ライフサイエンスコーパス: primary cancer

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

2 t significantly mutated in any type of human primary cancer.

3 patients experience pain at the site of the primary cancer.

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

5 4 men and 24,475 women were diagnosed with a primary cancer.

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

7 mechanically induced pain at the site of the primary cancer.

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

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

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

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

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

13 l failure after prior definitive therapy for primary cancer.

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

15 them resistant to therapies targeted to the primary cancers.

16 ere with survival in relatively benign first primary cancers.

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

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

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

20 stic methods for the evaluation of uncertain primary cancers.

21 cerous morphology, closely mimicking that of primary cancers.

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

23 suppressor that is targeted for mutation in primary cancers.

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

25 g classification problems imposed by unknown primary cancers.

26 ckie-adenovirus receptor expression on human primary cancers.

27 rosatellite instability (MI) associated with primary cancers.

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

29 radiation therapy is the induction of second primary cancers.

30 genomic and transcriptomic heterogeneity of primary cancers.

31 all patients had complete responses of their primary cancers.

32 ing familial clustering with certain defined primary cancers.

33 cations for metastases found at diagnosis of primary cancers.

34 patients had pancreatic NENs, 11 had unknown primary cancer, 6 had midgut NENs, 3 had gastric NENs, a

35 , 635 individuals developed recurrent or new primary cancer, 72 of whom had received anti-TNFalpha th

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

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

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

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

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

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

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

43 ce of initial cancer or development of a new primary cancer after treatment with anti-TNFalpha therap

44 We aimed to analyse the risk of subsequent primary cancers after treatment with carbon ion radiothe

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

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

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

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

49 hat exclude recurrence or progression of the primary cancer and external causes, but include the late

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

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

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

53 003 and 2005 who survived after diagnosis of primary cancer and participated in the biennial national

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 58), 170 (15%) of 1162 probands had multiple primary cancers, and 155 (17%) of 911 families with info

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 hagectomy, gastrectomy, and colectomy) for a primary cancer between 2008 and 2012.

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

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

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

108 Primary cancer cell dissemination is a key event during

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

110 Expression of genes was knocked down in primary cancer cells and pancreatic cancer cell lines by

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

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

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

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

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

116 Metastasis is the process through which the primary cancer cells spread beyond the primary tumor and

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

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

119 aled that cell fitness in cancer cell lines, primary cancer cells, and fibroblasts under unhindered g

120 proliferation, enable in vitro expansion of primary cancer cells, and induce an epithelial-to-mesenc

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

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

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

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

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

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

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

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

129 apy was not associated with recurrent or new primary cancer development in patients with previous can

130 The incidence of recurrent or new primary cancer development was 30.3 cases (95% CI 24.0-3

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

132 diagnosis did not influence recurrent or new primary cancer development.

133 D), rheumatoid arthritis, or psoriasis and a primary cancer diagnosed between Jan 1, 1999 and Dec 31,

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

135 Adult patients (>=18 years of age) with a primary cancer diagnosis (except skin cancer) during at

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

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

138 Age at primary cancer diagnosis and menstrual and reproductive

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

140 t cancer rate decreased 18% every 5 years of primary cancer diagnosis era (rate ratio [RR], 0.82; 95%

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

142 anti-TNFalpha treatment and recurrent or new primary cancer diagnosis was 2.8 years (IQR 1.7-5.4).

143 No other primary cancer diagnosis was associated with an elevated

144 27.3 years (range, 12.2 to 46.0 years) from primary cancer diagnosis was performed.

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

146 sed at age younger than 15 years (matched on primary cancer diagnosis, including leukaemia, lymphoma,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

161 ational profiles consistent with independent primary cancer formation.

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

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

164 697 women) were followed up for diagnoses of primary cancers from January 1, 1994, to December 31, 20

165 When comparing primary cancers from patients with and without metastase

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

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

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

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

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

171 rrence that are not significantly mutated in primary cancers, implicate membrane progesterone signali

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

173 y outcome of development of recurrent or new primary cancer in patients who received anti-TNFalpha th

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

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

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

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

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

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

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

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

182 associated with a higher risk of subsequent primary cancers in patients treated with carbon ion radi

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

184 The risk of subsequent primary cancers in patients with prostate cancer after t

185 s been made between periodontal diseases and primary cancers in the absence of a mechanistic understa

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

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

188 A new primary cancer is a serious late effect of a pre-existin

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

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

191 tern of SPANXB1 was determined using matched primary cancer, lymph node metastatic tissues and circul

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

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

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

195 A second primary cancer more than 1 year after prostate cancer di

196 26% of the US population, to identify first primary cancers (n = 236,850) occurring in persons aged

197 nuation in 6 patients (6%) because of second primary cancers (n = 4) and infection (n = 2).

198 Second primary cancers occurred in 18 patients who received len

199 Thirteen second primary cancers occurred.

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

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

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

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

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

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

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

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

208 Data on primary cancers of the esophagus, stomach, colorectum, l

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

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

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

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

213 ar after diagnosis, (4) occurrence of second primary cancer or death within 1 year or less after diag

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

215 hnology holds promise for early detection of primary cancer or metastasis.

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

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

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

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

220 The primary cancer originated in the lung (n = 17 [39%]), br

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

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

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

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

225 Regional adoption of effective primary cancer prevention strategies has a vast potentia

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

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

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

229 Primary cancer registry data were used to determine whic

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

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

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

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

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

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

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

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

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

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

240 Primary cancer site or ocular tumor features (size, loca

241 Accuracy also varied by primary cancer site, BM volume, and scanner model pairin

242 The ITPP benefits also affected the primary cancer site.

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

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

245 comprehensive data on the risk of subsequent primary cancers (SPCs) among survivors of adult-onset ca

246 Second primary cancers (SPCs) are becoming a common cancer enti

247 ile and vulvar/vaginal cancers and in second primary cancers (SPCs) following these cancers are limit

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

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

250 noma (CRC) invasion, we collected live human primary cancer specimens at the time of surgery and moni

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

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

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

254 ndance and low mutational load found in most primary cancer specimens.

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

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

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

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

259 s associated with a lower risk of subsequent primary cancers than photon radiotherapy (hazard ratio [

260 associated with a higher risk of subsequent primary cancers than surgery (HR 1.18 [1.02-1.36]; p=0.0

261 py appear to have a lower risk of subsequent primary cancers than those treated with photon radiother

262 Primary cancers that expressed ROR1 more commonly expres

263 2.19) in a multivariable model that included primary cancer therapy exposures.

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

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

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

267 tained evDNA and nuclear DNA (nDNA) from the primary cancer tissues of colon cancer patients.

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

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

270 tastatic breast cancer tissues compared with primary cancer tissues.

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

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

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

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

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

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

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

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

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

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

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

282 tively spared from metastasis, regardless of primary cancer type.

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

284 Although the primary cancer was an embryonal rhabdomyosarcoma and the

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

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

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

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

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

290 ncers in the United States, several types of primary cancer were significantly associated with greate

291 234 subsequent primary cancers were diagnosed in the carbon ion radioth

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

293 Over 80,000 first primary cancers were identified for each invasive and in

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

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

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

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

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

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

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