ライフサイエンスコーパス: RET gene

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1 ction of the corresponding mutation into the ret gene.

2 orted with loss of function mutations in the Ret gene.

3 cing to phase two variants 9 kb apart in the RET gene.

4 those caused by mutations in the SOX10 or c-RET genes.

5 in the proximal promoter region of the human RET gene (-51 to -33 relative to transcription start sit

6 an 18 Mb region on 10q11.2-21 containing the RET gene and its recombination partners, the H4 and NCOA

7 lar biology behind specific mutations of the RET gene and their prognostic implications have led to t

8 angement is formed by fusion of the ELE1 and RET genes, and is highly prevalent in radiation-induced

9 Rearrangements involving the RET gene are common in radiation-associated papillary th

10 Mutations in the RET gene are responsible for approximately half of famil

11 For the detection of C533G mutation of the RET gene, biotinylated oligonucleotide probes were used.

12 ain how putative activating mutations of the RET gene can produce a phenotype usually associated with

13 zygous mutations in the coding region of the RET gene cause a severe form of Hirschsprung disease (to

14 tions in the REarranged during Transfection (RET) gene cause MEN2A, MEN2B, and familial medullary thy

15 ximately 8 Mb in length, which positions the RET gene close to both, the NCOA4 and H4, loci.

16 Cis-acting sequences around the RET gene, conserved in mammals but not in fish, are able

17 entified an intronic enhancer variant in the RET gene disrupting SOX10 binding and increasing Hirschs

18 phenotype can be largely rescued by reducing Ret gene dosage.

19 The c-ret gene encodes a receptor tyrosine kinase that is expr

20 The RET gene, encoding a receptor tyrosine kinase, is unusua

21 s well as 1 EML4-ALK gene fusion and 1 KIF5B-RET gene fusion.

22 s identified 11 additional tumors with KIF5B-RET gene fusions (2.0%; 95% CI 0.8-3.1%).

23 ALK, ROS1 and RET gene fusions are important predictive biomarkers for

24 Novel configurations of BRAF, NTRK3, and RET gene fusions resulting from chromosomal translocatio

25 d with transcriptional activation of mutated RET gene in human medullary thyroid carcinoma TT cells.

26 al role in transcriptional regulation of the RET gene in vivo, providing insight into a novel strateg

27 haracterized the breakpoints in the ELE1 and RET genes in 12 post-Chernobyl pediatric papillary carci

28 transcriptional profiling indicates that the retS gene is required for expression of the Type III sec

29 ) p53(+/-) mice, amplified the region of the Ret gene known to be mutated in human MTC, and detected

30 on profile of MTC with regard to the type of RET gene mutation and the cancer genetic background (her

31 risk-stratification scheme based on type of RET gene mutation informs the age at which prophylactic

32 We also noticed that the site of the RET gene mutation slightly influenced the gene expressio

33 The absence of germline VHL and RET gene mutations in many of these families suggested t

34 Identification of RET gene mutations in patients at-risk for the developme

35 iers of germline pathogenic mutations of the RET gene, or were first-degree relatives with histologic

36 In humans and mice, mutations in the Ret gene result in Hirschsprung's disease and renal defe

37 ine kinase, which is believed to convert the RET gene to an oncogene by altering the enzyme's substra

38 tic screening for a germline mutation at the RET gene was performed in 11 family members.

39 can bind to and activate expression of the c-RET gene, which is often mutated in Hirschsprung disease

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