ライフサイエンスコーパス: solid cancer

1 sttransplantation tumors (18 skin, 2 PTLD, 8 solid cancers).

2 nant transformation across multiple types of solid cancer.

3 range 5-34); 60,271 (9%) developed a second solid cancer.

4 lts with chronic lung disease, diabetes, and solid cancer.

5 valuate the risk of the development of a new solid cancer.

6 d higher mortality relative to patients with solid cancer.

7 al load is associated with the occurrence of solid cancer.

8 denocarcinoma has the worst mortality of any solid cancer.

9 naling axis enhances bone metastases in many solid cancers.

10 ive microenvironments that exist within many solid cancers.

11 tor expression, derived from seven different solid cancers.

12 herapeutic target in curative treatments for solid cancers.

13 heral blood at advanced metastatic stages of solid cancers.

14 rs of disease progression in hematologic and solid cancers.

15 eing evaluated in clinical trials of several solid cancers.

16 mide conditioning are at risk for developing solid cancers.

17 ventions, including hyperthermic ablation of solid cancers.

18 elates with poor outcome in murine and human solid cancers.

19 enotype has been identified in the stroma of solid cancers.

20 s been shown to promote tumor progression in solid cancers.

21 f malignancies, including haematological and solid cancers.

22 inical studies in non-Hodgkin's lymphoma and solid cancers.

23 omplicons, characterize many hematologic and solid cancers.

24 th antiangiogenic drugs for the treatment of solid cancers.

25 ied in human haematological malignancies and solid cancers.

26 d in poor prognoses in a number of different solid cancers.

27 uent challenge in patients with extracranial solid cancers.

28 somatic tissues, is re-expressed in diverse solid cancers.

29 ause of a lack of antitumor activity against solid cancers.

30 employed this mechanism to treat established solid cancers.

31 oradic colon cancers as well as other common solid cancers.

32 iation were associated with a higher risk of solid cancers.

33 nal evolution in a significant proportion of solid cancers.

34 limit side effects and broaden their use to solid cancers.

35 act, especially in genetically heterogeneous solid cancers.

36 t is widely used in the treatment of various solid cancers.

37 ysts but also other large targets, including solid cancers.

38 g combinations and clinical trial designs in solid cancers.

39 several human diseases, particularly various solid cancers.

40 s innately overexpressed in several types of solid cancers.

41 As species to a variety of hematological and solid cancers.

42 to optimize CAR T efficacy in patients with solid cancers.

43 immune diseases, fibrotic complications, and solid cancers.

44 promising therapeutic strategy for targeting solid cancers.

45 w CD3+ and CD4+ T cells were associated with solid cancers.

46 may lead to durable anti-tumour responses in solid cancers.

47 remains a mainstay in the treatment of most solid cancers.

48 ed by promoter hypermethylation in all major solid cancers.

49 mprove the therapeutic outcome of late stage solid cancers.

50 criptomic, and clinical parameters across 21 solid cancers.

51 can contribute to therapeutic resistance in solid cancers.

52 nes significantly contribute to a variety of solid cancers.

53 may define new options for the treatment of solid cancers.

54 ed risks for breast cancer, sarcoma, and all solid cancers.

55 role of the CAR as a prognostic indicator in solid cancers.

56 are present in the microenvironment of most solid cancers.

57 the cellular process level across a range of solid cancers.

58 and proposes G9a as a therapeutic target for solid cancers.

59 data from The Cancer Genome Atlas for seven solid cancers.

60 CAR may be a potential prognostic marker in solid cancers.

61 are rare in individuals with advanced-stage solid cancers.

62 logeneic T-cell therapy of hematopoietic and solid cancers.

63 s an attractive therapeutic approach against solid cancers.

64 o epithelial-mesenchymal transition (EMT) in solid cancers.

65 This cluster was upregulated in a number of solid cancers.

66 component of tumor microenvironment in most solid cancers.

67 or a cure, for patients with advanced-stage solid cancers.

68 but its overexpression is protumorigenic in solid cancers.

69 ression of both hematologic malignancies and solid cancers.

70 h tumor formation and progression of various solid cancers.

71 r therapeutic intervention in the setting of solid cancers.

72 nown to be associated with hematological and solid cancers.

73 remains poor, in particular in metastasizing solid cancers.

74 g optimal cancer care across the spectrum of solid cancers.

75 thways enriched in blood cancers compared to solid cancers.

76 ration of trial treatment (>/=7.5 years: all solid cancers, 0.69, 0.54-0.88, p=0.003; gastrointestina

77 orkers, the authors evaluated mortality from solid cancers (1,921 deaths) among 25,619 workers (865,7

78 tacle in the control of pancreatic and other solid cancers(1-3).

79 urrence of brain abscess neurosurgery (12%); solid cancer (11%); ear, nose, and throat infections (7%

80 atologic cancers, 44.8% (2.7%) in those with solid cancers, 23.1% (8.3%) in those with solid organ tr

81 matologic cancer, 51.9% (2.7%) in those with solid cancers, 26.9% (8.7%) in those with solid organ tr

82 atologic cancers (813 patients [8.40%]), and solid cancers (274 patients [2.83%]).

83 s evaluated, risk was highest in adults with solid cancer (300.4), HIV/AIDS (422.9), and hematologica

84 s (83; 9) and was lowest in breast and other solid cancers (38; 4).

85 Glypican-3 (GPC3) is expressed in a group of solid cancers(5-10), and here we report the evaluation i

86 udy of 183 patients with posttransplantation solid cancers (58 SCCs, 125 non-SCCs) and 501 matched co

87 The aORs were 4.12 (95% CI 3.37-5.04) for solid cancer; 8.77 (95% CI 5.66-13.6) for hematological

88 d 1.4x higher than expected rate of invasive solid cancers (95% confidence interval, 1.08-1.79, P = .

89 In solid cancers, a localized tumor mass allows alternative

90 germ cell tumors (TGCTs) are the most common solid cancers affecting young men.

91 Twenty-nine patients developed solid cancers after BMT, which represents a two-fold inc

92 Increased risks of solid cancers after chemotherapy were observed in most f

93 here have been no data on long-term risks of solid cancers after growth hormone treatment.

94 evaluated the incidence and risk factors for solid cancers after HCT using high-dose busulfan-cycloph

95 c chemotherapeutic agents in the etiology of solid cancers after Hodgkin's disease require detailed i

96 specific drug treatments in the etiology of solid cancers after NHL deserves further investigation.

97 , 1.31-3.09]), but this was not the case for solid cancers (aHR for 1-2 years prior, 0.90 [95% CI, .7

98 Risks of secondary solid cancers among allogeneic hematopoietic cell transp

99 s reporting significantly increased risks of solid cancers among patients with testicular nonseminoma

100 We quantified the site-specific risk of solid cancers among testicular nonseminoma patients trea

101 151 patients with cancer (95 patients with solid cancer and 56 patients with haematological cancer)

102 s broad impact in their applicability to any solid cancer and associated biomarkers shed, thereby all

103 rvational, evaluation study of patients with solid cancer and extracranial oligometastases treated wi

104 in our understanding of T-cell migration in solid cancer and immunotherapy based on the adoptive tra

105 e cells, leading to effective eradication of solid cancer and metastases.

106 gic analyses demonstrated that patients with solid cancer and patients without cancer had a similar i

107 yads, which comprised patients with stage IV solid cancer and their caregivers, were recruited from o

108 n interesting therapeutic target in multiple solid cancers and a good biomarker to stratify patients

109 apsular oncocells are universally present in solid cancers and appear in hematologic cancers in immun

110 Hh may be a promising therapeutic target for solid cancers and bone metastases.

111 ure in CCSs increases the risk of subsequent solid cancers and breast cancer, whereas cyclophosphamid

112 e/threonine Pim kinases are overexpressed in solid cancers and hematologic malignancies and promote c

113 is known to be elevated in various types of solid cancers and is associated with poor prognosis, how

114 stiffening is a physical hallmark of several solid cancers and is associated with therapy failure.

115 Lactate accumulation is a hallmark of solid cancers and is linked to the immune suppressive ph

116 ular carcinoma (HCC) is one of the deadliest solid cancers and is the third leading cause of cancer-r

117 issue factor (TF) is aberrantly expressed in solid cancers and is thought to contribute to disease pr

118 altered or functionally inactivated in many solid cancers and leukaemias, and is therefore a tumour

119 a panel of kinases and cell lines including solid cancers and leukemia cell models to explore its po

120 bsolute excess risks and cumulative risks of solid cancers and leukemia, however, were greater at old

121 ile episodes (FEs) among 1,565 patients with solid cancers and lymphomas receiving cyclical, myelosup

122 rt, the in vitro CXCR4 expression profile of solid cancers and metastases described in the previous l

123 wth factor receptor (EGFR) occurs in various solid cancers and often correlates with poor outcome.

124 se treatments remain largely ineffective for solid cancers and require significant time and resources

125 (CIN) underlies malignant properties of many solid cancers and their ability to escape therapy, and i

126 enzyme exhibits elevated expression in most solid cancers and therefore is a potential cancer-specif

127 ontrols; 21 (38%; 26-51) of 56 patients with solid cancer, and eight (18%; 10-32) of 44 patients with

128 16 healthy controls, 25 patients with solid cancer, and six patients with haematological cance

129 sease was an independent risk factor for all solid cancers, and especially cancers of the oral cavity

130 eceiving fluorouracil-based chemotherapy for solid cancers, and for the prevention of severe oral muc

131 Macrophage infiltration is a hallmark of solid cancers, and overall macrophage infiltration corre

132 cose positron emission tomography imaging of solid cancers, and targeting metabolic pathways in cance

133 In regard to most of the solid cancers, another potential strategy is to consider

134 Solid cancers are a major adverse outcome of orthotopic

135 Solid cancers are able to escape immune surveillance and

136 ecades after mutation by carcinogens and why solid cancers are aneuploid, although conventional mutat

137 pothesis in view of the fact that nearly all solid cancers are aneuploid, that many carcinogens are n

138 1971C, R2017Q, and R2017L observed mostly in solid cancers are catalytically inactive suggesting that

139 Advanced solid cancers are complex assemblies of tumor, immune, a

140 re certain leukemias and lymphomas, but most solid cancers are only curable at early stages.

141 hat inactivates T cell responses; and third, solid cancers are typified by phenotypic diversity and t

142 which immune responses are generated against solid cancers are well characterized and knowledge of th

143 tumor (WT), one of the most common pediatric solid cancers, arises in the developing kidney as a resu

144 cial role in the management of patients with solid cancers, as it helps selecting and prioritising th

145 The cumulative-incidence of solid cancers at 5 and 10 years after HCT was 0.6% and 1

146 inostat has activity against hematologic and solid cancers at doses well tolerated by patients.

147 Overall, patients developed new solid cancers at twice the rate expected based on genera

148 Given a proband with solid cancer, both Latinos (SIR = 4.98; 95% CI: 3.82-6.3

149 e been reported to have an increased risk of solid cancers but most studies are small and have limite

150 riately in a wide range of hematological and solid cancers, but clinically available therapies target

151 d induces durable responses in patients with solid cancers, but data on clinical efficacy in leukemia

152 e is a prognostic factor for the majority of solid cancers, but the role for PDAC in predicting survi

153 ll dysfunction impedes antitumor immunity in solid cancers, but the underlying mechanisms are diverse

154 be associated with increased risk of certain solid cancers, but there have been no data on long-term

155 (SOCS1) is inactivated in hematopoietic and solid cancers by promoter methylation, miRNA-mediated si

156 Loss and gain of chromosomal material in solid cancers can alter gene expression over large chrom

157 udies have shown that genomic alterations in solid cancers can be characterized by massively parallel

158 Hematological and solid cancers catabolize the semiessential amino acid ar

159 sistance in two different platinum-resistant solid cancer cell lines and demonstrated strong synergis

160 Conversely, CDCP1 downregulation in multiple solid cancer cell lines decreased both cell growth and S

161 cell death in approximately 36% (45/126) of solid cancer cell lines in vitro at subnanomolar concent

162 s low cytotoxicity against hematological and solid cancer cell lines, AP1 represents a valuable tool

163 Solid cancer cells commonly enter the blood and dissemin

164 round incidence rates were higher for second solid cancers, compared with first solid cancers, until

165 Extrapolation to other solid cancers demonstrated highly recurrent and tumor-ty

166 ncer drugs, proved effective against several solid cancer-derived cell lines.

167 Of 17,285 trial participants, 987 had a new solid cancer diagnosed during mean in-trial follow-up of

168 The risk of second solid cancers did not appear to be lower among patients

169 The cumulative incidence of second solid cancers did not differ according to study period (

170 Many solid cancers display cellular hierarchies with self-ren

171 Effective therapies for most solid cancers, especially those that have progressed to

172 To explain why solid cancers grow or are rejected, we examined how the

173 Participants with hematological and solid cancer had higher relative risks of zoster than th

174 We show that the spatial structure of a solid cancer has a major impact on the detection of clon

175 f this approach for myeloid malignancies and solid cancers has been limited by the paucity and hetero

176 hematologic malignancy, the success against solid cancers has been more moderate.

177 profound immunosuppression in patients with solid cancers has impeded efficacious immunotherapy.

178 tigen receptor T cell (CAR-T) treatments for solid cancers have been compromised by limited expansion

179 pharmacological blockade of its function in solid cancers have been unsuccessful.

180 Genomic analyses of many solid cancers have demonstrated extensive genetic hetero

181 inducing ligand (TRAIL)-induced apoptosis in solid cancers have yet to be clearly defined.

182 pirin groups than in the control groups (all solid cancers, HR 0.80, 0.72-0.88, p<0.0001; gastrointes

183 , HR 0.54, 95% CI 0.38-0.77, p=0.0007; other solid cancers, HR 0.82, 95% CI 0.53-1.28, p=0.39), due m

184 688 men were diagnosed with a second primary solid cancer (IMRT, 1306; 3DCRT, 1382).

185 necessitating kidney replacement therapy and solid cancer in ICU patients.

186 Prostate cancer, the most frequent solid cancer in older men, is a leading cause of cancer

187 s, 2844 (5.5%) had received a diagnosis of a solid cancer in the 2-year follow-up period and 3869 (7.

188 ATC is one of the most aggressive solid cancers in humans and is resistant to currently av

189 microenvironment to improve immunotherapy of solid cancers in patients.

190 been studied in leukemia but are critical in solid cancers in the context of metastasis and interacti

191 d cancer drugs approved for the treatment of solid cancers in the USA and Europe (Germany and Switzer

192 erm cells tumors (TGCTs) are the most common solid cancers in young men.

193 rtunities for addressing clonal evolution in solid cancers, in particular those where double-strand b

194 pha2) is overexpressed in a variety of human solid cancers including pancreatic cancer, we investigat

195 However, CPPB inhibits migrations of several solid cancers including pancreatic cancers that require

196 related with good prognosis in several other solid cancers including prostate, cervical, and lung.

197 racellular glycoprotein expressed in several solid cancers, including malignant gliomas, upon adoptio

198 alyses revealed that CHIP is associated with solid cancers, including non-melanoma skin cancer and lu

199 It is estimated that approximately 80% of solid cancers, including non-small cell lung cancer (NSC

200 ratumoral heterogeneity occurs in nearly all solid cancers, including ovarian cancer, contributing to

201 ant IRE1alpha pathway activation in multiple solid cancers, including TNBC.

202 trait of host resistance to both ascites and solid cancers induced by transplantable cells.

203 Both haematological and solid cancers initially gain chromosome arms, while only

204 In solid cancers, invasion and metastasis account for more

205 all survival of patients with several of the solid cancers investigated in The Cancer Genome Atlas da

206 For girls, a radiation-induced solid cancer is projected to result from every 300 to 39

207 tigen receptor (CAR) T cell immunotherapy in solid cancer is severely limited by the absence of ideal

208 Although the etiology of solid cancers is multifactorial, with environmental and

209 ctivity range, 2.1-8.9 GBq) for treatment of solid cancers known to produce carcinoembryonic antigen.

210 ion of dose-response relationships, types of solid cancers, latency patterns, and interactions with o

211 ransplantation have an increased risk of new solid cancers later in life.

212 ilized GemiNI for analyzing six data sets of solid cancers (liver, kidney, prostate, lung and germ ce

213 ting into the routine management of advanced solid cancers may expand the delivery of molecularly gui

214 Therefore, up-regulation of BER in solid cancers may represent an adaptive survival respons

215 Purpose Trop-2, expressed in most solid cancers, may be a target for antibody-drug conjuga

216 Many solid cancers metastasize to the bone and bone marrow (B

217 olon, and pancreatic tumors, we identified a solid cancer miRNA signature composed by a large portion

218 with T cell inflammation for the majority of solid cancers; moreover, EDMC enrichment, in accordance

219 tasis to distant organs is a major cause for solid cancer mortality, and the acquisition of migratory

220 ciations between radiation and site-specific solid cancer mortality.

221 omplete and durable responses, in a range of solid cancers, most notably in melanoma.

222 al of [(177)Lu]Lu-AKIR001for CD44v6-positive solid cancers (NCT06639191) is currently recruiting pati

223 ments in clinical outcomes for patients with solid cancers observed over the past 3 decades have been

224 es (SIR, 1.43; 95% CI, 1.18 to 1.73; n = 111 solid cancers) occurred after chemotherapy.

225 cohort study included patients with BMs from solid cancers, of which at least 1 lesion received preop

226 e a compelling therapeutic strategy, such as solid cancers or metabolic syndromes, and also caution a

227 not differ between first and second primary solid cancers (P = 0.70).

228 s associated with increased risks of several solid cancers, particularly more than 20 years after exp

229 D) and its therapy may increase the risk for solid cancers, particularly squamous-cell carcinomas (SC

230 or type, stage, and treatment, virus-exposed solid cancer patients display a dominant impact of SARS-

231 Furthermore, while recovered solid cancer patients' immunophenotypes resemble those o

232 Solid cancer, pneumonia in hematologic malignancies, and

233 The multivariate analyses identified solid cancer, pneumonia in hematologic patients, and do-

234 t doxorubicin-related increased risks of all solid cancers ( Ptrend < .001) and breast cancer ( Ptren

235 onducted to identify CPGs and CSs for common solid cancers published between January 2003 and October

236 ythropoietin and erythropoietin receptors in solid cancers, raise concern about the safety of ESA adm

237 cancer, zoster risk among participants with solid cancers receiving chemotherapy was greater than in

238 In various models of solid cancers refractory to immunotherapies, including h

239 wever, optimal cell surface targets for many solid cancers remain elusive.

240 e disorders were predominant (77%); however, solid cancers (renal, sarcomas, genital, thyroid) were s

241 were diagnosed with a first primary invasive solid cancer reported in the SEER registries between Jan

242 ppressive population of CD4(+) T cells, into solid cancers represents a barrier to cancer immunothera

243 ed by 3 fold and 6.5 fold in hematologic and solid cancers respectively before and after 1980.

244 ia (low O2) is a pathobiological hallmark of solid cancers, resulting from the imbalance between cell

245 population-based studies, however, focus on solid cancer risk among survivors of TC managed with non

246 us on individual chemotherapeutic agents and solid cancer risk.

247 Moreover, the detectability of solid cancers seems to be generally lower for (68)Ga-pen

248 Highly tumorigenic subpopulations of several solid cancers share characteristics with somatic stem ce

249 s initially gain chromosome arms, while only solid cancers subsequently preferentially lose multiple

250 s a standard chemotherapeutic agent to treat solid cancers such as breast, colon, head, and neck.

251 iated at young ages, face increased risks of solid cancers, supporting strategies to promote lifelong

252 For evaluation of tracer accumulation in solid cancers, SUVmax and tumor-to-background (T/B) rati

253 In solid cancers, T cells typically function as cytotoxic e

254 nts were at significantly higher risk of new solid cancers than the general population (observed case

255 Aneuploidy is a hallmark of human solid cancers that arises from errors in mitosis and res

256 ed a total of 3266 (2862-3670) excess second solid cancers that could be related to radiotherapy, tha

257 Seventy-nine patients with advanced solid cancers that were unresponsive to standard therapy

258 ted cellular polarity (DCP) is a hallmark of solid cancer, the malignant disease of epithelial tissue

259 In participants with solid cancers, the estimated duration of nAbs against th

260 Similar to human solid cancers, the resulting tumors evolved subtetraploi

261 hough S100A8 and S100A9 have been studied in solid cancers, their functions in hematological malignan

262 In expanding the utility of CFZ to solid cancer therapy, the poor aqueous solubility and in

263 MEN1 knockout in multiple solid cancer types does not impact cell proliferation in

264 pan-cancer analysis on 226 samples across 10 solid cancer types to profile the TME at single-cell res

265 In most human solid cancer types, a high frequency of intratumoral neu

266 g pathway, is somatically mutated in diverse solid cancer types, and aberrant AKT activation promotes

267 ributes to the metastatic spread of multiple solid cancer types, but its direct target genes that med

268 expressed on Fate-1 TI Treg cells in several solid cancer types, but not on other TI or peripheral Tr

269 s (ICI) have revolutionized the treatment of solid cancer types, ICI are still restricted to a very s

270 mour-specific antigens expressed on multiple solid cancer types, remains a major challenge.

271 id not inhibit growth of several IDH1 mutant solid cancer types.

272 or second solid cancers, compared with first solid cancers, until about age 70 years for men and 80 y

273 mic administration of siRNA to patients with solid cancers using a targeted, nanoparticle delivery sy

274 ul treatment of large numbers of people with solid cancers using this strategy is unlikely to be stra

275 encases vascular structures and, unlike most solid cancers, usually presents with substantial metasta

276 of next-generation immunotherapies targeting solid cancers utilizing viral vectors and adoptive cell

277 95% CI: 0.24-0.64; P=0.0002) and for de novo solid cancer was 0.44 (0.24-0.82; P=0.0092).

278 ve probability (+/- SE) for development of a solid cancer was 6.1% +/- 1.6% at 10 years.

279 The incidence of any solid cancer was not elevated in RA (HR 0.80 [95% CI 0.5

280 h that for the US population, mortality from solid cancers was significantly lower than expected amon

281 t study to date to evaluate risk factors for solid cancers, we studied a multi-institutional cohort o

282 Projected lifetime attributable risks of solid cancer were higher for younger patients and girls

283 ut one eighth of genome based treatments for solid cancer were rated as likely to offer a high benefi

284 Twenty-four patients with advanced solid cancer were treated at seven dose levels (700 to 4

285 While findings on several types of solid cancers were less consistent, several studies prov

286 Two hundred ten second solid cancers were observed.

287 Sixty-six solid cancers were reported at a median of 6 years after

288 Thirty-two patients with advanced solid cancers were treated at seven dose levels (12.5 to

289 t type of primary brain tumor, is one of the solid cancers where cancer stem cells have been isolated

290 one (SIR, 0.93; 95% CI, 0.76 to 1.14; n = 99 solid cancers), whereas significantly increased 40% exce

291 lature with tumor blood vasculature of other solid cancers, which correlated with the overall surviva

292 In contrast to solid cancers, which often require genetic modifications

293 All adults with a diagnosis of solid cancers who underwent surgery during the study per

294 tant factor in the tumor microenvironment of solid cancers, whose growth often exceeds the growth of

295 cells to treat the majority of patients with solid cancers will require major technical, manufacturin

296 6 and autophagy is also synergistic in other solid cancers with an intact G1/S checkpoint, providing

297 , is a potential treatment approach to human solid cancers with high levels of CCR4-expressing tumor-

298 el CXCR4-targeted PET probe in patients with solid cancers with reported in vitro evidence of CXCR4 o

299 g tested in clinical trials in patients with solid cancer, with the aim of enhancing the efficacy of

300 ity increased significantly in patients with solid cancer within 2 weeks of a vaccine boost at day 21