrogen therapy given for at least 6 months, or had

20 gression while receiving continuous adjuvant antiestrogen therapy, had experienced relapse within 12

21 While ERalpha-dependent cancers respond to antiestrogen therapy, Her-2/neu-overexpressing cancers t

22 tic lung lesions, is frequently treated with antiestrogen therapy, i.e., progesterone and/or oophorec

23 storing ERalpha expression and responding to antiestrogen therapy in a subset of breast cancers.

24 ggest that these data warrant the testing of antiestrogen therapy in females with CF and propose an a

25 ceived included the following: initiation of antiestrogen therapy in patients with hormone receptor-p

26 both ER subtypes may explain the failure of antiestrogen therapy in some breast cancer patients.

27 Antiestrogen therapy induces the unfolded protein respon

28 on estrogen for continued tumor growth, then antiestrogen therapy may be effective in the treatment o

29 Among participants eligible for antiestrogen therapy, navigated participants (n = 380) h

30 (P < .0001), younger age (P < .008), and no antiestrogen therapy (P < .02).

31 mains unanswered, but predicting response to antiestrogen therapy requires only measurement of ERalph

32 Although antiestrogen therapies targeting estrogen receptor (ER)

33 are resistant to and others are worsened by antiestrogen therapy; the data suggest that hER-alpha36

34 Prior neoadjuvant/adjuvant antiestrogen therapy was allowed.

35 ptor/progesterone receptor-positive disease, antiestrogen therapy with an aromatase inhibitor is a re

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