ライフサイエンスコーパス: primary cancer

1 ncer types (first cancer, recurrence, second primary cancer).

2 4 men and 24,475 women were diagnosed with a primary cancer.

3 , of whom 1,088 were diagnosed with a second primary cancer.

4 an: 4.7 years), 279 women developed a second primary cancer.

5 agnosis of primary cancer, and SEER stage of primary cancer.

6 data base, 114 patients were identified with primary cancer.

7 ustifying its use in patients with high-risk primary cancer.

8 a matter of stage and adequate treatment of primary cancer.

9 l failure after prior definitive therapy for primary cancer.

10 r recurrence, and 57 (2%) developed a second primary cancer.

11 he CRLM, and the subsequent resection of the primary cancer.

12 s known about its effect on risk of multiple primary cancers.

13 ive risks of second primary cancers as first primary cancers.

14 stic methods for the evaluation of uncertain primary cancers.

15 cerous morphology, closely mimicking that of primary cancers.

16 ls than Skp2 in breast cancer cell lines and primary cancers.

17 suppressor that is targeted for mutation in primary cancers.

18 itions such as obesity, diabetes, and second primary cancers.

19 all patients had complete responses of their primary cancers.

20 g classification problems imposed by unknown primary cancers.

21 ckie-adenovirus receptor expression on human primary cancers.

22 rosatellite instability (MI) associated with primary cancers.

23 ted to be overexpressed in a number of human primary cancers.

24 ing familial clustering with certain defined primary cancers.

25 cations for metastases found at diagnosis of primary cancers.

26 them resistant to therapies targeted to the primary cancers.

27 ng suggestion of an increased risk of second primary cancers.

28 ases in the recurrent cancer relative to the primary cancer, a characteristic which may parallel the

29 ncer resulted in retarded progression of the primary cancer, a reduced metastatic load, and prolongat

30 eveloped countries can now be cured of their primary cancer--a remarkable achievement for a childhood

31 is patient was also diagnosed with two other primary cancers: a synchronous lobular breast carcinoma

32 IP% significantly increased as SEER stage of primary cancer advanced for all primary sites.

33 ively) and recipients who developed a second primary cancer after transplantation (aHRs, 1.01; 95%CI,

34 ients with cancer recurrence and/or a second primary cancer after transplantation are unknown.

35 However, whether and how primary cancer alters T cell glycolytic metabolism and a

36 try were used to evaluate the risk of second primary cancers among a retrospective population-based c

37 s a critical step in the development of both primary cancer and advanced-stage disease.

38 In patients who have been treated for a primary cancer and are judged to be at high risk of a co

39 bservations of prognostic gene signatures in primary cancer and how tumor growth can both lead to met

40 change in the expression of 14 genes in the primary cancer and liver metastasis compared with normal

41 T12/24) weeks of age, and the development of primary cancer and metastatic disease was compared to no

42 Median interval between primary cancer and SMN was 5 years (range, <1 to 35 year

43 s represent a potential common nidus for the primary cancer and the recurrent cancer that arises afte

44 n expression is detected in situ in 14 of 14 primary cancers and 14 of 16 metastatic sites of human p

45 gulated in ACC by immunohistochemistry of 28 primary cancers and 20 normal tissues.

46 KAI1 were analyzed using a tissue bank of 98 primary cancers and 32 metastases.

47 has been found to be mutated in a number of primary cancers and cancer-derived cell lines.

48 nce significant excesses of death from other primary cancers and cardiac disease.

49 trials yielded rate ratios (RRs) for second primary cancers and cause-specific mortality and excess

50 of follow-up, the AER for deaths from second primary cancers and circulatory causes increased from 8

51 xcess number of deaths observed while second primary cancers and circulatory deaths together accounte

52 ildhood cancer, excess mortality from second primary cancers and circulatory diseases continued to oc

53 edoxin is overexpressed by a number of human primary cancers and its expression is decreased during d

54 trials, possibly due to TRAIL-resistance of primary cancers and its inherent short half-life.

55 environment (soil) promoting growth of both primary cancers and metastases (seeds).

56 g tumor cells (CTC) released into blood from primary cancers and metastases reflect the current statu

57 o poorly differentiated and undifferentiated primary cancers and metastatic tumors.

58 ected CD133 on ovarian cancer cell lines, in primary cancers and on purified epithelial cells from as

59 on and resorption, suggesting a link between primary cancers and the bone microenvironment prior to m

60 g cell differentiation but down-regulated in primary cancers and transformed cell lines.

61 tations or methylation in GATA genes both in primary cancers and tumor lines including breast.

62 ata after bisulfite treatment indicated that primary cancers and two cell lines with loss of expressi

63 utations occur in human tumor cell lines and primary cancers , and Fbw7 loss in cultured cells causes

64 urring tumor dormancy precedes occurrence of primary cancer, and (ii) conventional cancer therapies r

65 ted clonal deletion, reduced the size of the primary cancer, and completely prevented metastasis late

66 utcomes are breast cancer recurrence, second primary cancer, and death.

67 usive (and competing) outcomes: CRC, another primary cancer, and death.

68 dition, RNA was extracted from normal colon, primary cancer, and liver metastasis in a patient with m

69 CI), site and lymph node involvement (pN) of primary cancer, and postoperative chemotherapy.

70 primary site, race, sex, age at diagnosis of primary cancer, and SEER stage of primary cancer.

71 (by trial centre) and minimisation (by age, primary cancer, and sex) with allocation concealment.

72 of interest (race, sex, age at diagnosis of primary cancer, and Surveillance, Epidemiology, and End

73 58), 170 (15%) of 1162 probands had multiple primary cancers, and 155 (17%) of 911 families with info

74 with multiple gene abnormalities had second primary cancers, and an additional patient had multifoca

75 ecurrence sites, time of relapse, subsequent primary cancers, and causes of death in the natural hist

76 Distant metastases, second primary cancers, and deaths before LRR were censored.

77 died of recurrent cancer, two died of second primary cancers, and four died of other causes.

78 e breast cancer (TNBC) lines and dissociated primary cancers, and in lung cancer lines.

79 Improvement of all primary cancer- and anemia-specific QOL domains, includi

80 history of malignancy, recurrent and second primary cancers are infrequent after renal transplantati

81 ormal tissue, heterozygous variants found in primary cancers are often subtle and difficult to detect

82 enal cell carcinoma (RCC) is the most common primary cancer arising from the kidney in adults, with c

83 back-Liebler divergence associated with each primary cancer as compared with data for all cancer type

84 onfers equally high relative risks of second primary cancers as first primary cancers.

85 lance and screening for recurrence or second primary cancers, assessment and management of long-term

86 east cancer recurrence, screening for second primary cancers, assessment and management of physical a

87 Hepatocellular carcinoma (HCC) is a common primary cancer associated frequently with hepatitis C vi

88 found that compared with normal fibroblasts, primary cancer-associated fibroblasts (CAF) and fibrobla

89 in vitro studies indicated that exposure of primary cancer-associated fibroblasts to MEDI-575 can di

90 at might have originally been present in the primary cancer at low frequency but that have expanded u

91 of metastatic colorectal cancer with that of primary cancers, benign colorectal tumors, and normal co

92 Ten long-term CR patients developed second primary cancers: breast (3), ovary (2), pancreas (1), en

93 luciferase reporter model, the growth of the primary cancer can be followed noninvasively by biolumin

94 ion due to 4HPR exposure compared with their primary cancer cell counterparts.

95 Primary cancer cell dissemination is a key event during

96 t occur at the DNA methylation level between primary cancer cells and metastases.

97 crofluidic cultures of difficult-to-maintain primary cancer cells as a useful tool for precision canc

98 cause a number of studies have reported that primary cancer cells express only low levels of CAR, our

99 Current attempts to culture these primary cancer cells focus on long-term maintenance unde

100 mechanism is clinically significant, because primary cancer cells from patients with metastatic RCC s

101 tifying genes and pathways that modulate how primary cancer cells respond to targeted therapeutics an

102 ransfer their amoeboid phenotype to isogenic primary cancer cells through exosomes, and that this mor

103 a before reverse-engineering the response of primary cancer cells to a proliferative (protumorigenic)

104 The method is validated in cell lines and in primary cancer cells, and may have potential application

105 regulation of CDK2 to TGF-beta resistance in primary cancer cells, and they suggest that disruption o

106 e in cells, and its pattern of expression in primary cancer cells.

107 genes is proposed to be a common feature of primary cancer cells.

108 g poorly differentiated and undifferentiated primary cancers chosen to resemble those that present as

109 In addition, the primary cancers could be propagated in nude mice or nont

110 In breast lines and primary cancer culture, VEGFA rapidly upregulates SOX2 e

111 rom 2 months until the diagnosis of a second primary cancer, death, loss to follow-up, or December 31

112 ignant cells at the primary site, leading to primary cancer development, and at distant sites, leadin

113 on of CHC burden in survivors with differing primary cancer diagnoses was observed.

114 lated myeloid neoplasms at the time of their primary cancer diagnosis and before they have been expos

115 lated myeloid neoplasms at the time of their primary cancer diagnosis and before they have been expos

116 Age at primary cancer diagnosis and menstrual and reproductive

117 ncer incidence was evaluated with respect to primary cancer diagnosis and therapy, age at and time si

118 The mean interval from primary cancer diagnosis to retinal metastasis was 63 mo

119 No other primary cancer diagnosis was associated with an elevated

120 27.3 years (range, 12.2 to 46.0 years) from primary cancer diagnosis was performed.

121 essed overall, synchronous (< 6 months after primary cancer diagnosis), and subsequent (ie, metachron

122 risks of neurologic sequelae > 5 years after primary cancer diagnosis, including seizures (HR, 10.0;

123 gnosis and peripheral blood from the time of primary cancer diagnosis.

124 es ranging from 11 months to 9 years after a primary cancer diagnosis.

125 h remained confined within the ducts so that primary cancer did not develop.

126 re categorized according to whether they had primary-cancer-directed surgery (CDS) or no CDS within 4

127 from the structure recently reported for the primary cancer DNA phenotype.

128 duals with cancer for the early detection of primary cancers, early detection of cancer relapse, moni

129 Following treatment of the primary cancer, emotional and psychosocial factors withi

130 bserved significant increases in risk of the primary cancer endpoint.

131 ynthesized and evaluated in vitro in a human primary cancer explant assay.

132 PCPs, expectations were most incongruent for primary cancer follow-up (agreement rate, 35%), with PCP

133 In the case of primary cancer follow-up, both PCPs and oncologists indi

134 dances in perceptions of their own roles for primary cancer follow-up, cancer screening, and general

135 tations regarding physician participation in primary cancer follow-up, screening for other cancers, g

136 ational profiles consistent with independent primary cancer formation.

137 different PDX groups obtained by implanting primary-cancer fragments harvested from patients into mi

138 patients alive, recurrence-free, and second primary cancer-free (disease-free survival [OS|DFS]).

139 697 women) were followed up for diagnoses of primary cancers from January 1, 1994, to December 31, 20

140 When comparing primary cancers from patients with and without metastase

141 cer cell lines and in more than 50% of human primary cancers from various tissues.

142 in vitro models that accurately reflect the primary cancers from which they are derived.

143 ce of the following brain cancer cell lines: primary cancers (glioblastoma multiforme and neuroblasto

144 In breast cancer, Akt1 induces primary cancer growth, but is reported to inhibit metast

145 ed tumors were more likely to develop second primary cancers (HR = 2.76, 95% CI, 1.34 to 5.70; P = .0

146 nce imaging correctly identified residual or primary cancer in 55 of 58 cases and accurately predicte

147 taging, PET/CT aided in the detection of the primary cancer in patients with metastatic uveal tumors.

148 ngs, matching metastatic location in CUP and primary cancer in relatives, could be reconciled if thes

149 st cancer will subsequently develop a second primary cancer in the contralateral breast.

150 Seven (12%) patients developed a new primary cancer in the contralateral breast.

151 noma (ICC) is the second most common type of primary cancer in the liver.

152 However, the incidence of a second primary cancer in transplanted patients has never been s

153 retinoids prevent the development of second primary cancers in head/neck and lung cancer patients wh

154 Do second primary cancers in humans arise from radiation-induced s

155 screening for cardiac disease and subsequent primary cancers in patients with HL-BC is warranted.

156 ing tumour cells (CTCs) shed into blood from primary cancers include putative precursors that initiat

157 or diagnosis of suspected cancer (or unknown primary cancer), initial cancer staging, restaging, and

158 occur during malignant dormancy even before primary cancer is clinically detectable; and (iii) chron

159 resent and maintain the genetic diversity of primary cancers is uncertain.

160 Parallel laboratory studies using primary cancer material for which endocrine response is

161 er a single miRNA can regulate metastasis in primary cancer models in vivo.

162 irect intratumoral injection in a variety of primary cancer models.

163 26% of the US population, to identify first primary cancers (n = 236,850) occurring in persons aged

164 Second primary cancers occurred in 18 patients who received len

165 Thirteen second primary cancers occurred.

166 DNA methylation profiling predicted a primary cancer of origin in 188 (87%) of 216 patients wi

167 r in prostatic intraepithelial neoplasia and primary cancer of prostate, some others occur in late st

168 or more adenomas, number with more than one primary cancer of the colorectum or endometrium, and mea

169 Uveal melanoma is the most common primary cancer of the eye and often results in fatal met

170 Intrahepatic cholangiocarcinoma (ICC) is a primary cancer of the liver that is increasing in incide

171 Intrahepatic cholangiocarcinoma (IHCC) is a primary cancer of the liver with an increasing incidence

172 Hepatocellular carcinoma, the most common primary cancer of the liver, results in significant morb

173 standing conundrum on the cell of origin for primary cancers of the brain.

174 Aberrant methylation of TIMP-3 occurred in primary cancers of the kidney, brain, colon, breast, and

175 d 14,048 participants diagnosed with a first primary cancer, of whom 1,088 were diagnosed with a seco

176 Contaminating normal stromal cells of primary cancers often limit mutational analyses.

177 ease progression or the development of a new primary cancer or death assessed at 4.5 years after rand

178 y tumor, and not from the bulk, higher-grade primary cancer or from a lymph node metastasis resected

179 orrelate with age, surgical treatment of the primary cancer, or chemotherapy.

180 arch 15, 2005, 394 events (recurrent, second primary cancer, or death before recurrence) had been rep

181 urrence at other sites, occurrence of second primary cancer, or death resulting from noncancer causes

182 ime from randomization to recurrence, second primary cancer, or death.

183 igens as each was shared among human ovarian primary cancers, ovarian cancer cell lines, and normal f

184 us ovarian cell lines and tissues, including primary cancers, ovarian surface epithelia cells, and cy

185 ncer should be carefully screened for second primary cancers, particularly for cancers that are radia

186 in cancer cell line populations compared to primary cancer populations.

187 andomized, double-blind, placebo-controlled, primary cancer prevention trial; participants were Finni

188 s, and implementation of policies to improve primary cancer prevention.

189 Hospice use varied by type of primary cancer ranging from 31.8% of patients with pancr

190 The rate of patients undergoing palliative primary cancer resection decreased from 68.4% in 1998 to

191 The benefit of palliative primary cancer resection persisted during the time perio

192 ion analysis after propensity score matching primary cancer resection was associated with a significa

193 In contrast, CD133+ cells in primary cancer samples showed a unique genomic aberratio

194 ng genetic and functional data in studies of primary cancer samples, both in xenograft models and in

195 er mutational load in metastatic compared to primary cancer samples, however, after correction for mu

196 ns of the B-MYB gene in human cell lines and primary cancer samples, we frequently isolated two nonsy

197 variants in a Final Model containing age at primary cancer, sex, and cranial radiation therapy dose

198 ial exposures who are diagnosed with a first primary cancer should be carefully screened for second p

199 or more), gender, number of hepatic tumors, primary cancer site (colon vs. rectum), and age, the nom

200 The ITPP benefits also affected the primary cancer site.

201 tion, PET has the advantage of assessing the primary cancer sites and detecting other metastases.

202 We investigated the incidence of a second primary cancer (SPC) in 7,636 patients who underwent a k

203 tigating the distribution and risk of second primary cancers (SPCs) in multiple myeloma (MM) survivor

204 iple human cancer cell lines and dissociated primary cancer specimens and NK transfer in NSG mice har

205 n cancer cell lines in vitro and dissociated primary cancer specimens ex vivo.

206 expression is decreased in mesenchymal-like primary cancer specimens in vivo and following induction

207 reased with activation of the ERK pathway in primary cancer specimens in vivo and in cancer cell line

208 included as cases if they were treated for a primary cancer, subsequently developed therapy-related m

209 ecreasing the probability of eradicating the primary cancer, substantially increase the risk of later

210 ions that these miRNAs are underexpressed in primary cancers support the idea that miR-192 and miR-21

211 linical trial (patients scheduled to undergo primary cancer surgery are treated briefly with an inves

212 Primary cancers that expressed ROR1 more commonly expres

213 However, it is unknown whether changes in primary cancer therapy have improved rates of long-term

214 kocyte infusions (DLIs) were administered as primary cancer therapy in a phase I trial to determine (

215 he rates of treatment-related deaths, second primary cancers, thromboembolic events, and peripheral n

216 measure the impact of targeted inhibition on primary cancer tissues.

217 f the promoter as a cancer-specific event in primary cancer tissues.

218 tastatic breast cancer tissues compared with primary cancer tissues.

219 f collagen expression and also methylated in primary cancer tissues.

220 n of 24.0 years (range, 10 to 34 years) from primary cancer to breast cancer.

221 The median interval from primary cancer to meningioma diagnosis was 22 years (5 t

222 evolution of the lethal cell clone from the primary cancer to metastases through samples collected d

223 tcome of patients who had resection of their primary cancer to those who did not.

224 Measures were repeated 6 and 18 months after primary cancer treatment (cancer survivors) or within a

225 How early translocations appear during primary cancer treatment has not been investigated.

226 LL gene translocations are a complication of primary cancer treatment with DNA topoisomerase II inhib

227 hich providers handle their care needs after primary cancer treatment.

228 astatic disease and in four of the high-risk primary cancer trials, albeit with no impact on overall

229 is not a surrogate of local tumor invasion, primary cancer type, or aggressive phenotype and is asso

230 The primary outcome was the detection of new primary cancers using FDG-PET/CT scanning.

231 Although the primary cancer was an embryonal rhabdomyosarcoma and the

232 The incidence of second primary cancers was 3.1 per 100 patient-years in the len

233 estimated detection rate for new, localized primary cancers was 7% (95% CI, 5%-9%).

234 pidemiology, and End Results [SEER] stage of primary cancer) was calculated with 95% CIs.

235 e survival (with events that included second primary cancers) was significantly improved with lenalid

236 hology, size and number of polyps, and other primary cancers) was used in conjunction with age at ons

237 Colon cancer cell lines and primary cancers were examined for mutations in HDAC2 by

238 ation exposure and risks of first and second primary cancers were quantified using Poisson regression

239 d similar pooled incidence values for new or primary cancers when immunosuppression was initiated wit

240 The primary cancers, which included 11 solid tumors and eigh

241 y metastases, particularly in the setting of primary cancer with a known tendency to metastasize to t

242 inferior treatment of favorable stage early primary cancer with worsened survival.

243 as strikingly similar between cell lines and primary cancers with a few obvious exceptions such as lo

244 e hundred five women (12.8%) developed other primary cancers, with 49 (46.6%) occurring in the contra