ライフサイエンスコーパス: prolactinoma

1 as only seen in patients with acromegaly and prolactinoma.

2 ctor 3 subunit B1 (SF3B1(R625H)) in 19.8% of prolactinomas.

3 nction, we examined these receptors in human prolactinomas.

4 s, 118 (12%) craniopharyngiomas, and 93 (9%) prolactinomas.

5 roups of pituitary adenomas, except for most prolactinomas.

6 in all groups of pituitary adenomas, except prolactinomas.

7 e detected in nearly all adenomas except for prolactinomas.

8 tatistically significance when compared with prolactinomas.

9 secretion (30-40%; P < 0.05) in four of six prolactinomas.

10 -secreting adenomas and giant and aggressive prolactinomas.

11 e that could differentiate micro- from macro-prolactinomas.

12 practice on the diagnosis and management of prolactinomas.

13 on (PCR) analysis of tissue samples from 227 prolactinomas.

14 yrate (BHB) in serum and whole-blood (WB) of prolactinomas (0.481 +/- 0.211/0.329 +/- 0.228 mM in ser

15 Prolactinomas account for 32% to 66% of adenomas and pre

16 These results show ErbB3 expression in human prolactinomas and a novel ErbB3-mediated mechanism for P

17 and, most recently, familial acromegaly and prolactinomas and other tumors caused by mutations in th

18 between a gain-of-function PRLR variant and prolactinomas and reveal a new etiology and potential th

19 Prolactinomas are the most frequent type of pituitary tu

20 present the first reported pediatric case of prolactinoma associated with SLE, in a 13-year-old white

21 oming the preferred drug in the treatment of prolactinomas because of higher response rate and less s

22 cohort study of 114 patients diagnosed with prolactinomas between 2007 and 2017 was conducted.

23 ated in both serum and WB when compared with prolactinomas but it met the statistical significance cr

24 TR5 exclusively regulates PRL secretion from prolactinoma cells.

25 First-line therapy for prolactinomas consists of bromocriptine or cabergoline,

26 recommendations for paediatric patients with prolactinomas, Cushing disease, growth hormone excess ca

27 Prolactinomas develop in mice lacking the prolactin rece

28 Thus, hst may directly facilitate prolactinoma development via paracrine or autocrine acti

29 phic hyperplastic response, angiogenesis and prolactinoma development, we propose a previously unknow

30 These patients with mutant prolactinomas display higher prolactin (PRL) levels (p =

31 We have shown previously that human prolactinomas express transforming sequences of the hepa

32 ranssphenoidal pituitary surgery, except for prolactinomas, for which medical therapy, either bromocr

33 Management of prolactinoma in special situations is discussed, includi

34 ility are outlined, as well as management of prolactinomas in children and adolescents, patients with

35 eceptor induced hyperprolactinemia and large prolactinomas in females.

36 present the latest evidence on treatment of prolactinoma, including efficacy, adverse effects and op

37 For prolactinomas, initial therapy is generally dopamine ago

38 Surgery as a primary treatment of prolactinomas is considered in 64 centers (25.2%).

39 Pharmacological treatment of prolactinomas is mainly based on dopamine agonists.

40 cle-stimulating (LH/FSH)-secreting (n = 24), prolactinomas (n = 14), and non-functional (NF) (n = 9)

41 The various histologic types include prolactinomas, nonfunctioning adenomas, somatotropinomas

42 A samples (35 leucocytes, 15 tumors) from 46 prolactinoma patients (59% males, 41% females).

43 ificantly higher frequencies (P < 0.0001) in prolactinoma patients than in 60 706 individuals of the

44 ients [gonadotropic (LH/FSH-secreting) = 17; prolactinomas (PRL-secreting) = 11, Cushing's disease (A

45 s use, renal failure, hypothyroidism, and by prolactinoma - PRL secreting tumors.

46 asis and corresponding clinical relevance of prolactinomas remain poorly understood.

47 Prolactinomas represent the most common type of secretor

48 ld be useful for the treatment of aggressive prolactinomas resistant to conventional therapy.

49 e control of PRL secretion and tumor load in prolactinomas resistant to dopaminergic treatment, or fo

50 Symptomatic hyperprolactinemia and prolactinomas should be treated to lower PRL levels, dec

51 een serum prolactin (PRL) concentrations and prolactinoma size, and to determine a cut-off PRL value

52 ss of normally produced hormones and include prolactinomas, somatotropinomas, corticotropinomas, and

53 d not suppress PRL release from six cultured prolactinomas studied.

54 In about 25% of the centers, prolactinoma surgery may be regarded as first-line treat

55 ial mechanism underlying the pathogenesis of prolactinomas that may lead to the development of target

56 In prolactinomas this is the case in 194 centers, (76.4%),

57 malignant) while the remaining tumour was a prolactinoma; three ectopic secretors of ACTH (two bronc

58 genome sequencing (WGS) on 21 patients with prolactinomas to detect somatic mutations and then valid

59 tant to dopaminergic treatment, or for those prolactinomas undergoing rare malignant transformation.

60 The diagnosis of pituitary prolactinoma was based on the histologic features and th

61 elucidate the role of the PRLR gene in human prolactinomas, we determined the PRLR sequence in 50 DNA

62 pituitary tumours assessed, two (including a prolactinoma) were essentially negative, while the third

63 Approximately 53% of pituitary adenomas are prolactinomas, which can cause hypogonadism, infertility