ライフサイエンスコーパス: cancer

1 /= 65 years who reported a history of breast cancer.

2 creen individuals for the early diagnosis of cancer.

3 eptor mutations and metastasis in colorectal cancer.

4 nd the death rate was second to that of lung cancer.

5 ndpoint in patients with advanced colorectal cancer.

6 diseases, including metabolic disorders and cancer.

7 t-tissue sarcoma, and central nervous system cancer.

8 ndent diseases like endometriosis and breast cancer.

9 strategy to target mutant p53 in pancreatic cancer.

10 e molecular scale, to more effectively study cancer.

11 e for non-Hodgkin lymphoma and melanoma skin cancer.

12 time of patients with metastatic colorectal cancer.

13 poor oral hygiene, tobacco smoking, and oral cancer.

14 s, such as ciliopathies and certain types of cancer.

15 tous carcinogen in sunlight that causes skin cancer.

16 bsequent neoplasms in survivors of childhood cancer.

17 to evaluate statin therapy in patients with cancer.

18 s in patients with early TOP2A-normal breast cancer.

19 ny diseases such as myelodysplasia (MDS) and cancer.

20 al methylation in human diseases, especially cancer.

21 ent tumor-suppressive and oncogenic roles in cancer.

22 diseases, as well as several other types of cancer.

23 al gatekeepers in common forms of intestinal cancer.

24 progression in an aggressive model of breast cancer.

25 percentile vs.<25th percentile) and bladder cancer.

26 ial therapeutic target for metastatic breast cancer.

27 contribute to aging, neurodegeneration, and cancer.

28 responding to treatment in advanced gastric cancer.

29 ired resistance to platinum drugs in ovarian cancer.

30 2nd Hit) transforms the expanding clone into cancer.

31 for the involvement of this region in breast cancer.

32 spectively, and 82% had stage I or II breast cancer.

33 vel regulatory mechanism in human pancreatic cancer.

34 Diagnosis with favorable-risk prostate cancer.

35 hemically in patients with metastatic breast cancer.

36 of pelvic drainage after rectal surgery for cancer.

37 recurrent cancer and 27 (10.5%) from de novo cancer.

38 tes modulated in certain types of colorectal cancers.

39 enetic marker for guiding therapy of certain cancers.

40 tic potential of targeting Nck in aggressive cancers.

41 of liver metastasis derived from colorectal cancers.

42 rd to classification of active compounds for cancers.

43 e and constituted <10% of all reported liver cancers.

44 patients with metastatic prostate or breast cancers.

45 treat colorectal and other gastrointestinal cancers.

46 educe the observed disparities for digestive cancers.

47 for clinical imaging of other hematological cancers.

48 vival [OS], 69%), followed by basal prostate cancers (10-year bRFS, 39%; DMFS, 73%; PCSS, 86%; OS, 80

49 ; PCSS, 86%; OS, 80%) and luminal A prostate cancers (10-year bRFS, 41%; DMFS, 73%; PCSS, 89%; OS, 82

50 disease (41 patients, 182 scans), colorectal cancer (70 patients, 286 scans), melanoma (69 patients,

51 In 13 breast cancers, 8 had a low binding (mean density, 844 +/- 168

52 melanoma (69 patients, 271 scans), and lung cancer (84 patients, 286 scans).

53 The primary tumors were breast cancer (92 patients, 426 scans), non-Hodgkin lymphoma (7

54 y-stage disease (American Joint Committee on Cancer [AJCC] stage 0, I, or II), and 48 (51.6%) were di

55 6 recipients died, 35 (13.7%) from recurrent cancer and 27 (10.5%) from de novo cancer.

56 mutated in 7.6% (484 of 6353) of colorectal cancer and 9.1% (29 of 317) of SBA samples, but V600E mu

57 ign, important for managing diseases such as cancer and Alzheimer's disease.

58 re we adopt this powerful approach to breast cancer and analyse 515 cells from 11 patients.

59 rategies, to the most recent applications in cancer and inflammation management, including therapeuti

60 data uncover a direct role for RANK in lung cancer and may explain why female sex hormones accelerat

61 ence of breast cancer was the highest of any cancer and the death rate was second to that of lung can

62 ivor is open to debate by people living with cancer and those caring for them.

63 tion of the genomic landscape of a patient's cancer and, ideally, the ability to monitor therapy-indu

64 omplex genomic rearrangements (CGRs) in many cancers and various congenital disorders in humans.

65 ctivity of adoptively transferred polyclonal cancer antigen-reactive T cells deficient in the regulat

66 ance cue receptor DCC (deleted in colorectal cancer) appear to confer resilience or susceptibility to

67 and rarer cancers, with breast and prostate cancer as baseline categories for women and men, respect

68 ecurrence remains the main reason for breast cancer-associated mortality, and there are unmet clinica

69 actors that alone or in combination increase cancer-associated thrombosis.

70 nt solutions to benefit patients with breast cancer at high risk of recurrence.

71 n CHCs in all patients treated for childhood cancer at the St Jude Children's Research Hospital who s

72 Breast cancer (BC) has a higher incidence in young Lebanese wom

73 The study of both cancer-bearing mouse models in wild types and their corr

74 years when diagnosed with localized prostate cancer between October 1994 and October 1995 in one of s

75 016, as part of the Reproducibility Project: Cancer Biology, we published a Registered Report, that d

76 sitive electrochemical detection of a breast cancer biomarker microRNA (miRNA), mir-21 was achieved v

77 as the age-adjusted incidence of HPV-related cancer (both cervical and non-cervical) in all women in

78 anscription factors (TF) is a key feature of cancer, but its global influence on drug sensitivity has

79 at drives progression of many types of human cancer, but the basis for its actions remains obscure.

80 pressor or as an oncogene in different human cancers, but direct evidence for its role in tumorigenes

81 ing the tumor suppression function of p53 in cancer by dual targeting of the negative regulators HDM2

82 egies to prevent cancer metastasis in breast cancer cases.

83 P NPs are able to induce efficient apoptotic cancer cell death both in vitro and in vivo through tumo

84 sphorylation-mediated LDHA activity promotes cancer cell invasion and anoikis resistance through redo

85 Cancer cell invasion from primary tumors is mediated by

86 The metabolic phenotype of a cancer cell is determined by its genetic makeup and micr

87 iNVICT on simulated data as well as prostate cancer cell lines and cfDNA obtained from castration-res

88 noxide (CO) reduced GSH/GSSG in three breast cancer cell lines by inhibiting CBS.

89 have analyzed a panel of 17 KRAS mutant lung cancer cell lines classified as K-Ras-dependent or -inde

90 s to suppress let-7 target genes in multiple cancer cell lines such as HMGA2 and MYC.

91 nalyzed the proteomes of 10 human pancreatic cancer cell lines to a depth of >8,700 quantified protei

92 ial-mesenchymal transition in human prostate cancer cell lines, and stable overexpression of miR-194

93 wound closing in three types of immortalized cancer cell lines.

94 -refractory papillary and follicular thyroid cancer cell lines.

95 ive tool for exploring the thermodynamics of cancer cell migration and invasion.

96 This also induced PC3 cancer cell motility and increased colony size in 2D cul

97 In this issue of Cancer Cell, Chen et al. describe complementary approach

98 ity mostly (if not only) as a consequence of cancer cell-intrinsic effects.

99 lso inhibit endothelial phenotypes of breast cancer cells adopted in response to a nutrient-deficient

100 Here, we first demonstrated that breast cancer cells and pancreatic adenocarcinoma cells generat

101 nd to what extent TRAIL/TRAIL-R signaling in cancer cells can affect the immune microenvironment.

102 -kappaB, Bcl-2 and p53) in these NPs-treated cancer cells compared to 5-fluorouracil (5-FU) treated c

103 ration typical of most tissues, we find that cancer cells depend on high levels of the iron-sulfur cl

104 Previously, we found that in cancer cells derived from pancreatic ductal adenocarcino

105 The effect of the G4-ligands on Panc-1 cancer cells has also been examined.

106 studies with orthotopically injected breast cancer cells in wild-type and RAGE-knockout C57BL6 mice.

107 Invasive cancer cells interact with the surrounding extracellular

108 l conditions, maintained mTORC1 signaling in cancer cells promotes survival by suppressing endogenous

109 vides a better understanding of how prostate cancer cells respond heterogeneously to androgen depriva

110 tumorigenesis, the high metabolic demand of cancer cells results in increased production of reactive

111 Cancer cells share several metabolic traits, including a

112 e the unique transhesive profiles for breast cancer cells that are adapted to colonize different meta

113 rtially permissive for the majority of human cancer cells that harbor defects in antiviral signaling,

114 Herein we show in a diverse array of human cancer cells that IMP2 overexpression stimulates and IMP

115 may inhibit cell proliferation of esophageal cancer cells through Orai1-mediated intracellular Ca(2+)

116 f phospho-deficient LDHA Y10F sensitized the cancer cells to anoikis induction and resulted in attenu

117 ptome profiling of 144 single LNCaP prostate cancer cells treated or untreated with androgen after ce

118 nt of MRP1 functional activity in individual cancer cells using scanning electrochemical microscopy (

119 ion, induced a phenotypic switch in prostate cancer cells via mechanotransduction.

120 the plasticity and heterogeneity of prostate cancer cells with regard to androgen dependence, definin

121 otent stem cells with trisomy 21, as well as cancer cells.

122 tion of DNA damage via Ku70/Ku80 in prostate cancer cells.

123 critical for sustained EMT traits of ovarian cancer cells.

124 rgeted siRNA delivery to EFGR-overexpressing cancer cells.

125 mutated peptides presented on the surface of cancer cells.

126 Ambra1 binds to both FAK and Src in cancer cells.

127 expression of which is often dysregulated in cancer cells.

128 e invadopodial maturation in invasive breast cancer cells.

129 evention and Orai1-SOCE signaling pathway in cancer cells.

130 ndrogen regulation of DNA repair in prostate cancer cells.

131 other concurrent patients at the MD Anderson Cancer Center who were eligible for this trial but decli

132 rch 2, 2011, and May 21, 2013, at 8 academic cancer centers.

133 , we recruited patients at a single tertiary cancer centre in the USA.

134 ess disease relapse after 5-FU-based gastric cancer chemotherapy.

135 se regression in treatment-refractory breast cancer chest wall metastases but responses are short-liv

136 Triple-negative breast cancer, compared with non-TNBC, likely arises from diffe

137 AIMS: Among subjects screened for colorectal cancer (CRC) by the guaiac fecal occult blood test, inte

138 nflammatory potential and risk of colorectal cancer (CRC) in 87,042 postmenopausal women recruited fr

139 0 to 2012 were identified using the National Cancer Data Base, which includes more than 70% of patien

140 l adenocarcinoma from the 2006-2012 National Cancer Database who received neoadjuvant chemoradiothera

141 ong nonelderly patients with newly diagnosed cancer declined substantially after the ACA, especially

142 Unspecified liver cancer decreased over time and constituted <10% of all r

143 The probability of cancer detection for PI-RADS category 2, 3, 4, and 5 les

144 the guaiac fecal occult blood test, interval cancers develop in 48% to 55% of the subjects.

145 alcitonin is intimately connected with human cancer development and proliferation.

146 Calcipotriol suppressed skin cancer development in mice in a TSLP-dependent manner.

147 lain why female sex hormones accelerate lung cancer development.

148 nal transplanted patients with pretransplant cancer diagnoses in the Uppsala-Orebro region, Sweden.

149 (1) How accurate is teledermatology for skin cancer diagnosis compared with usual care (face-to-face

150 ated molecules could be beneficial for early cancer diagnosis, monitoring and surveillance.

151 understanding hypoxia-mediated mechanisms in cancer disease and other biological processes, and disco

152 and sepsis were associated with worse colon cancer disease-specific survival [(+)transfusion: hazard

153 Cancers display elevated O-GlcNAcylation and suppression

154 nt of both EMT-dependent and EMT-independent cancer dissemination programs.

155 ective in inhibiting ERalpha-negative breast cancer due at least in part to epigenetic reactivation o

156 Eighty-six patients (12.9%) developed a cancer during follow-up.

157 ally confirmed limited-stage small-cell lung cancer, Eastern Cooperative Oncology Group performance s

158 required lower concentrations to exert anti-cancer effects and preferentially affected GSCs and telo

159 Chromosomal instability (CIN) contributes to cancer evolution, intratumor heterogeneity, and drug res

160 l-to-cell heterogeneity is a major driver of cancer evolution, progression, and emergence of drug res

161 the retrospective cohort, luminal B prostate cancers exhibited the poorest clinical prognoses on both

162 We demonstrate that ovarian cancer exhibits a targetable alteration in iron metaboli

163 ated to the incidence and mortality of these cancers exist.

164 The majority of breast cancers expresses the estrogen receptor (ER(+)) and is t

165 CSCs initiate cancer formation and are linked to metastasis and resist

166 mammary stem cell (MaSC) activity and breast cancer formation remain poorly understood.

167 positive section margins in nonmelanoma skin cancer from 8.4% to 12.8%.

168 Guidelines for cancer genetic testing based on family history may miss

169 scription factors (TFs), our analysis of The Cancer Genome Atlas database (TCGA) found that patients

170 Men with low-risk, localised prostate cancer (Gleason pattern 3) who had received no previous

171 In six of the 52 patients, breast cancer had been diagnosed at an outside institution.

172 esented the risk of AK as not progressing to cancer had the lowest proportion of individuals who chos

173 subsequent therapy for metastatic colorectal cancer has clinical benefit in patients with colorectal

174 low-Up Study (1986 to 2012) who were free of cancer, heart disease, and stroke at baseline.

175 lled with porphyrin molecules, for effective cancer imaging and therapy.

176 bsets with properties critical for improving cancer immunotherapy.

177 optogenetics to overcome critical hurdles in cancer immunotherapy.

178 ll-molecule target for preventing colorectal cancer in high-risk groups such as those with familial a

179 ce had lower thyroidectomy rates for thyroid cancer in Massachusetts and the control states compared

180 ohort study, we evaluated the risk of breast cancer in relation to indoor heating and cooking practic

181 estimated by comparing the observed rates of cancer in relatives with population-expected rates estim

182 an 70% of patients newly diagnosed as having cancer in the United States.

183 ive was to assess the risk of posttransplant cancer in this patient group.

184 Prostate cancer (PCa) is one of the leading cancers in men in the USA.

185 y be an important factor in the reduction of cancer incidence.

186 o the contribution of mutagenic exposures to cancer incidence.

187 and suppression of O-GlcNAcylation inhibits cancer invasion and metastasis.

188 Although cancer is typically associated with somatic variations,

189 defining hallmark of primary and metastatic cancers is the migration and invasion of malignant cells

190 atory mechanisms control PD-L1 expression in cancer, it remains unknown whether such regulatory loops

191 The first evidence of prostate cancer lesion visualization in men using (68)Ga-NeoBOMB1

192 can play an important role in individualized cancer medicine.

193 eview focuses on the applications of SIRM to cancer metabolism and its use in understanding drug acti

194 tion of kinesin-1 motor functions and breast cancer metastasis and suggest PLD2 as a potential therap

195 n for future treatment strategies to prevent cancer metastasis in breast cancer cases.

196 icroenvironment that exert potent effects on cancer metastasis.

197 JAM-C can be potentially targeted to control cancer metastasis.

198 strated that miR-194 is a driver of prostate cancer metastasis.

199 as a regulatory mechanism to impact ovarian cancer metastatic success.

200 has been achieved in muscle-invasive bladder cancer (MIBC).

201 aintained AR expression in multiple prostate cancer model systems, was required for cell proliferatio

202 During the same period, deaths after breast cancer (n = 134) were significantly reduced (40 deaths [

203 herent cells to prove their applicability as cancer nanotherapeutics.

204 detection of clinically significant prostate cancer, no difference was found in the diagnostic perfor

205 s improved patient outcomes in several human cancers, no such advance has been achieved in muscle-inv

206 Neurons promote the growth of cancers of the brain, skin, prostate, pancreas, and stom

207 Patients with lung or colorectal cancer often exhibit leukocytosis.

208 effector of SPOP mutation in human prostate cancer or mouse models.

209 Colorectal cancer originates within immunologically complex microen

210 zed data from 249,010 hospital-based English Cancer Patient Experience Survey responders with sexual

211 Here, we show in mice and cancer patients (n = 70) that lung adenocarcinomas incre

212 reporting 593 TB cases occurring in 324,041 cancer patients between 1950 and 2011 were identified.

213 supports Honokiol as a promising therapy for cancer patients receiving Dox treatment.

214 e prognostic biomarker in ER positive breast cancer patients, and predictive of preclinical sensitivi

215 ificantly increase response rates for breast cancer patients, especially those with HER2 and ER negat

216 glutamate metabolism metal transport in oral cancer patients.

217 obtained from castration-resistant prostate cancer patients.

218 dependent data sets with totally 1079 breast cancer patients.

219 l properties in both healthy individuals and cancer patients.

220 elate with metastatic status in human breast cancer patients.

221 Prostate cancer (PCa) is one of the leading cancers in men in the

222 ility of (64)CuCl2 PET/CT to detect prostate cancer (PCa) recurrence in patients with biochemical rel

223 are limited for genetic testing for prostate cancer (PCA).

224 Rare cancers pose challenges for diagnosis, treatments, and c

225 nse, which will have a significant impact on cancer precision medicine.

226 a possible molecular basis for zinc-induced cancer prevention and Orai1-SOCE signaling pathway in ca

227 ns unclear whether MSA exerts its effects on cancer prevention by influencing angiogenesis within Se

228 programs controlled by these isoforms affect cancer progression and outcomes.

229 tionships between Twist1 and Foxa1 in breast cancer progression are unknown.

230 report that a 0.1 Gy radiation dose reduces cancer progression by deactivating the JAK1/STAT3 pathwa

231 h oncogenic and tumour-suppressing roles for cancer progression, such as the insulin-like growth fact

232 fects that likely contribute to HPV-mediated cancer progression.

233 n factor is a critical barrier to pancreatic cancer progression.

234 g a large whole-genome sequencing data bank, cancer registry and colorectal tumour bank we determine

235 changes in sexual quality of life using the Cancer Rehabilitation Evaluation System sexuality subsca

236 eptor tyrosine kinases, including the highly cancer relevant insulin-like growth factor type 1 recept

237 sample data are available at dmri.slicer.org Cancer Res; 77(21); e101-3.

238 Methods ASCO, Friends of Cancer Research, and the US Food and Drug Administration

239 Single gene tests to predict whether cancers respond to specific targeted therapies are perfo

240 n was found between TRT and overall prostate cancer risk (odds ratio [OR], 1.03; 95% CI, 0.90 to 1.17

241 ms of overnutrition, a confirmed independent cancer risk factor, remain poorly understood.

242 density (MD) is one of the strongest breast cancer risk factors.

243 ing to genetic risk based on lifetime breast cancer risk from birth, as estimated by BOADICEA (Breast

244 25 to 76 years of age with increased breast cancer risk who underwent CE spectral mammography and MR

245 nce of these disparities in gastrointestinal cancer risk, as well as approaches that apply precision

246 the prevalence of Lynch syndrome, associated cancer risks and pathogenicity of several variants in th

247 mic and/or epigenomic profiles for any given cancer sample.

248 ic changes with established implications for cancer screening or prevention.

249 To describe a skin cancer screening quality initiative in a large health ca

250 of 857 mug/kg, and exceeded the human health cancer screening value of 12 mug/kg in 48% of the nation

251 re we show that in a mouse model of prostate cancer, SIN3B provides a barrier to malignant progressio

252 e over- or under-represented among different cancer sites.

253 otka-Volterra equations with three competing cancer "species": androgen dependent, androgen producing

254 tastasis-free survival [DMFS], 53%; prostate cancer-specific survival [PCSS], 78%; overall survival [

255 bly contributes to poorer overall and breast cancer-specific survival.

256 pression significantly increases at advanced cancer stages, providing an improved opportunity for con

257 epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) acquisitions.

258 Y cells and proved even to efficiently block cancer stem cell growth.

259 ion, tumorsphere formation and ALDH-positive cancer stem cell population, in vitro.

260 uivalents of blastomeres, the most primitive cancer stem cells reported to date.

261 or rectal (FFT: 44% vs LFT: 35%, P = 0.330) cancer subgroups.

262 Recent evolutions in rectal cancer surgery led to transanal dissection of the rectum

263 Only 40% of patients with advanced ovarian cancer survive more than 5 years.

264 Methotrexate-treated cancer survivors had significantly lower cerebral blood

265 The specialty of cancer survivorship has been developing and growing sinc

266 explore specific microRNAs (miRs) in rectal cancer that would predict response to radiation and iden

267 action may represent a therapeutic target in cancers that express ephrinB1.

268 In prostate cancer, the development of castration resistance is pivo

269 ive contributions of mTORC1 versus mTORC2 in cancer, their role in tumor-associated blood vessels and

270 Since reovirus shows promise as a cancer therapy, efficient reovirus reverse genetics resc

271 tate the optimization and personalization of cancer therapy.

272 with beta-catenin and PKM2 levels in breast cancer tissues.

273 mly assigned 731 men with localized prostate cancer to radical prostatectomy or observation.

274 Purpose Survivors of childhood cancer treated with cranial radiation therapy are at ris

275 apy and radiotherapy is often encountered in cancer treatment, and there is a lack of effective treat

276 re at risk for receiving nonguideline breast cancer treatment, which probably contributes to poorer o

277 potent and specific AEP inhibitor useful for cancer treatment.

278 Cancer treatments are associated with subsequent neoplas

279 arched ClinicalTrials.gov for phase II to IV cancer trials of Food and Drug Administration-approved i

280 ivery approach for the treatment of prostate cancer tumors, and possibly other carcinomas where Sef i

281 s should measure multiple biomarkers in each cancer type to determine whether combinations of biomark

282 dium of 2218 primary tumours across 12 human cancer types and systematically screen for homozygous de

283 genes are overexpressed in several different cancer types and their elevated expression is associated

284 y to create scarless isogenic cell models of cancer variants in 1 month.

285 s from 2009 to 2013, the incidence of breast cancer was the highest of any cancer and the death rate

286 To gain understanding of MRN in cancer, we engineered mice with B lymphocytes lacking MR

287 5 women undergoing PM for Stage 0-III breast cancer were randomized to undergo either standard PM ("n

288 al, patients with HER2-positive early breast cancer were randomly assigned to receive treatment with

289 ly expressed in diseases, as best studied in cancers, where bromodomain proteins impact the expressio

290 ute a large subgroup of patients with breast cancer who are at risk for receiving nonguideline breast

291 nts with incidentally discovered gallbladder cancer who underwent reoperation and had available data

292 o investigate whether associations of breast cancer with body mass index (BMI; weight (kg)/height (m)

293 evel, or (c) had a prior history of prostate cancer with increasing PSA level.

294 expression of pro-apoptotic genes in breast cancer with mutant p53.

295 ith metastatic castration-resistant prostate cancer with the addition of custirsen to cabazitaxel and

296 ance: Illustrating the challenge in treating cancers with targeted drugs, which by selecting for drug

297 s as covariate-38 different common and rarer cancers, with breast and prostate cancer as baseline cat

298 ular Z line do not develop HGD or esophageal cancer within 5 years after index endoscopy.

299 GFR activation was also seen in a colorectal cancer xenograft.

300 ventions are available for both these common cancers, yet for so many women access to these is beyond