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

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

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

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

6 denocarcinoma has the worst mortality of any solid cancer.

7 nant transformation across multiple types of solid cancer.

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

9 rs of disease progression in hematologic and solid cancers.

10 mide conditioning are at risk for developing solid cancers.

11 ventions, including hyperthermic ablation of solid cancers.

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

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

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

15 f malignancies, including haematological and solid cancers.

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

17 omplicons, characterize many hematologic and solid cancers.

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

19 th antiangiogenic drugs for the treatment of solid cancers.

20 ied in human haematological malignancies and solid cancers.

21 uent challenge in patients with extracranial solid cancers.

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

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

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

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

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

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

28 nes significantly contribute to a variety of solid cancers.

29 s an attractive therapeutic approach against solid cancers.

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

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

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

33 component of tumor microenvironment in most solid cancers.

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

35 but its overexpression is protumorigenic in solid cancers.

36 ression of both hematologic malignancies and solid cancers.

37 h tumor formation and progression of various solid cancers.

38 nown to be associated with hematological and solid cancers.

39 remains poor, in particular in metastasizing solid cancers.

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

41 thways enriched in blood cancers compared to solid cancers.

42 naling axis enhances bone metastases in many solid cancers.

43 ive microenvironments that exist within many solid cancers.

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

45 tor expression, derived from seven different solid cancers.

46 herapeutic target in curative treatments for solid cancers.

47 heral blood at advanced metastatic stages of solid cancers.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

62 Risks of secondary solid cancers among allogeneic hematopoietic cell transp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

84 Solid cancers are a major adverse outcome of orthotopic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

101 Solid cancer cells commonly enter the blood and dissemin

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

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

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

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

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

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

108 Many solid cancers display cellular hierarchies with self-ren

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

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

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

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

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

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

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

116 , 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

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

118 microenvironment to improve immunotherapy of solid cancers in patients.

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

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

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

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

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

124 In solid cancers, invasion and metastasis account for more

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

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

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

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

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

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

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

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

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

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

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

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

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

138 Solid cancer, pneumonia in hematologic malignancies, and

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

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

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

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

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

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

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

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

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

148 us on individual chemotherapeutic agents and solid cancer risk.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

165 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).

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

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

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

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

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

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

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

173 Two hundred ten second solid cancers were observed.

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

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

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

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

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

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

180 6 and autophagy is also synergistic in other solid cancers with an intact G1/S checkpoint, providing

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

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

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