ライフサイエンスコーパス: metachronous

1 ion (synchronous) or after a period of time (metachronous).

2 Lesion development was synchronous and metachronous.

3 Five patients (15.2%) developed metachronous adenocarcinoma at a median of 6 years (rang

4 reduction in the odds of any and nonadvanced metachronous adenoma after adjustment for baseline adeno

5 nor was any single SNP in VDR related to any metachronous adenoma after correction for multiple compa

6 elation coefficients <0.2) between unrelated metachronous adenoma-cancer pairs.

7 was found for any single SNP and the odds of metachronous adenoma.

8 ively) having an 89% lower odds for advanced metachronous adenomas (OR, 0.11; 95% CI, 0.01-0.80) when

9 elated to most histologic characteristics of metachronous adenomas among men but not among women.

10 uence in the APC gene and individual risk of metachronous adenomatous polyps.

11 and 100 histologically proven synchronous or metachronous adenomatous polyps.

12 Risk of a metachronous advanced adenoma was higher among patients

13 plasia was not associated independently with metachronous advanced neoplasia after adjustment for oth

14 ted significantly with an increased risk for metachronous advanced neoplasia, as were the number and

15 We evaluated 13 cases of metachronous and 23 cases of synchronous primary and met

16 noma, 1 with sebaceous carcinoma, and 1 with metachronous bilateral lymphomas were treated.

17 The risk of metachronous breast cancer is low in patients with known

18 e patients who presented with synchronous or metachronous breast plus colorectal cancer.

19 One patient died of metachronous cancer after STC.

20 olorectal cancer risk approaching 80%, and a metachronous cancer rate of approximately 25%.

21 , given the mentioned increased frequency of metachronous cancer.

22 uent high-risk adenomas and 3 (8%) developed metachronous cancer.

23 ciated with a genetic defect, synchronous or metachronous cancers in the same individual, growth abno

24 Stages of the metachronous cancers were I-16, II-18, III-12, and IV-2.

25 ave increased risk of developing synchronous/metachronous cancers, including nonhematologic and hemat

26 ncludes a history of multiple synchronous or metachronous cancers.

27 5)] but saw no absolute reduction in risk of metachronous CBC (MCBC).

28 d 341 patients who underwent hepatectomy for metachronous CLM (disease-free interval >/=12 months, 19

29 er patients treated with liver resection for metachronous CLM after adjuvant FOLFOX for CRC have wors

30 and inferior outcomes after hepatectomy for metachronous CLM.

31 nomas in situ, pseudomelanosis coli, and two metachronous colon cancers.

32 Metachronous colorectal adenoma and carcinoma developmen

33 ) in the APC gene and the odds of developing metachronous colorectal adenomas as a surrogate measure

34 213 participants in 7 prospective studies of metachronous colorectal adenomas were pooled to assess w

35 support for the association between BMI and metachronous colorectal adenomas, particularly among men

36 We hypothesized that metachronous colorectal liver metastases (CLM) have diff

37 202 small (0.8-4.0 cm; mean: 2.2 cm +/- 1.1) metachronous colorectal liver metastases underwent ultra

38 chieved local control in a large majority of metachronous colorectal liver metastases.

39 icate that allelic variation in RXRA affects metachronous colorectal neoplasia, perhaps of particular

40 tions in RXRA and VDR and odds of recurrent (metachronous) colorectal neoplasia in a pooled populatio

41 nt anti-CD4 therapy; and (2) simultaneous or metachronous combined liver-heart and kidney-heart trans

42 HL survivors had an increased risk of metachronous contralateral breast cancer (adjusted hazar

43 The incidence of metachronous contralateral RCC is stable on long-term fo

44 ease, either at diagnosis (nine of 53) or as metachronous contralateral recurrence (two of 53).

45 etermine the observed and expected number of metachronous contralateral renal tumors developing after

46 was 89.2%, and the 2-year cumulative risk of metachronous contralateral WT was 3.1%.

47 The 2-year disease-free (relapse and metachronous contralateral WT) survival rate was 86.5%.

48 2-year disease-free survival rate (excluding metachronous contralateral WT) was 89.2%, and the 2-year

49 isk of relapse, including the development of metachronous contralateral WT, of 13.5% 2 years after di

50 Three patients developed metachronous, contralateral WT 1.1, 1.4, and 2.3 years a

51 50SerfsTer23), a 39-year old individual with metachronous CRC (p.Leu61GlufsTer11 mutation), and a 41-

52 The rates of metachronous CRC and of rectal cancer were evaluated, to

53 s of hepatic metastasectomy in patients with metachronous CRC liver metastases.

54 -effective option for selected patients with metachronous CRC metastases limited to the liver.

55 The risk of death in patients with metachronous CRC was 6-fold increased.

56 l survival between patients with and without metachronous CRC were evaluated using a time-dependent C

57 clearing and for postoperative prevention of metachronous CRC, specific considerations for the detect

58 Seventeen patients (26.2%) had metachronous CRC.

59 ia carry a high risk of rectal cancer and of metachronous CRC.

60 s associated with a significant reduction in metachronous CRC.

61 Synchronous and metachronous CRCs are extremely common.

62 The results were correlated with metachronous distant metastasis risk (n = 22 patients).

63 ICD insertion is indicated in CABG patients, metachronous endocardial implantation should be consider

64 Five H/DC tumors were metachronous, following FL by 2 months to 12 years; tumo

65 hronous group were younger than those in the metachronous group (median age 54 v 68 years).

66 patent processus vaginalis and contralateral metachronous hernia development in children justify the

67 rgoing partial colectomy have a high rate of metachronous high-risk adenomas and carcinomas.

68 not present at the initial diagnosis, termed metachronous hormonal syndromes (MHSs).

69 Metachronous hormonal syndromes developed after a median

70 Metachronous hormonal syndromes were identified more oft

71 onoscopy significantly increased the risk of metachronous HRA compared to the reference group (no ind

72 eased risk of metachronous large SPs but not metachronous HRA.

73 colonoscopy significantly increased risk of metachronous HRA.

74 71 (relative increase = 70%), contralateral metachronous IHR decreased from 29 to 11 (RR = 62%), and

75 The egg cytoplasm, therefore, is metachronous in terms of cell-cycle progression; multipl

76 cancer was 77% (several deaths secondary to metachronous invasive cancer), compared with 43% in thos

77 eas 5 (15%) developed clinically significant metachronous IPMNs.

78 dex STSA with no index HRA increased risk of metachronous large SPs but not metachronous HRA.

79 ignificantly associated with the odds of any metachronous lesion among men (odds ratio = 1.36, 95% co

80 try to evaluate risk of clinically important metachronous lesions associated with SPs detected during

81 For those with metachronous lesions liver lesions, the median time inte

82 Metachronous lesions or recurrence of cancer developed d

83 rge SPs (>1 cm) on surveillance colonoscopy (metachronous lesions).

84 history, colorectal subsite, or features of metachronous lesions.

85 reduction in odds was observed for advanced metachronous lesions.

86 py should be performed in 1 year to look for metachronous lesions.

87 an gastric mucosa in either a synchronous or metachronous manner.

88 ynchronous (LS-group)], and (3) resection of metachronous metastases >14 months after resection of th

89 nt reduction in the expression of p27 in the metachronous metastases (mean positive cells: 14.5%) whe

90 ma, we observed that cell lines derived from metachronous metastases arising over a decade retained a

91 ors from patients with either synchronous or metachronous metastases than those who were disease-free

92 paration of outcomes between synchronous and metachronous metastases were excluded.

93 ere from patients with either synchronous or metachronous metastases.

94 ients had synchronous metastases and 58% had metachronous metastases.

95 with synchronous metastasis than those with metachronous metastasis (12 months v 31 months, generali

96 apse (p = 0.02), and increased likelihood of metachronous metastasis (p = 0.001), including after sta

97 Development of metachronous metastasis is assumed to be governed largel

98 er median overall survival than those with a metachronous metastasis.

99 actor receptor (EGFR) somatic aberrations in metachronous multiple lung cancers to differentiate mult

100 Ninety-seven metachronous multiple lung cancers were identified to in

101 on rate of tumor clonality (77.3%; 75/97) in metachronous multiple lung cancers.

102 nts need to be aware of substantial risk for metachronous neoplasia after proctectomy.

103 rt an approximately 30% reduction in odds of metachronous neoplasia arising in the proximal colon amo

104 sess whether the association between BMI and metachronous neoplasia varied by these factors.

105 tion between RXRA SNP rs7861779 and proximal metachronous neoplasia was of borderline statistical sig

106 RA and any (P = 0.04) or proximal (P = 0.03) metachronous neoplasia.

107 cancer are at risk for recurrent cancer and metachronous neoplasms in the colon.

108 ity state of TAC (relative to SEG), rates of metachronous occurrence, and stage of cancer at the time

109 patients with NSCLC with those identified in metachronous or synchronous metastases.

110 ntify distinct mechanisms for development of metachronous or synchronous neoplasms in patients with I

111 For 11 patients who developed metachronous OS 24 months or more from initial diagnosis

112 iagnosis of primary OS to the development of metachronous OS was 1.4 years (range, 0.2 to 11.3 years)

113 small subset of patients who developed late metachronous OS, combined-modality therapy with surgery

114 Only 2 patients (0.5%) developed metachronous PDAC.

115 , a solitary site of first metastasis, and a metachronous presentation with recurrence.

116 ients undergoing total colectomy developed a metachronous rectal cancer (18.2%).

117 entified in synchronous nodal metastases and metachronous recurrent tumors, respectively, were transm

118 ar to their paired index primary tumors than metachronous recurrent tumors.

119 s lymph node metastases and 10 patients with metachronous recurrent tumors.

120 on reports of a high incidence of apparently metachronous second cancers in the first 2 years after r

121 We investigated the incidence and outcome of metachronous skeletal OS after initial treatment of the

122 mary OS may be applied to patients with late metachronous skeletal OS.

123 The prognosis for patients who develop metachronous skeletal osteosarcoma (OS) has been conside

124 significantly increased the risk of a large metachronous SP.

125 imary cancer diagnosis), and subsequent (ie, metachronous) stage-specific CBC occurrences in women wh

126 All the primary and metastatic tumors in the metachronous subgroup showed high levels of p27 mRNA exp

127 In the metachronous subgroup, 54% of the primary tumors were lo

128 r bed (n = 4), and abdomen (n = 2), with one metachronous tumor in the contralateral kidney (n = 1) a

129 erations at GC-rich regions of the genome in metachronous tumors and their derived cell lines from tw

130 umors were present in 33 patients (22%), and metachronous tumors developed in an additional 14 patien

131 ranscriptome, and deep-focused sequencing of metachronous tumors from 29 patients initially diagnosed

132 Because most metachronous tumors of the same histologic type have dif

133 tic analysis revealed a common origin of the metachronous tumors, with a higher proportion of clonal

134 ancer or adenoma because of the high rate of metachronous tumors.

135 y of multifocal IPMNs (86% synchronous, 100% metachronous) were composed of branch duct lesions, and