ライフサイエンスコーパス: solid tumor

1 epigenetic therapy to gain FDA approval in a solid tumor.

2 ), is the most common pediatric extracranial solid tumor.

3 er stem cell population may be maintained in solid tumors.

4 distinct from processes in inflammation and solid tumors.

5 of heart disease, ILD, infections, AEs, and solid tumors.

6 r tyrosine kinase and an oncoprotein in many solid tumors.

7 o classification or PET Response Criteria in Solid Tumors.

8 elivery of imaging and therapeutic agents to solid tumors.

9 tility of P2-6R for treating NSCLC and other solid tumors.

10 are largely ineffective in the treatment of solid tumors.

11 ortant role in the growth and progression of solid tumors.

12 adult and pediatric patients with Trk-driven solid tumors.

13 989) in patients with metastatic TP53 mutant solid tumors.

14 otherapy, but hurdles remain, especially for solid tumors.

15 ort further development of NHWD-870 to treat solid tumors.

16 H1 (mIDH1) under evaluation in patients with solid tumors.

17 for therapeutic-targeting of DHP activity in solid tumors.

18 in a variety of hematologic malignancies and solid tumors.

19 rves as a metric for metastatic potential of solid tumors.

20 n study of ivosidenib in patients with mIDH1 solid tumors.

21 slation for the treatment of both liquid and solid tumors.

22 has become a standard of care in a subset of solid tumors.

23 reclinical mouse models of hematological and solid tumors.

24 ed as a promising target in the treatment of solid tumors.

25 rolizumab in patients with selected advanced solid tumors.

26 ticity, which may also be relevant for other solid tumors.

27 nvestigated in a number of hematopoietic and solid tumors.

28 se as a selective treatment for a variety of solid tumors.

29 pressed by various types of human epithelial solid tumors.

30 et toxicity and is often ineffective against solid tumors.

31 nd spreading dynamics distinct that of other solid tumors.

32 ity of Th17 cells against large, established solid tumors.

33 lasting antitumor responses in patients with solid tumors.

34 cation of CAR-T cell therapy, especially for solid tumors.

35 utgrow the local vasculature, as observed in solid tumors.

36 -L1 has revolutionized the treatment of many solid tumors.

37 te promyelocytic leukemia, but also in other solid tumors.

38 cell renal cell carcinoma (ccRCC) and other solid tumors.

39 ivation and recruitment in immunosuppressive solid tumors.

40 esistant cancer cells found in heterogeneous solid tumors.

41 ralized to alpha-radioimmunotherapy in other solid tumors.

42 ssociated with CD8(+) T cell infiltration in solid tumors.

43 ly potent for the eradication of established solid tumors.

44 t effective treatment for most patients with solid tumors.

45 ped for sustained delivery of active drug to solid tumors.

46 immune responses against a broad spectrum of solid tumors.

47 ing modified Response Evaluation Criteria in Solid Tumors.

48 etreated patients with mesothelin-expressing solid tumors.

49 improvement for more effective treatment of solid tumors.

50 gimens are frequently used for treatments of solid tumors.

51 ne responses and play a central role against solid tumors.

52 preclinical and clinical studies of various solid tumors.

53 R-T therapy is currently approved for use in solid tumors.

54 now supports testing for MSI in all advanced solid tumors.

55 dio combination therapy for locally advanced solid tumors.

56 bles genomic biomarker detection in advanced solid tumors.

57 been adapted as an immunotherapy in several solid tumors.

58 inhibitors (ICI) presents many challenges in solid tumors.

59 s of anti-PD-L1 have been limited in several solid tumors.

60 in an ongoing phase Ib/II study of selected solid tumors.

61 for the diagnosis and therapy monitoring of solid tumors.

62 els able to predict the molecular profile of solid tumors.

63 ommonly correlated with enhanced invasion in solid tumors.

64 opes, making this platform applicable to all solid tumors.

65 etics of MP0250 in 45 patients with advanced solid tumors.

66 ell survival and overexpressed in almost all solid tumors.

67 rategy to improve outcomes for patients with solid tumors.

68 veness of chemotherapeutics for treatment of solid tumors.

69 enhanced cytotoxic T-cell response in human solid tumors.

70 h prostate cancer and neovasculature of most solid tumors.

71 ortant adjunct to standard cancer therapy of solid tumors.

72 ronic lymphocytic leukemia, and a variety of solid tumors.

73 gnificantly limit prognosis of patients with solid tumors.

74 uding developmental disorders, leukemia, and solid tumors.

75 the fastest increasing incidence rates among solid tumors.

76 analog used in the treatment of a variety of solid tumors.

77 orts of patients with advanced or metastatic solid tumors (0.15-7.5 mg/kg) received anetumab ravtansi

78 assessed by Response Evaluation Criteria in Solid Tumors 1.1), a decrease in prostate-specific antig

79 according to Response Evaluation Criteria in Solid Tumors 1.1.

80 stress under the constant strain imposed by solid tumor, a matrix property termed stress relaxation.

81 Because all solid tumors accumulate MDSCs and TAMs, a general strate

82 procedure, the microprobe can stay within a solid tumor and be repeatedly used as needed.

83 ion, which has been identified previously in solid tumor and histiocytosis patients, caused hyperacti

84 imics many of the complexities of an in vivo solid tumor and tumor microenvironment, and are often us

85 fer resistance to immune-based therapies for solid tumors and current advancements in stroma-targeted

86 sm of MEK/ERK pathway inhibitor addiction in solid tumors and found it does not apply to ALCL.

87 mTOR signaling is observed in virtually all solid tumors and has been an attractive drug target.

88 TP) 4A3 is frequently overexpressed in human solid tumors and hematologic malignancies and is associa

89 ple T cell functions and enhance ACT against solid tumors and hematologic malignancies.

90 tant active RAS is a driver in many types of solid tumors and hematological malignancies.

91 failure of NK cell therapy in patients with solid tumors and highlight the crucial role of a 3-D env

92 iplatin, are a mainstay in the management of solid tumors and induce cell death by forming intrastran

93 Intratumoral hypoxia occurs in 90% of solid tumors and is associated with a poor prognosis for

94 requently overexpressed in ovarian and other solid tumors and is involved in interactions between tum

95 Hypoxia is a common phenomenon in solid tumors and is strongly linked to hallmarks of canc

96 ere-binding protein POT1 are associated with solid tumors and leukemias.

97 ical investigation in patients with advanced solid tumors and lymphomas (NCT03188965).

98 is can occur following surgical resection of solid tumors and metastasis is the main cause of cancer

99 ITH is a widely recognized feature of solid tumors and poses distinct challenges related to th

100 t in understanding the underlying biology of solid tumors and predict tumor response to therapies.

101 on (CNV) in 20 categories and 45 subtypes of solid tumors and quantified differential expression (DE)

102 ed for more than 60 years against a range of solid tumors and still remains the cornerstone for the t

103 HDACi offers a dual therapeutic strategy in solid tumors and the opportunity to achieve previously u

104 to be applicable to treating a wide range of solid tumors and to circumvent problems associated with

105 ic patients with hematopoietic malignancies, solid tumors, and brain tumors.

106 cur in leukemias, as well as in a variety of solid tumors, and confer dependence on wild-type splicin

107 cal development in hematologic malignancies, solid tumors, and gliomas with mIDH1.

108 encouraging and surprising, given that most solid tumor antibodies that use Fc-dependent mechanisms

109 Solid tumors are characterized by intratumoral hypoxia,

110 Genomic profiling shows that many solid tumors are characterized by specific driver aberra

111 tment options, initial systemic regimens for solid tumors are dominated by a set of standard chemothe

112 t their effects on the tumor-invaded bone or solid tumors are elusive.

113 strategies to enhance CAR-T cell function in solid tumors are needed to make these living drugs widel

114 The progression and metastatic capacity of solid tumors are strongly influenced by immune cells in

115 s of cross-cancer heritability suggests that solid tumors arising across tissues share in part a comm

116 hemotherapy (Response Evaluation Criteria in Solid Tumors) as independent predictors of CSS.

117 ypoxia is a key microenvironmental stress in solid tumors associated with acquired resistance to conv

118 ing modified Response Evaluation Criteria in Solid Tumors at 6 weeks and 6-12 months after radioembol

119 digital histopathological images of a whole solid tumor based on current technology is feasible.

120 In solid tumors, blood vessels are abnormal and dysfunction

121 In preclinical models of solid tumors, both pro-metastatic and anti-metastatic ef

122 ls lead to enhanced clearance of leukemia or solid tumor burden, providing the first metabolic modifi

123 a zinc metalloenzyme that is upregulated in solid tumors but not in the corresponding normal tissues

124 ads to a uniquely acidic microenvironment in solid tumors, but exploiting the labile extracellular pH

125 Irinotecan treats a range of solid tumors, but its effectiveness is severely limited

126 wn thermal therapy platform studied to treat solid tumors, but its use for monotherapy is limited due

127 challenge for antibody-based therapeutics of solid tumors, but proper dosing can improve the tissue p

128 inhibitors used to treat high-risk pediatric solid tumors, but they often show poor efficacy due to i

129 st some hematologic cancers, but efficacy in solid tumors can be limited by restrictive tumor microen

130 ificant difference in VE among patients with solid tumor cancer receiving active chemotherapy.

131 nity, they are present around many different solid tumor cancers and their role in tumor microenviron

132 An unmet clinical need in solid tumor cancers is the ability to harness the intrin

133 treatments for a variety of hematologic and solid tumor cancers, the results thus far have been mixe

134 ncers, but further advances are required for solid tumor CAR therapy.

135 function against a panel of blood cancer and solid tumor cells as compared to IL-2-activated non-expa

136 45R0 lymphocytes, were determined within the solid tumor center, the invasive margin, and tumor strom

137 CC (modified Response Evaluation Criteria in Solid Tumors classification, European Association for th

138 eta) R2-41BB chimeric receptor that improved solid tumor clearance.

139 nsion in IL6-driven Th17 ACT provide greater solid tumor control and robust immune memory, highlighti

140 Ns) are increasingly recognized to influence solid tumor development, but why their effects are so co

141 can provide another mechanism for decreased solid tumor development.

142 Although more common in solid tumors, different forms of aneuploidy represent th

143 k, in which 13,895 men developed an incident solid tumor during follow-up.

144 t enrolled patients with Nectin-4-expressing solid tumors (eg, metastatic urothelial carcinoma [mUC])

145 rapy in patients with metastatic TP53 mutant solid tumors, especially in those with metastatic sarcom

146 ght to be inappropriate for the treatment of solid tumors, for which antibody penetration is limited

147 with Down syndrome have lower prevalence of solid tumor formation.

148 Here we report the genomic profiling of solid tumors from 131,668 cancer patients, identifying 9

149 tologic malignancies, but its application to solid tumors has been challenging(1-4).

150 ncentrations in the microenvironment of most solid tumors has been shown to accelerate FN assembly in

151 Extracellular matrix in solid tumors has emerged as a specific, stable, and abun

152 tologic malignancies, but its application to solid tumors has proven challenging.

153 igen receptor (CAR) T-cell therapy targeting solid tumors has stagnated as a result of tumor heteroge

154 imorphic regeneration and the progression of solid tumors have been uncovered by recent studies.

155 ancies, efforts to translate this success to solid tumors have met with limited success.

156 l transplants (HCT), cancer (hematologic and solid tumor), HIV, and solid organ transplant (SOT; kidn

157 tively transferred NK cells in patients with solid tumors, however, have thus far been unsuccessful.

158 omprise a class of viable genetic targets in solid tumors; however, their role in breast cancer remai

159 argely mediated by cytotoxic CD8+ T cells in solid tumors, HRSCs frequently lack major histocompatibi

160 rculation is a potential strategy to relieve solid tumor hypoxia in order to increase the effectivene

161 osine kinase highly expressed in a number of solid tumors, identified a number of Bicycle families wi

162 ies over the last decades have shown that in solid tumors, IGFBP2 is upregulated and promotes several

163 vancement in the field of ACT application to solid tumor immunotherapy.See related article by Knochel

164 is the most commonly diagnosed extracranial solid tumor in children.

165 here is a paucity of targeted treatments for solid tumors in children, adolescents, and young adults

166 xy)-5-methylbenzamide ((18)F-ISO-1) to image solid tumors in lymphoma, breast cancer, and head and ne

167 for the delivery of CCL21 to other types of solid tumors in the future and as a slow-release deliver

168 -T cells against established hematologic and solid tumors in vivo.

169 phenomenon, well-described in MEK-ERK-driven solid tumors, in which drug-target overexpression promot

170 ng T cells is increasingly utilized to treat solid tumors including non-small cell lung cancer (NSCLC

171 rane glycolipid GD2 is expressed by multiple solid tumors, including 88% of osteosarcomas and 98% of

172 recognized as an oncogenic driver in several solid tumors, including colorectal cancer (CRC).

173 state cancer and the neovasculature of other solid tumors, including CRC.

174 nt tumor therapies against various malignant solid tumors, including drug-resistant tumors and metast

175 y may represent a key therapeutic target for solid tumors, including glioblastoma.

176 Wee1, with single-agent activity in multiple solid tumors, including sarcoma, glioblastoma, and head

177 ation and metastatic colonization in various solid tumors, including those of the breast, prostate, a

178 for drug screening and mechanism studies on solid tumor interactions with functional blood vessels.

179 Growth in most solid tumors is dependent upon remodeling 'stroma', comp

180 Characterizing the complex composition of solid tumors is fundamental for understanding tumor init

181 the development of CAR-T cell therapies for solid tumors is hampered by the lack of truly tumor-spec

182 markable promise, but their efficacy in many solid tumors is limited, in part due to the low frequenc

183 Oxygen heterogeneity in solid tumors is recognized as a limiting factor for ther

184 Hypoxia in solid tumors is thought to be an important factor in res

185 ents with advanced, metastatic, or recurrent solid tumors known to express the tumor-differentiation

186 this respect, ccRCC might differ from other solid tumors like esophageal squamous-cell carcinoma or

187 MEK1/2 inhibitor trametinib in patients with solid tumors, lymphomas, or multiple myeloma whose tumor

188 n attractive class of therapeutic agents for solid tumors, mainly because of their high target select

189 se 2 study of pembrolizumab in patients with solid tumor malignancies and LMD (NCT02886585).

190 llowed by hematologic malignancies, SOT, and solid tumor malignancies, and were lowest in people livi

191 cancer that remains among the most lethal of solid tumor malignancies.

192 , from 2.6 (95% CI, 2.6-2.7) in those with a solid tumor malignancy to 12.3 (95% CI, 11.3-13.2) in th

193 ay yield cellular products able to withstand solid tumor metabolic-deficient environments.

194 The role of neutrophils in solid tumor metastasis remains largely controversial.

195 most abundant hematopoietic cell type in the solid tumor microenvironment.

196 nges due to the biological complexity of the solid-tumor microenvironment (TME).

197 multivalent macromolecular agent in multiple solid tumor mouse models, overcoming common mechanisms o

198 In two xenograft and two syngeneic solid tumor mouse models, p40-Td CAR T cells showed supe

199 Modified Response Evaluation Criteria in Solid Tumors (mRECIST) criteria was used to evaluate CNS

200 te (Modified Response Evaluation Criteria in Solid Tumors (mRECIST) criteria) to the first DEB-TACE (

201 ing modified Response Evaluation Criteria in Solid Tumors (mRECIST) on cross-sectional images, time t

202 In a series of 11 solid tumors (n = 2936), LOF mutations are not associate

203 Underlying malignancies were solid tumors (n = 362; 17.6%) or hematologic malignancie

204 n-Hodgkin lymphoma, n = 13; leukemia, n = 6; solid tumor, n = 25; unspecified malignancy, n = 4).

205 ed a Phase I clinical trial in patients with solid tumors (NCT03076372).

206 Neuroblastoma is a common solid tumor of young children that arises from anomalies

207 stem tumors are the most common extracranial solid tumors of childhood and include neuroblastoma, gan

208 ation therapy (RT) is commonly used to treat solid tumors of the breast, lung, and esophagus; however

209 Conclusion: For solid tumors of the pelvis, the repeatability of the eva

210 95% CI 1.84-2.46; p < 0.001), and metastatic solid tumor (OR 1.70; 95% CI 1.19-2.43; p = 0.004) were

211 I study in patients with advanced/metastatic solid tumors, patients with anaplastic thyroid carcinoma

212 Particularly, solid tumors present unique challenges due to the biolog

213 uation of the radiologic response to them in solid tumors presents many challenges.

214 rmation and its possible connection to lower solid tumor prevalence, we developed the first model of

215 ations, introducing a potential paradigm for solid tumor prevention and treatment.

216 by means of response evaluation criteria in solid tumors (RECIST) 1.1 and Immuno-related Response Cr

217 Response per Response Evaluation Criteria in Solid Tumors (RECIST) 1.1, other radiographic changes in

218 entrally per Response Evaluation Criteria in Solid Tumors (RECIST) v1.1.

219 with use of Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1 and classification of

220 nse rate per Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1 by blinded independent

221 nd point was Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1 progression-free survi

222 asurable disease as per Response Criteria in Solid Tumors (RECIST) version 1.1, absence of brain meta

223 s defined by Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1.

224 results with Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1.

225 ding to both Response Evaluation Criteria in Solid Tumors (RECIST), version 1.1, in the response-eval

226 by modified Response Evaluation Criteria in Solid Tumors (RECIST).

227 disease per Response Evaluation Criteria in Solid Tumors (RECIST; version 1.1) assessed by independe

228 disease (by Response Evaluation Criteria in Solid Tumors [RECIST] version 1.1) regardless of histolo

229 and mortality rates, but most diagnostics on solid tumors rely on imaging tests with limited sensitiv

230 g (AS) in the development and progression of solid tumors remains to be defined.

231 antigen receptor (CAR)-modified T cells, to solid tumors requires combinatorial strategies to overco

232 Solid tumors reside in harsh tumor microenvironments (TM

233 id substitutions associated with leukemia or solid tumors, respectively.

234 inct morphological and metabolic stages of a solid tumor, starting with an avascular tumor and progre

235 etic basis of Hh pathway activation in adult solid tumors, such as small-cell lung cancer (SCLC), is

236 ent the long sought-after, ideal targets for solid tumor targeting by high-potency oncology compounds

237 While it is known that solid tumors tend to have higher mechanical rigidity, al

238 cis-X may be applied to pediatric and adult solid tumors that are aneuploid and heterogeneous.

239 fective against hematologic malignancies and solid tumors that are typically resistant to NK cell-med

240 otherapy shows limited efficacy against many solid tumors that originate from epithelial tissues, inc

241 our enhanced understanding of Trk biology in solid tumors, the importance of Trk signaling in hematol

242 iew, we highlight the role of macrophages in solid tumors, the progress made with macrophage-focused

243 re widely used in cancer treatments, but for solid tumors they often leave a residual tumor-cell popu

244 Compared with patients with solid tumors, those with hematologic malignancies also e

245 tion and worse outcome in different types of solid tumors, thus highlighting a critical role of corta

246 We hypothesize that the resistance of solid tumors to CAR-T can be overcome by similar means a

247 Responses of solid tumors to chimeric antigen receptor (CAR) T cell t

248 o known as UTMD, has been shown to sensitize solid tumors to radiation in preclinical models through

249 agents that exploit the inherent acidity of solid tumors to selectively graft cancer cells with immu

250 In a current series of solid tumors treated with ICB, we are unable to demonstr

251 itabine, a standard chemotherapy for various solid tumors, triggers hallmark immunostimualtory DAMP r

252 rt that ONM-100 was well tolerated, and four solid tumor types could be visualized both in- and ex vi

253 antitumor activity in patients with selected solid tumor types.

254 ofile consistent with that reported in other solid tumor types.

255 rognosis and high recurrence across multiple solid tumor types.

256 hort of what has been achieved in many other solid tumor types.

257 Pediatric cancers, particularly high-risk solid tumors, urgently need effective and specific thera

258 Since solid tumors utilize aberrant angiogenesis for their gro

259 In solid tumors, vascular structure and function varies fro

260 dy, we introduce a microfluidic model of the solid tumor-vascular interface composed of a human umbil

261 survival per Response Evaluation Criteria in Solid Tumors version 1.1 and overall survival, assessed

262 according to Response Evaluation Criteria in Solid Tumors version 1.1 based on two imaging assessment

263 eview as per Response Evaluation Criteria in Solid Tumors version 1.1 for radiological scans and WHO

264 igator using Response Evaluation Criteria in Solid Tumors version 1.1 in patients who received at lea

265 etermined by Response Evaluation Criteria in Solid Tumors version 1.1 in the intention-to-treat evalu

266 ommon in the Response Evaluation Criteria in Solid Tumors version 1.1 literature.

267 according to Response Evaluation Criteria in Solid Tumors version 1.1) and duration of response, and

268 according to Response Evaluation Criteria in Solid Tumors version 1.1) before study entry.

269 rding to the Response Evaluation Criteria in Solid Tumors version 1.1, and an Eastern Cooperative Onc

270 survival per Response Evaluation Criteria in Solid Tumors version 1.1.

271 according to Response Evaluation Criteria in Solid Tumors version 1.1.

272 according to Response Evaluation Criteria in Solid Tumors version 1.1.

273 s defined by Response Evaluation Criteria in Solid Tumors version 1.1.

274 sease as per Response Evaluation Criteria in Solid Tumors (version 1.1), and an Eastern Cooperative O

275 rding to the Response Evaluation Criteria in Solid Tumors (version 1.1), as assessed by an independen

276 herapy using Response Evaluation Criteria in Solid Tumors, version 1.1 (RECIST), and cancer antigen 1

277 uish between Response Evaluation Criteria in Solid Tumors, version 1.1 objective response rates of 20

278 ollow-up CT (Response Evaluation Criteria in Solid Tumors, version 1.1) were assessed.

279 according to Response Evaluation Criteria in Solid Tumors, version 1.1), which was assessed locally;

280 ted by using Response Evaluation Criteria in Solid Tumors, version 1.1.

281 sease as per Response Evaluation Criteria in Solid Tumors, version 1.1.

282 rding to the Response Evaluation Criteria in Solid Tumors, version 1.1.

283 ability in tumor growth rate and tumor size, solid tumors versus tumor heterogeneity and a necrotic p

284 Cy5.5-CTLs were clearly observed at targeted solid tumors via non-invasive NIRF imaging.

285 Because of the hypoxic nature of solid tumors, we investigated if oxygen, via hypoxia-ind

286 on germline DNA of 1,507 C-AYA patients with solid tumors, we show 12% of these patients carrying ger

287 11 subjects with advanced solid tumors were imaged by MRI at baseline and 2-3 days

288 alpha or Notch signaling routes prevalent in solid tumors were not activated.

289 Solid tumors were rare (2.8%); nearly all were young mal

290 Adult patients with solid tumors were treated in four cohorts: part A, to de

291 toma, the most common extracranial pediatric solid tumor, where MYCN amplification heralds a poor pro

292 that introduces truncated CD19 expression in solid tumors, which are then eradicated by CD19-specific

293 ssion of IL-17RD is downregulated in certain solid tumors, which has led to the hypothesis that it ma

294 patients with metastatic TP53 hotspot mutant solid tumors who were treated with ixazomib and vorinost

295 Within solid tumors, why monocytes preferentially differentiate

296 Neuroblastoma is a deadly pediatric solid tumor with infrequent recurrent somatic mutations.

297 ersus untreated observation in patients with solid tumors with CIT.

298 pulses (HVEPs) in clinical oncology to treat solid tumors with irreversible electroporation (IRE) and

299 rent status of immune profiling of pediatric solid tumors, with emphasis on tumor types that represen

300 In two solid tumor xenograft mouse models, a single infusion of