ライフサイエンスコーパス: EGFR gene

1 sease caused by a homozygous mutation in the EGFR gene.

2 nt in the tyrosine kinase (TK) domain of the EGFR gene.

3 ond that resulting from amplification of the EGFR gene.

4 were revealed for SNPs within the TM9SF2 and EGFR genes.

5 ion of the epidermal growth factor receptor (EGFr) gene.

6 ape of the epidermal growth factor receptor (EGFR) gene.

7 ons in the epidermal growth factor receptor (EGFR) gene.

8 fication and expression of the EGF receptor (EGFR) gene.

9 21 of the epidermal growth factor receptor (EGFR) gene.

10 ing on three functional polymorphisms in the EGFR gene [-216G/T, intron 1 (CA)n, and R497K].

11 xamine the intragenic mutations in the human EGFR gene, a panel of normal and malignant human oral ke

12 apoptosis of HCC827, a NSCLC cell line with EGFR gene amplification and an exon 19 deletion.

13 EGFR gene amplification and EGFRvIII are associated with

14 EGFR gene amplification and mutation are common in gliob

15 Neither EGFR kinase domain mutations nor EGFR gene amplification appear to be essential for respo

16 By quantitative PCR, we found EGFR gene amplification in 2 of 8 tumors.

17 The extent of EGFR gene amplification or mutation of the EGFR tyrosine

18 udied 14 glioblastomas for TP53 mutation and EGFR gene amplification status, using fluorescence in si

19 eptor (EGFR) overexpression (with or without EGFR gene amplification) that is often associated with i

20 glioblastoma tumors and two cell lines with EGFR gene amplification.

21 e genetic alterations, such as EGF receptor (EGFR) gene amplification and mutation, plays a major rol

22 Epidermal growth factor receptor (EGFR) gene amplification and mutations are the most comm

23 Epidermal growth factor receptor (EGFR) gene amplification is the most common genetic alte

24 Epidermal growth factor receptor (EGFR) gene amplification occurs in glioblastomas as so-c

25 Epidermal growth factor receptor (EGFR) gene amplification, mutations, and/or aberrant act

26 re discovered in the 5'-regulatory region of EGFR gene and 2 common single nucleotide polymorphisms (

27 balanced disomy (40%) and trisomy (38%) for EGFR gene and chromosome 7 (40%), whereas balanced polys

28 It will be important to evaluate EGFR gene and EGFR protein status and signal protein exp

29 e of somatic mutations of the RAS, BRAF, and EGFR genes and association of cetuximab efficacy with th

30 nth) as best candidates to silence c-MET and EGFR genes and of two endogenous miRNAs (miR-15a and miR

31 example, somatic activating mutations in the EGFR gene are present in approximately 20% of patients w

32 ons of the epidermal growth factor receptor (EGFR) gene are common in some forms of cancer and the mo

33 ain of the epidermal growth factor receptor (EGFR) gene are found in human lung adenocarcinomas and a

34 nts of the epidermal growth factor receptor (EGFR) gene are frequently found in glioblastoma multifor

35 ain of the epidermal growth factor receptor (EGFR) gene are reportedly associated with sensitivity of

36 No mutation of KRAS, BRAF, and EGFR genes at the investigated loci was found.

37 we established that a portion of VANGL1 and EGFR gene body methylation in human tissue DNA samples i

38 EK expands the known mechanisms by which the EGFR gene contributes to oncogenesis and represents the

39 cancer (LA-HNC) and correlate outcomes with EGFR gene copy number alterations.

40 EGFR and K-ras mutation analyses and EGFR gene copy number analyses were performed on DNA fro

41 Increased EGFR gene copy number based on FISH analysis is demonstr

42 High EGFR gene copy number by FISH is frequent in HNSCC and i

43 xpression by immunohistochemistry (IHC), and EGFR gene copy number by fluorescent in situ hybridizati

44 Increased EGFR gene copy number correlated with LOH-positive statu

45 Increased EGFR gene copy number detected by FISH is associated wit

46 se domain mutations were not identified, and EGFR gene copy number did not relate to response or PFS,

47 omain of EGFR were associated with increased EGFR gene copy number in NSCLC.

48 High EGFR gene copy number may be associated with poor outcom

49 High EGFR gene copy number was a predictor of a gefitinib-rel

50 EGFR gene copy number was a predictor of clinical benefi

51 EGFR gene copy number was assessed by fluorescent in sit

52 In 31 patients with available tissue, high EGFR gene copy number was associated with worse overall

53 The EGFR gene copy number was not predictive of erlotinib ef

54 ochemistry for p16, and fluorescence ISH for EGFR gene copy number were performed on tissue microarra

55 nt in situ hybridization (FISH) to determine EGFR gene copy number, by polymerase chain reaction and

56 mal growth factor receptor (EGFR), increased EGFR gene copy number, cyclin D1 polymorphisms, specific

57 ed lung cancer cell lines for alterations in EGFR gene copy number, enhanced expression of EGFR and o

58 r (EGFR) protein expression and/or with high EGFR gene copy number.

59 The EGFR gene copy numbers in 134 HNSCC tumors were determin

60 The status of EGFR gene copy numbers was analyzed with clinical parame

61 s included epidermal growth factor receptor (EGFR) gene copy number by fluorescence in situ hybridiza

62 Epidermal growth factor receptor (EGFR) gene copy number detected by fluorescent in situ h

63 High epidermal growth factor receptor (EGFR) gene copy number is associated with poor prognosis

64 ed MET and epidermal growth factor receptor (EGFR) gene copy numbers, or mutated (somatic mutation ra

65 with high epidermal growth factor receptor (EGFR)-gene-copy number in the intention-to-treat populat

66 periority of gefitinib in patients with high EGFR-gene-copy number (85 vs 89 patients) was not proven

67 high-risk patients with LOH-positive or high-EGFR-gene-copy-number OPLs.

68 through connection with the previously known eGFR gene DAB2 and extends understanding of the megalin

69 Egfr gene deficiency blocked TPA-induced ERK activity an

70 Our experimental model suggests that EGFR gene delivery might be an effective future therapy

71 of TP53 protein or expressing mutant KRAS or EGFR genes did not induce or expand PNECs, but tumors re

72 tion is inevitably associated with increased EGFR gene dosage.

73 These experiments indicate that EGFR gene expression and function is critical for SCCHN

74 63gamma is involved in the regulation of the EGFR gene expression through interactions with basal tra

75 and cervix, a strong association of FAT1 and EGFR gene expressions was identified.

76 ybridization, and mutational analyses of the EGFR gene have all been proposed as candidates to help p

77 ts associated with the risk of glioma in the EGFR gene have also been associated with specific somati

78 specifically target mutational points in the EGFR gene have significantly reduced suffering and provi

79 ons of the epidermal growth factor receptor (EGFR) gene have been identified in specimens from patien

80 ivated upon HIF1 binding to intron 18 of the EGFR gene in cell lines in which EGFR was induced by hyp

81 ntified in the tyrosine kinase domain of the EGFR gene in eight of nine patients with gefitinib-respo

82 The DNA sequence of the EGFR gene in his tumor biopsy specimen at relapse reveal

83 This study analyzed the genetic nature of EGFR gene in HNSCC and its clinical correlations.

84 mutations in the coding region of the human EGFR gene in normal and malignant human oral keratinocyt

85 We searched for mutations in the EGFR gene in primary tumors from patients with non-small

86 mutations of the HRAS, KRAS, NRAS, BRAF, and EGFR genes in patients with advanced cSCC treated with c

87 ion of the epidermal growth factor receptor (EGFR) gene in gliomas.

88 Somatic activating mutations of the EGFR gene, increased gene copy number and certain clinic

89 r (EGFR) because of somatic mutations of the EGFR gene is commonly observed in tumors of non-small ce

90 ave been identified in gliomas, in which the EGFR gene is frequently amplified and rearranged.

91 However, when a functional EGFR gene is introduced in these cells, they become grow

92 Southern analysis indicates that the EGFR gene is not amplified in these cells; however, thes

93 The epidermal growth factor receptor (EGFR) gene is amplified or mutated in 30%-50% of human g

94 ncers, the epidermal growth factor receptor (EGFR) gene is amplified, mutated, or both.

95 The epidermal growth factor receptor (EGFR) gene is commonly amplified and rearranged in gliob

96 The epidermal growth factor receptor (EGFR) gene is frequently amplified and rearranged in mal

97 tion and/or gain-of-function mutation of the EGFR gene leading to the activation of multiple signalin

98 and mouse epidermal growth factor receptor (EGFR) genes located on chromosomes 7p11.2 and 11, respec

99 ins of the epidermal growth factor receptor (EGFR) gene locus on chromosome 7, an association for whi

100 at the local haplotype structures across the EGFR gene may favor the development of cellular malignan

101 Somatic mutations of the EGFR gene, most commonly L858R (exon 21) and short in-fr

102 ave yet demonstrated any association between EGFR gene mutations and survival.

103 Specific EGFR gene mutations have been identified associated with

104 We show that the EGFR-DMP can detect EGFR gene mutations within 20 min in a label-free and re

105 l types of epidermal growth factor receptor (EGFR) gene mutations have been reported in glioblastomas

106 Epidermal growth factor receptor (EGFR) gene mutations, which are correlated with sensitiv

107 Alterations of the EGFR gene occur frequently in human gliomas where the mo

108 ons of the epidermal growth factor receptor (EGFR) gene occur frequently in human malignant gliomas.

109 ent of the epidermal growth factor receptor (EGFR) gene occur frequently in malignant gliomas.

110 ion of the epidermal growth factor receptor (EGFR) gene occur in MPNST formation.

111 ons in the epidermal growth factor receptor (EGFR) gene or anaplastic lymphoma kinase (ALK) gene rear

112 ons of the epidermal growth factor receptor (EGFR) gene play a crucial role in pathogenesis of gliobl

113 ion of the epidermal growth factor receptor (EGFR) gene, present in approximately 40% of glioblastoma

114 CDK6, SOX9, and EGFR, genes previously implicated in chordoma biology, a

115 sor of the epidermal growth factor receptor (EGFR) gene promoter, we have now shown that PML's repres

116 Each tumor cell is equipped with an EGFR gene-protein interaction network module that also c

117 rming growth factor alpha (TGFalpha) induced EGFR-gene-protein interaction network.

118 rst intron-exon splice junction of the human EGFR gene resulted in decreased EGFR protein production

119 inding sites within introns 26 and 17 of the EGFR gene resulting in the formation of a chimeric intro

120 EGFR gene sequencing of the tyrosine kinase domain and g

121 We report that the EGFR gene spans nearly 200 kb and that the full-length 1

122 ons in the epidermal growth factor receptor (EGFR) gene that cause constitutive receptor activation.

123 alignant melanoma driver gene xmrk, a mutant egfr gene, that is driven by a pigment cell-specific mit

124 to compare three major molecular aspects of Egfr gene: the relative expression levels, gene network

125 Within the EGFR gene there are two functional polymorphisms of inte

126 vian retroviral vectors to transfer a mutant EGFR gene to glial precursors and astrocytes in transgen

127 ngements fusing the 3' coding portion of the EGFR gene to the 5'-UTR of the SEC61G, yielding products

128 nhibitors (TKIs) by concurrently stimulating EGFR gene transcription and protein dephosphorylation.

129 d repressive role for AP-2alpha in governing EGFR gene transcription as cells exit the basal layer an

130 Either wild-type or EGFR gene transduced C6 glioma cells (C6EGFR), which exp

131 ther F98 wild-type (F98(WT)) receptor (-) or EGFR gene-transfected F98(EGFR) cells, which expressed 5

132 A human GBM in which the EGFR gene was amplified without truncation was immunoneg

133 n the 3'-untranslated region (3'-UTR) of the EGFR gene was identified, which was mutated by either mo

134 ons in the epidermal growth factor receptor (Egfr) gene were common in SB-induced liver tumors from m

135 l lung cancer have specific mutations in the EGFR gene, which correlate with clinical responsiveness

136 small interfering RNA (siRNA) targeting the EGFR gene, with a focus on optimizing complexation effic

137 in Xiphophorus, by assessing mutation of the EGFR gene, Xmrk.