ライフサイエンスコーパス: solid tumor

1 ma is the most common childhood extracranial solid tumor.

2 ed to produce uniform mild hyperthermia in a solid tumor.

3 hibitors induce response in diverse types of solid tumors.

4 hich may inhibit their functionality against solid tumors.

5 cles are used to deliver anticancer drugs to solid tumors.

6 ase-relevant genes in CRC and possibly other solid tumors.

7 e in the nanoparticle delivery efficiency to solid tumors.

8 unique insights into biological processes in solid tumors.

9 is a prominent feature of malignant cells in solid tumors.

10 ical role in the treatment of most pediatric solid tumors.

11 treatment of hematological malignancies and solid tumors.

12 transfer (ACT) is much curtailed in treating solid tumors.

13 ouraging preclinical and clinical results in solid tumors.

14 ch are overexpressed in selected tissues and solid tumors.

15 logic malignancies and 5 (10%) patients with solid tumors.

16 target for colorectal and potentially other solid tumors.

17 However, their function is attenuated in solid tumors.

18 n correlated with a negative outcome in most solid tumors.

19 ic DNA rearrangements in childhood and adult solid tumors.

20 d poor efficacy have hampered application to solid tumors.

21 irected CAR T cells to control the growth of solid tumors.

22 a, and acute myeloid leukemia, as well as in solid tumors.

23 have superior antitumor efficacy on various solid tumors.

24 be beneficial for the therapy of many other solid tumors.

25 red with that observed in cells derived from solid tumors.

26 eutics are being used to treat patients with solid tumors.

27 Exposures: Molecular profiling across solid tumors.

28 broad applications in treating VEGF-mediated solid tumors.

29 gy should be efficacious for a wide range of solid tumors.

30 nown about the effects of DHA on established solid tumors.

31 Hypoxia is a common feature of solid tumors.

32 expressed on angiogenic endothelial cells in solid tumors.

33 VIPER facilitates effective gene transfer to solid tumors.

34 nt a substantial barrier to drug delivery in solid tumors.

35 are associated with childhood leukemias and solid tumors.

36 ing and in vivo imaging of both leukemia and solid tumors.

37 in patients with lymphoma or INI1-deficient solid tumors.

38 ed in patients with inoperable or metastatic solid tumors.

39 that 0.7% of nanoparticles are delivered to solid tumors.

40 HATs are recurrently mutated in leukemia and solid tumors.

41 % of newly diagnosed pediatric patients with solid tumors.

42 potent and selective arsenical drugs against solid tumors.

43 T cell therapies, which redirect T cells to solid tumors.

44 le hypoxic cancer cells found widely in most solid tumors.

45 al blockade as an antimetastatic strategy in solid tumors.

46 mmune responses that can induce rejection of solid tumors.

47 svascular mechanisms for their delivery into solid tumors.

48 lymphoma, highlighting key differences from solid tumors.

49 pacity to traffic to, regress and survive in solid tumors.

50 apeutic potential for both hematological and solid tumors.

51 egulated metabolism are defining features of solid tumors.

52 50 with hematologic malignancies and 50 with solid tumors.

53 al therapeutic approach to control growth of solid tumors.

54 n cancers and is an oncogenic driver in many solid tumors.

55 on modified Response Evaluation Criteria in Solid Tumors.

56 s and their application to the management of solid tumors.

57 arily focus on studies of epithelial-derived solid tumors.

58 n blocking the transport of nanoparticles to solid tumors.

59 often leads to severe glutamine depletion in solid tumors.

60 he extracellular acidosis that characterizes solid tumors.

61 ancer and within the neovasculature of other solid tumors.

62 is recurrently mutated in hematopoietic and solid tumors.

63 tic effect in a hypoxic environment, such as solid tumors.

64 imaging and therapeutic targeting of MEMs in solid tumors.

65 242 in patients with wild-type TP53 advanced solid tumors.

66 A hypoxic microenvironment is a hallmark for solid tumors.

67 rive the heterogeneous hypoxic landscapes in solid tumors.

68 al evaluation of CFI-402257 in patients with solid tumors.

69 vity of varlilumab in patients with advanced solid tumors.

70 s) are hallmark features of inflammation and solid tumors.

71 mittee using Response Evaluation Criteria in Solid Tumors 1.1 in the intention-to-treat population, a

72 the basis of Response Evaluation Criteria in Solid Tumors 1.1, 38% of these patients had a tumor as w

73 8%) were immunocompromised, distributed into solid tumors (122), hematologic malignancies (106), and

74 20 of 32) of patients with CNS metastases of solid tumors, 50% (six of 12) of patients with primary b

75 ids, here we identify hypoxia, a hallmark of solid tumors [9], as an inducer of the collective-to-amo

76 In most cancer cell lines derived from solid tumors, ABBV-075 triggers prominent G1 cell-cycle

77 Patients (99,590) with a solid tumor and 13,538 patients with a hematological mal

78 red laser-triggered photothermal ablation of solid tumor and simultaneous inhibition of PTT-induced i

79 es to hypoxic and metabolic gradients in the solid tumor and to an aggressive tumor phenotype.

80 predictive biomarker of radiosensitivity in solid tumors and a generally applicable druggable target

81 herapy is essential to the treatment of most solid tumors and acquired or innate resistance to this t

82 ytic, but whether they can also traffic into solid tumors and engulf cancer cells is questionable, gi

83 e the effectiveness of CAR T cell therapy in solid tumors and help protect against the emergence of e

84 ponses to hypoxia and are often activated in solid tumors and hematologic malignancies due to intratu

85 cal trials, alone or in combination, in both solid tumors and hematologic malignancies.

86 emonstrate that GNA13 is upregulated in many solid tumors and impacts survival and metastases in pati

87 s 1 and 2 (CtBP1 and 2) occurs in many human solid tumors and is associated with poor prognosis.

88 uppressor cells (MDSCs) has been observed in solid tumors and is correlated with tumor progression; h

89 the tumors and was effective against distant solid tumors and lung metastases.

90 ogenesis is essential for the development of solid tumors and metastatic disease.

91 Hypoxic regions exist within most solid tumors and often lead to altered cellular metaboli

92 roenvironment influences the pathogenesis of solid tumors and plays an outsized role in some.

93 vel method for the in silico dissociation of solid tumors and presents novel insights that have impli

94 t mediates epigenetic silencing in unrelated solid tumors and provide strong support for an instructi

95 tly in phase II clinical trials for advanced solid tumors and refractory lymphoma.

96 sing RECIST (Response Evaluation Criteria in Solid Tumors) and an exploratory analysis of vascular re

97 malignancy was classified into skin cancer, solid tumor, and posttransplant lymphoproliferative diso

98 ally impacted the diagnosis and treatment of solid tumors, and common themes regarding the use of kin

99 disease per Response Evaluation Criteria in Solid Tumors, and had an Eastern Cooperative Oncology Gr

100 Tissue factor (TF) is upregulated in many solid tumors, and its expression is linked to tumor angi

101 sorders, hemophagocytic lymphohistiocytosis, solid tumors, and other diseases.

102 , this success has yet to be extrapolated to solid tumors, and the reasons for this are being activel

103 Regions of hypoxia occur in most solid tumors, and they are associated with a poor progno

104 mor populations, as well as other liquid and solid tumor antigens.

105 elated with asparaginase efficacy in certain solid tumors as well.

106 ukemia, but have been much less effective in solid tumors, because neutralizing antibodies develop an

107 s and through cell-non-autonomous effects on solid tumor biology.

108 Similar to most solid tumors, breast cancer is a heterogeneous disease w

109 ted APOBEC3B expression has been detected in solid tumors, but expression of APOBEC3A (A3A) in cancer

110 roduces therapeutic activity in a variety of solid tumors, but most patients exhibit partial or compl

111 unotherapy for hematological malignancies or solid tumors by administration of monoclonal antibodies

112 Close to half of all solid tumors carry inactivating mutations in the TP53 ge

113 ntify candidate microRNA biomarkers in a rat solid tumor cell line.

114 best growth inhibition of both leukemia and solid tumor cell lines.

115 improved capacity to graft both leukemic and solid tumor cells compared with NSI, NOG, and NDG mice.

116 Uptake of CLR1404 by pediatric solid tumor cells was tested in vitro by flow cytometry

117 ietic stem cells (as well as hematologic and solid tumor cells) and their protective microenvironment

118 itors when treating ovarian cancer and other solid tumors characterized by increased IL-8/CXCL8 expre

119 Solid tumor chemotherapy regimens pose a risk for hepati

120 programmed death ligand 1-positive, advanced solid tumor cohorts.

121 ophages on soft (like marrow) or stiff (like solid tumors) collagenous gels demonstrated a stiffness-

122 not efficiently target CAR T cells; second, solid tumors create an immunosuppressive microenvironmen

123 en under shear flow in communication with 3D solid tumors cultured in a tumor compartment.

124 tinued until Response Evaluation Criteria in Solid Tumors-defined disease progression while receiving

125 In contrast to solid tumor-derived cells, cMyc and Sp transcriptions ar

126 pecific obstacles to drug delivery that make solid tumors difficult to treat, as well strategies to o

127 Patients with solid tumors displayed increased in-hospital mortality (

128 the delivery efficiency of nanoparticles to solid tumors either through the engineering of multifunc

129 r kinases, overactive in selected subsets of solid tumors, elicit improved response rates and surviva

130 hematological diseases, however, studies on solid tumors failed due to widely unknown reasons.

131 Patients age >/= 65 years with a solid tumor, fluent in English, and who were scheduled t

132 igh) T cells persist in and regress multiple solid tumors following adoptive cell transfer.

133 ligand and receptor expression is common in solid tumors for activin and TGF-beta pathway members.

134 CAR T cell treatments are less effective in solid tumors for several reasons.

135 Solid tumors, for instance, get their nourishment from n

136 oach could also be applied to treat numerous solid tumors from individual patients.

137 been reported to play a more active role in solid tumor growth and metastatic dissemination than sim

138 tudy was initiated in patients with advanced solid tumors harboring genetic alterations in fibroblast

139 The spatial and temporal heterogeneity of solid tumors has been a critical barrier to the developm

140 However, clinical activity in solid tumors has been disappointing and toxicity has bee

141 oportion of relapsed or refractory pediatric solid tumors have actionable alterations.

142 However, most human solid tumors have an abnormal karyotype implying that ga

143 The challenges in solid tumor immunotherapy comprise heterogenously expres

144 1 in 6 patients who undergo treatment for a solid tumor in the United States.

145 Notably, this intron was expressed in solid tumors in a stage-dependent manner.

146 Here, we show that PMPs infiltrate solid tumors in humans and mice and transfer platelet-de

147 ith intratumoral bacteria injection to treat solid tumors in mice.

148 ve been shown to strongly suppress growth of solid tumors in mice.

149 des a unique model for studying vascularized solid tumors in vitro.

150 s first report on pHLIP-PNA lncRNA targeting solid tumors in vivo suggests a novel cancer therapeutic

151 or therapeutic response or prognosis in many solid tumors, including BC.

152 Refractoriness of solid tumors, including colorectal cancers (CRCs), to im

153 malignancies, it has been less effective in solid tumors, including EOC.

154 associated with a poor prognosis in several solid tumors, including epithelial ovarian cancer (EOC).

155 on and as a key oncogenic factor in numerous solid tumors, including glioblastoma.

156 osase expressed in the majority of childhood solid tumors, including lethal rhabdoid tumors.

157 berrantly overexpressed or activated in most solid tumors, including pancreatic ductal adenocarcinoma

158 cell (EC) barriers in normal tissues and in solid tumors, including paracellular and transcellular p

159 account of various unique characteristics of solid tumors, including some mechanisms that are still n

160 (CTCs)-rare cells that enter the blood from solid tumors, including those of the breast, prostate gl

161 ng a variety of hematologic malignancies and solid tumor indications.

162 racellular matrix within and surrounding the solid tumor is a critical determinant of metastasis.

163 T-cell infiltration of solid tumors is associated with improved prognosis and f

164 However, the efficacy of ATRA against solid tumors is limited due to its short half-life of 45

165 However, their efficacy in solid tumors is marginal and drug resistance hampers the

166 driving the emergence of drug resistance in solid tumors is tumor hypoxia, which leads to the format

167 oid cancer (ATC), one of the most aggressive solid tumors, is characterized by rapid tumor growth and

168 lthough EGFL7 is aberrantly overexpressed in solid tumors, its role in leukemia has not been evaluate

169 mmune cells in the hypoxic cores of advanced solid tumors leads to a chain reaction of stimuli that e

170 proteasome inhibitor PS-341 (bortezomib) in solid tumors led to the invention of MLN9708 (ixazomib),

171 Solid tumors limit the effectiveness of immunotherapeuti

172 atocellular carcinoma samples and show these solid tumors maintain circadian function but with aberra

173 , while no increased risk of the most common solid tumor malignancies was observed.

174 an immunotherapy target in hematological and solid tumor malignancies.

175 shown limited efficacy for the management of solid tumor malignancies.

176 cacy with a small-molecule BET degrader in a solid-tumor malignancy and potentially represents an imp

177 ges that CAR T cells have to surmount in the solid tumor microenvironment and new approaches that are

178 In a solid tumor mouse model allowing simultaneous monitoring

179 to modified Response Evaluation Criteria in Solid Tumors (mRECIST).

180 Treatment failure in solid tumors occurs due to the survival of specific subp

181 toma, the most common extracranial malignant solid tumor of the central nervous system in infants and

182 Neuroblastoma, the most common solid tumor of young children, frequently presents with

183 However, we have evidence that for solid tumors of epithelial origin, extreme levels of gen

184 mics studies have been performed to evaluate solid tumors of the body, and there is much to explore.

185 Solid tumors often contain hypoxic regions which are res

186 ioma without associated iris or ciliary body solid tumor on clinical examination and ultrasound biomi

187 f leukoreduction and platelet transfusion in solid tumors or chronic, stable severe thrombocytopenia)

188 in patients with hematologic malignancies or solid tumors or in those who undergo invasive procedures

189 rticularly B19 parvovirus; thymoma and other solid tumors; or a variety of other disorders, drugs, or

190 erapy' - is a highly effective treatment for solid tumors, particularly prostate cancer.

191 In solid tumor patients admitted between 2009 and 2013, hos

192 ICU admission between 1997 and 2013; 39,734 solid tumor patients and 6,652 patients with a hematolog

193 ts indicate that a significant proportion of solid tumor patients are eligible for immuno-targeted co

194 Solid tumor perfusion is a proven variable of interest f

195 In contrast to many other solid tumors, periampullary adenocarcinomas exhibited mo

196 king, and lipid transport, and contribute to solid tumor progression as routes of metastasis.

197 owever, tumor tissue tends to stiffen during solid tumor progression, and tissue stiffness is known t

198 dent mechanism.Angiogenesis is essential for solid tumor progression.

199 B activation is important in EGFR-associated solid-tumor progression.

200 led legumain, is highly expressed in various solid tumors, promoting cancer cell invasion, migration,

201 Methods In total, 189 patients with advanced solid tumors received selinexor (3 to 85 mg/m(2)) in 21-

202 disease with Response Evaluation Criteria in Solid Tumor (RECIST) measurable disease and evidence of

203 by modified Response Evaluation Criteria in Solid Tumors (RECIST) (target hazard ratio, 0.60).

204 ted by using Response Evaluation Criteria in Solid Tumors (RECIST) 1.1 guidelines, and the CT images

205 sessed using Response Evaluation Criteria in Solid Tumors (RECIST) and iodine-123 ((123)I) -metaiodob

206 only 31% met Response Evaluation Criteria in Solid Tumors (RECIST) for measurable metastatic disease.

207 12 weeks per Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 by independent central review

208 erapy beyond Response Evaluation Criteria in Solid Tumors (RECIST) v1.1-defined progression.

209 the modified Response Evaluation Criteria In Solid Tumors (RECIST) version 1.0 for pleural mesothelio

210 assessed by Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1 for NSCLC and by modif

211 t as per the Response Evaluation Criteria In Solid Tumors (RECIST) version 1.1 in the full analysis p

212 e disease by Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1, adequate haematologic

213 rding to the Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1, had adequate organ fu

214 ation (WHO), Response Evaluation Criteria in Solid Tumors (RECIST), modified RECIST (mRECIST), and Eu

215 according to Response Evaluation Criteria in Solid Tumors (RECIST), version 1.1.

216 response per Response Evaluation Criteria In Solid Tumors (RECIST, version 1.1).

217 ew using the Response Evaluation Criteria in Solid Tumors (RECIST; version 1.1).

218 esponse (via Response Evaluation Criteria in Solid Tumors [RECIST] version 1.1), and progression-free

219 (defined by Response Evaluation Criteria In Solid Tumors [RECIST] version 1.1), as assessed by a mas

220 sponse rate (Response Evaluation Criteria in Solid Tumors [RECIST] version 1.1), progression-free sur

221 according to Response Evaluation Criteria in Solid Tumors [RECIST], version 1.1) previously treated w

222 yelocytic leukemia (APL) but its activity in solid tumors remains to be explored.

223 etylases (HDACs) regulate differentiation in solid tumors remains unclear.

224 T cell dysfunction in solid tumors results from multiple mechanisms.

225 he Her2 antigen in two different established solid tumor settings.

226 The most common solid tumors show intrinsic multidrug resistance (MDR) o

227 -3.39), PTLD (SHR, 1.93; 95% CI, 1.01-3.66), solid tumor (SHR, 1.44; 95% CI, 1.04-1.99), death (HR, 1

228 ovarian cancer cells from patient ascites or solid tumors sorted for alpha2-6 sialylation grew as sph

229 orts from the phase 1 dose-expansion JAVELIN Solid Tumor study, patients aged 18 years and older with

230 A slow-releasing ATRA formulation inhibits solid tumors such as HCC, but can be used only in animal

231 Moreover, in solid tumors such as stage 4 neuroblastomas (NB), imatin

232 ing RNA (siRNA) delivery to the liver and to solid tumors, systemic siRNA delivery to leukocytes rema

233 For the treatment of solid tumors, systemically delivered drug carriers face

234 Thus, mAb against well-validated solid tumor targets, such as the epidermal growth factor

235 eity along three spatial dimensions (3-D) in solid tumors, termed the tumor ecosystem diversity index

236 n, it is highly immunogenic in patients with solid tumors that have normal immune systems, but much l

237 However, in solid tumors, the full potential of CAR T cell therapy i

238 Despite its wide application in a variety of solid tumors, the mechanisms of cancer cell resistance t

239 velop and disseminate quite differently than solid tumors, the pathways that regulate immune activati

240 In solid tumors, the presence of lymph node-like structures

241 disappointing results in clinical trials of solid tumors, therapeutic targets specific to HDAC3 func

242 iver CAR T cells directly to the surfaces of solid tumors, thereby exposing them to high concentratio

243 ited to the endothelium but may also include solid tumor tissue of nonprostatic cancers including mel

244 In practice, solid tumor tissue samples obtained from clinical settin

245 While in human solid tumors TP53 is mutated in more than half of cases,

246 c profiles and synergize their activities in solid tumor treatment, a need still unmet in the clinic.

247 , dose-escalation trial (part of the JAVELIN Solid Tumor trial) assessed four doses of avelumab (1 mg

248 nce of the CD73/adenosine pathway in several solid tumor types, and the initiation of phase I trials

249 for the prevention and treatment of certain solid tumor types.

250 ibed mtDNA copy number depletion across many solid tumor types.

251 ention of cancer progression across multiple solid tumor types.

252 cterize the mode of evolution across diverse solid tumor types.

253 t modes of evolution both within and between solid tumor types.

254 Six patients with advanced solid tumors underwent (11)C-erlotinib PET scans before

255 Radioimmunotherapy of solid tumors using antibody-targeted radionuclides has b

256 However, treatment of solid tumors using CAR T cells has been largely unsucces

257 of cancer therapeutics engineered to destroy solid tumors using different strategies such as nanocarr

258 Imaging metabolic dysfunction, a hallmark of solid tumors, usually requires radioactive tracers.

259 according to Response Evaluation Criteria In Solid Tumors v1.1), Eastern Cooperative Oncology Group p

260 sponse rate (Response Evaluation Criteria in Solid Tumors v1.1, central review) and safety.

261 Solid tumor vasculature is highly permeable, allowing th

262 nse rate per Response Evaluation Criteria in Solid Tumors version 1.1 (central review), assessed in p

263 according to Response Evaluation Criteria In Solid Tumors version 1.1 (RECIST v1.1) or death due to a

264 e disease by Response Evaluation Criteria In Solid Tumors version 1.1 (RECIST v1.1), tumour biopsy or

265 e lesion per Response Evaluation Criteria In Solid Tumors version 1.1 (RECIST v1.1), unresectable sta

266 activity per Response Evaluation Criteria in Solid Tumors version 1.1 and immune-related response cri

267 sponse rate (Response Evaluation Criteria In Solid Tumors version 1.1) for the expansion phase.

268 rding to the Response Evaluation Criteria In Solid Tumors version 1.1, and had at least one lesion ac

269 s defined by Response Evaluation Criteria in Solid Tumors version 1.1, and normal end-organ function.

270 etermined by Response Evaluation Criteria in Solid Tumors version 1.1, intervention by surgery or rad

271 s by central Response Evaluation Criteria in Solid Tumors version 1.1.

272 response per Response Evaluation Criteria In Solid Tumors version 1.1.

273 e disease by Response Evaluation Criteria in Solid Tumors version 1.1.

274 sessment per Response Evaluation Criteria In Solid Tumors (version 1.1) in all randomly assigned pati

275 sessment per Response Evaluation Criteria In Solid Tumors (version 1.1) in the total population, in p

276 ponse as per Response Evaluation Criteria in Solid Tumors (version 1.1).

277 , by RECIST (Response Evaluation Criteria in Solid Tumors) version 1.1.

278 col using Response to Evaluation Criteria in Solid Tumors, version 1.0.

279 a (irRC) and Response Evaluation Criteria in Solid Tumors, version 1.1 (RECIST v1.1) in patients with

280 rding to the Response Evaluation Criteria in Solid Tumors, version 1.1, as assessed by independent ce

281 ing to local Response Evaluation Criteria in Solid Tumors, version 1.1, assessed in the intention-to-

282 nse rate per Response Evaluation Criteria in Solid Tumors, version 1.1, by investigator review.

283 according to Response Evaluation Criteria in Solid Tumors, version 1.1, in the intention-to-treat pop

284 ed miRNAs transfer in vivo to tumor cells in solid tumors via infiltrating MPs, regulate tumor cell g

285 Dose escalation (3 + 3 design) in all solid tumors was followed by dose expansion in renal cel

286 patterns of MGMT expression across different solid tumors, we make a case for revisiting temozolomide

287 selected TILs in vivo In two mouse models of solid tumors, we show that PD-1 allows identification an

288 ted central nervous system (CNS) and non-CNS solid tumors were prospectively enrolled in the BASIC3 s

289 ells (TRM cells) accumulate in several human solid tumors, where they have been associated with a fav

290 e sufficient in patients with poor-prognosis solid tumors, whereas patients with hematologic malignan

291 progression-promoting potentials in certain solid tumors, which is largely attributed to the immunom

292 own one, as there exists hypoxia inside most solid tumors while oxygen is essential to enhance radiat

293 nteraction is a therapeutic target for human solid tumors "(Willingham et al., 2012).

294 Neuroblastoma is a pediatric solid tumor with high expression of the tumor associated

295 l-cell lung cancer (sqNSCLC; arm 1) or other solid tumors with FGFR genetic alterations (mutations/am

296 ing physical energy based modality to ablate solid tumors with high power, or increase local permeabi

297 can elicit a rapid and selective necrosis of solid tumors, with limited deleterious effects on surrou

298 and has the highest mortality rate among all solid tumors, with the majority of patients diagnosed at

299 vely employed for the clinical management of solid tumors, with therapeutic or palliative intents, fo

300 Having observed complete eradication of solid tumor xenografts, we conclude that targeted alpha-