ライフサイエンスコーパス: tumor

1 y reduces the survival time of the mice with tumor.

2 and a potential target for immune-refractory tumor.

3 0) = 17 nM) and in mice with H1975 xenograft tumor.

4 bility for T cells to infiltrate and repress tumors.

5 h an immunosuppressive TME in multiple human tumors.

6 llular adenomas (HCAs) are rare benign liver tumors.

7 to treat homologous recombination-deficient tumors.

8 lly considered a characteristic of malignant tumors.

9 ing force for different types of spontaneous tumors.

10 rejection of both virus-injected and distant tumors.

11 zyme B promoter (Tax(+)), develop osteolytic tumors.

12 umulates dose-dependently in GLP-1R-positive tumors.

13 ft tumor growth and induces survivin loss in tumors.

14 nocytes and facilitates their recruitment to tumors.

15 tabolic response for both WT-ER and Y537S-ER tumors.

16 commonly cooccur in muscle invasive bladder tumors.

17 d poorer survival in patients with grade III tumors.

18 rs will be useful in treating BRAF-dependent tumors.

19 fication revealed deleted in malignant brain tumors 1 (DMBT1) (also known by the aliases GP340 and SA

20 iomas (9 low-grade, 34 high-grade; 9 primary tumors, 34 recurrent tumors) who had preoperative (time

21 h stereotactic body radiotherapy (SBRT), and tumor ablation (with transarterial chemo- or radio-embol

22 zed the genomic landscape of 34 BI-ALCLs (15 tumor and 19 in situ subtypes) collected from 54 BI-ALCL

23 We obtained 93 pancreatic cancer specimens (tumor and adjacent nontumor tissues) from patients who u

24 ts, we were able to obtain distinct edges of tumor and blood flow mapping of the tumor microvascular

25 otype and were capable of trafficking to the tumor and mediating cell killing.

26 Tumor and stromal cells cooperated in forming niches; st

27 Ly6C(hi) monocyte levels and recruitment to tumors and depletion of these cells abrogated MI-induced

28 x/flox);PostnCre(+)) were completely free of tumors and had normal phospho-ERK activity compared with

29 le in long-term survivors of pediatric brain tumors and that metformin is safe to use and tolerable i

30 uate the growth of genetically defined renal tumors and their association with patient clinical and g

31 changes that are more common in high-ploidy tumors and thus support altered selection pressures upon

32 novel putative biomarker genes in different tumors, and microarray and metabolomics data from Arabid

33 ibited growth of mutant TP53, WT PTEN LN-229 tumors, and sensitized LN-229 tumors to TMZ therapy.

34 , without the need for a priori knowledge of tumor antigen, ex vivo cellular manipulation, or cellula

35 lies on T lymphocyte-mediated recognition of tumor antigens.

36 Obesity/diabetes-associated liver tumors are specifically vulnerable to cyclin D1 deficien

37 Earlier attempts to use oxygenation of tumors as a monotherapy or to improve radiotherapy have

38 dies (n = 294) or from within canine mammary tumor associated regions (n = 471).

39 med on 20 matched blood and aqueous samples; tumor-associated chromosomal changes were found in 0/20

40 n-like growth factor 1 (IGF1) is produced by tumor-associated microglia in response to interleukin-4

41 , it remains unclear whether activity in the tumor-associated stroma contributes to malignancy.

42 We detected increased expression of both tumor-associated truncated O-linked glycans and their re

43 Here, in vivo characterization of tumor-associated USP22 upregulation and unbiased interro

44 Atypical teratoid rhabdoid tumors (ATRTs) are challenging pediatric brain cancers t

45 ncluding IL6, IL17, MCP-1, and GM-CSF in the tumor-bearing host, and persisted as memory cells.

46 Genetic sequences from 320 MSI tumor biopsies and matched healthy tissues in The Cancer

47 l free DNA (cfDNA) and of matched metastatic tumor biopsies from patients with metastatic prostate ad

48 Most patients had baseline tumor biopsies positive for PD-L1 expression (n = 28/40

49 elected tumor gene expression to control for tumor burden, we identified a subgroup of patients with

50 rically more frequent in NCI-MATCH than TCGA tumors, but not markedly so.

51 ld significantly boost therapy of MYC-driven tumors by enhancing intrinsic MYC-driven apoptosis.

52 form clinical efforts in targeting KRAS-G12D tumors by immunotherapy and has general implications for

53 Colorectal cancer (CRC) tumors can be partitioned into four biologically distinc

54 her clonal or at low frequency; hypermutated tumors can only establish after the evolution of immune

55 tive descriptor of O2 carrier interaction in tumor capillary networks, we accounted for factors such

56 ne metastases, but the mechanisms regulating tumor cell dissemination from the primary site to the sk

57 In modeling simulations, tumor cell doubling time, administered antibody, antibod

58 ensuing proliferative response, but also for tumor cell growth and survival.

59 roduction, migration toward tumor cells, and tumor cell killing.

60 6 regulates cytoskeletal dynamics to promote tumor cell migration and invasion.

61 Tumor cell migration to LECs was inhibited by blocking C

62 and protein levels to identify mechanisms of tumor cell survival and proliferation in adherent and no

63 esting a mechanism for prolonged epithelioid tumor cell survival.

64 investigate the impact of cross-talk between tumor cell- and endothelial cell (EC)-secreted IL6 on HN

65 This review focuses on tumor cell-intrinsic alterations that blunt productive a

66 that allowed for granular assessment of both tumor cells and the tumor microenvironment.

67 Dormant tumor cells are quiescent, and thus, do not respond to c

68 other hand, the ROS not only directly kills tumor cells by photodynamic therapy but stimulates the d

69 ure is used for targeting fast-proliferating tumor cells during chemo-, radio-, and immunotherapy.

70 ate of (177)Lu (or labeled metabolites) from tumor cells had the strongest effect on the minimal perf

71 hen decreased proliferation and migration of tumor cells in different in vitro 2D and 3D co-cultures.

72 s redirect pre-existing CMV immunity against tumor cells in vitro and in mouse cancer models.

73 onally, we found that during this adaptation tumor cells might present unique, temporally restricted

74 dominantly core, structural ECM proteins and tumor cells produced a diverse array of ECM-associated p

75 Tumor cells require nominal increases in protein synthes

76 , infiltrating nerves not only influence the tumor cells themselves but also impact other cells of th

77 redominance and juxtaposition of M2 TAM near tumor cells were associated with poor survival.

78 reased cytokine production, migration toward tumor cells, and tumor cell killing.

79 In both murine and human tumor cells, HOTAIR-sbid impaired the ability of HOTAIR

80 east cancer cell lines and 4T1 mouse mammary tumor cells, PD-L1 expression was regulated by the nucle

81 ced in stroma following alpha3 deletion from tumor cells.

82 vity of C(3)-ZIF(MCF) to accumulate in MCF-7 tumor cells.

83 r cell-autonomous invasive properties of the tumor cells.

84 s are closely involved in drug resistance of tumor cells.

85 on Jurkat cells delivered DiD to ~15% of the tumor cells.

86 c niche that captures aggressive circulating tumor cells.

87 e L1 insertions in aneuploid than in euploid tumor cells.

88 lls with the potential to differentiate into tumor cells.

89 Tumor characteristics did not differ significantly from

90 ibromas are benign nerve sheath Schwann cell tumors characterized by biallelic mutations in the neuro

91 Notably, we also observed complete tumor clearance and subsequent full protection against t

92 Outcome analysis included tumor control, preservation of serviceable hearing based

93 ts, the coregistration of multimodal PET/MRI tumor data was improved by using the reverse phase encod

94 of primary resected tumors, we discover that tumor-derived oRG-like cells undergo characteristic mito

95 alpha-fetoprotein (AFP) at liver transplant, tumor diameter, tumor pathology, and vascular invasion,

96 idual cells evolve into tumors or aspects of tumors displaying different characteristics of the initi

97 Here, to evaluate the utility of circulating tumor DNA (ctDNA) genotyping, we compare trial enrollmen

98 rapy is the only option for the treatment of tumor dormancy.

99 RG1-2 = 44% vs 8%, P < 0.001) and a trend to tumor downstaging as compared to the control group.

100 of a metastable bioanalyte toward predicting tumor drug sensitivity.

101 hod to track spatial oxygen distributions in tumors during fractionated radiotherapy, using oxygen-de

102 and detected with increased intensity at the tumor edge.

103 n, which in turn facilitates the movement of tumor epithelial cells toward nutrient-rich territories.

104 onymous somatic mutations derived from 6,789 tumor exomes across 14 cancer types from The Cancer Geno

105 more potent and selective inhibitors for the tumor-expressed CA IX.

106 il that the histotype-specific regulation of tumor fibrosis in lung cancer is mediated through differ

107 Notably, the early-onset tumor formation observed in p53(5KR/5KR) and p53-null mi

108 o the endothelium, a first step in secondary tumor formation.

109 s anti-PD-1 therapy resistance, and NGFR(hi) tumor fractions are associated with immune exclusion.

110 It has also been noted that frequently a tumor from a single patient harbors more than one resist

111 sing PDX models of colon cancer and resected tumors from colon cancer patients, our data demonstrated

112 assifier, DeepC, can effectively distinguish tumors from normal samples with an accuracy of 90% for P

113 cluster of differentiation (CD)138-selected tumor gene expression to control for tumor burden, we id

114 the loss of VHL through analysis of primary tumor genomic and transcriptomic data.

115 The aggressive brain tumor glioblastoma (GBM) is characterized by rapid cellu

116 ever, its efficacy in highly malignant brain-tumors, glioblastomas (GBM), is limited.

117 ion in human cancers is associated with high tumor grade, poor survival, and resistance to chemothera

118 given orally effectively inhibits xenograft tumor growth and induces survivin loss in tumors.

119 Consistently, GBP2 dramatically promotes GBM tumor growth and invasion in mice and significantly redu

120 Ultraselective HDAC6 inhibitors can reduce tumor growth and invasiveness of breast cancer by noncan

121 on and colony formation in vitro, as well as tumor growth and metastasis in vivo.

122 Overexpression of Trop2 induces tumor growth and metastasis while loss of Trop2 suppress

123 (CYP) enzymes have been linked to increased tumor growth and metastasis, largely on the basis of ove

124 spheroids in ovarian cancer (OC) facilitate tumor growth and progression, and also pose major obstac

125 cer agents to inhibit chemotherapy-resistant tumor growth by consuming intracellular glutathione and

126 ng CIP, as well as attenuated suppression of tumor growth in mice.

127 nt as a combination with anti-PD1, SG7 slows tumor growth in multiple syngeneic mouse models.

128 L2 demonstrated dose-dependent inhibition of tumor growth in the PSMA(+) flank tumor model.

129 criptional activity and is required for TNBC tumor growth in vivo using an orthotopic xenograft model

130 26a was able to induce an 80% tumor growth inhibition of xenografts derived from the e

131 In xenografts, a significant tumor growth inhibition was seen after twice-weekly intr

132 andard clinical dose of Abraxane reduces the tumor growth rate as effectively as the standard clinica

133 ll intrinsic oncogenic properties, decreased tumor growth, reduced the incidence of lung metastasis a

134 iate into defined progenies and initiate the tumor growth.

135 for assessing hypoxia, microvasculature, and tumor growth.

136 epletion of these cells abrogated MI-induced tumor growth.

137 raming of proline metabolism is critical for tumor growth.

138 Patients' tumors harbored FGFR1 or FGFR2 amplification (n = 20), F

139 Extracellular matrix in solid tumors has emerged as a specific, stable, and abundant t

140 ic regeneration and the progression of solid tumors have been uncovered by recent studies.

141 design also enables characterization of non-tumor hemodynamics (e.g. brain), other preclinical disea

142 method to impart high accuracy in resolving tumor hemodynamics during bevacizumab therapy in two typ

143 d with reticuloendothelial system clearance, tumor heterogeneity, and complexity of the tumor microen

144 chemotherapies induce dynamic changes in the tumor immune microenvironment that vary by subtype and p

145 insic alterations that blunt productive anti-tumor immune responses by directly or indirectly excludi

146 Cancer immunotherapies enhance anti-tumor immune responses using checkpoint inhibitors, such

147 e expression was associated with higher anti-tumor immunity in most solid malignancies.

148 has already influenced our understanding of tumor immunology and immunotherapy.

149 ng MK2 and XPA to pre-existing p53-deficient tumors in a highly aggressive, immunocompetent mouse mod

150 ated with gene expression from E2F2 knockout tumors in an MMTV-Neu background.

151 ompared to single-agent sunitinib treatment, tumors in sunitinib-treated EpsilonC-betaKO mice showed

152 Furthermore, CRPC tumors in which Pten is lost are also resistant to eradi

153 mune suppression from the earliest stages of tumor inception to subvert adaptive T cell immunity.

154 Analysis of tumor-infiltrating cells in dual PARP-1/PARP-2-deficienc

155 Direct competition between tumor-infiltrating lymphocytes (TIL) and cancer cells fo

156 c Abs enhances the expansion and function of tumor-infiltrating lymphocytes (TILs) for treating cance

157 The distribution of tumor-infiltrating lymphocytes (TILs) within the tumor m

158 erexpressed in TMEs and induces apoptosis in tumor-infiltrating, Fas receptor-positive lymphocytes.

159 disease aggressiveness in GBM, particularly tumor infiltration (P = .0044) and hyperplastic blood ve

160 enuate cancer stem cell markers, inhibit the tumor-initiating cell's neurosphere-forming capacity, an

161 work highlights, at a biochemical level, how tumor-initiating ETS translocations result in reprogramm

162 Chemoresistance, i.e., tumor insensitivity to chemotherapy, shortens life expec

163 dance of mutation signatures partitions POLE tumors into distinct subgroups dependent on the nature o

164 In melanoma patients, a tumor-intrinsic NGFR signature predicts anti-PD-1 therap

165 tients with somatostatin receptor-expressing tumors is often performed using administration protocols

166 While caspase-8 expression is lost in some tumors, it is increased in others, indicating a conditio

167 Glioblastomas are aggressive primary brain tumors known for their inter- and intratumor heterogenei

168 However, tumors less than 1 cm in size still remain difficult to

169 ed to clarify the prognostic role of primary tumor location in NSCLC.

170 Clinical features vary depending on the tumor location.

171 Fluorescent imaging using 6qcNIR allows 100% tumor margin assessment by generating en face images tha

172 logies that can improve the visualization of tumor margins and adjuvant therapies to ablate remaining

173 s accompanied by worsened hypoxia inside the tumor mass, creating a positive feedback loop.

174 of the interactions between platelets and a tumor may promote or prevent cancer progression.

175 Responses were observed regardless of tumor MCPyV, PD-L1, or TMB status.

176 hondrial activity is a critical component of tumor metabolism, with profound implications for tumorig

177 emain suboptimal, suggesting that AKT-driven tumor metastasis needs to be further understood.

178 Immunosuppressive tumor microenvironment (TME) and ascites-derived spheroi

179 c cancer, the degree of heterogeneity of the tumor microenvironment (TME) and its molecular underpinn

180 owever, metabolic constraints imposed by the tumor microenvironment (TME) can dampen their ability to

181 iew summarizes current understandings of the tumor microenvironment and intercellular communications

182 to extensive reprogramming of the pancreatic tumor microenvironment and that patients who progress on

183 tic traits of cancer cells and of associated tumor microenvironment components have been shown to pro

184 tes to fluoresce in the acidic extracellular tumor microenvironment due to the mechanism of nanoscale

185 ne a new role for Notch3 in manipulating the tumor microenvironment in bone metastases.

186 r-infiltrating lymphocytes (TILs) within the tumor microenvironment provides strong prognostic value,

187 turnover and decreases heterogeneity of the tumor microenvironment, hence PI3Kbeta inhibition may be

188 derstanding of intratumor heterogeneity, the tumor microenvironment, metastasis, and therapeutic resi

189 produces a signal only in the protease-rich tumor microenvironment, was topically applied to 90 spec

190 , tumor heterogeneity, and complexity of the tumor microenvironment.

191 that suggest the development of a malignant tumor microenvironment.

192 nular assessment of both tumor cells and the tumor microenvironment.

193 tly excluding effector CD8+ T cells from the tumor microenvironment.

194 rcome immune suppression associated with the tumor microenvironment.

195 y CAFs as the specific source of FGF1 in the tumor microenvironment.

196 types and increased stromal cells within the tumor microenvironment.

197 intratumoral heterogeneity, and deleterious tumor microenvironmental (TME) crosstalk.

198 edges of tumor and blood flow mapping of the tumor microvascular with improved sensitivity up to 11.0

199 eas recombinant CXCL11 significantly induced tumor migration, epithelial-to-mesenchymal transition, a

200 e been shown to promote an immunosuppressive tumor milieu.

201 ibition of tumor growth in the PSMA(+) flank tumor model.

202 Tumor models of human PCa epithelia with CAF expanded si

203 nd that Ewing sarcoma and malignant rhabdoid tumor (MRT), two pediatric cancers that are sensitive to

204 though conventional genomic markers (such as tumor mutation burden and neoantigen load) and the degre

205 s, mutational signatures in whole exome, and tumor mutational burden in predicting NAC response.

206 several cytokines and chemokines, especially tumor necrosis factor alpha (TNF-alpha), CCL3, CCL4, and

207 s those observed in ECD kidneys, except that tumor necrosis factor alpha and monocyte chemotactic pro

208 We examined the outcome of anti-tumor necrosis factor and anti-interleukin-12/interleuki

209 Tumor necrosis factor receptor 2 (TNFR2) is strongly upr

210 /MRI before and after ILP with melphalan and tumor necrosis factor-alpha.

211 model predicts that, without immune escape, tumor neoantigens are either clonal or at low frequency;

212 nset of those caused by WT EBV, although the tumors occurred at a similar rate.

213 inoma (CCA) is a highly malignant epithelial tumor of the biliary tree with poor prognosis.

214 he WHO classification of the digestive tract tumors of 2010 the disease was grouped under a heterogen

215 sity significantly enhanced the incidence of tumors of diverse histotypes and increased stromal cells

216 variable number of somatic L1 insertions in tumors of the same type from patient to patient.

217 s, we show that individual cells evolve into tumors or aspects of tumors displaying different charact

218 cDC1 maturation to drive superior control of tumor outgrowth.

219 e (p < 0.0001), rim deposition within sparse tumors (p = 0.045), and peripheral deposition (p < 0.000

220 Surgical removal of the tumor partially resolved the CFs and contributes to impr

221 n (AFP) at liver transplant, tumor diameter, tumor pathology, and vascular invasion, female sex was a

222 new alternative strategy to control ovarian tumor progression based on selectively disrupting a prev

223 pite the importance of AKT overactivation in tumor progression, results from clinical trials of vario

224 ular communications in CCA and their role in tumor progression.

225 nt (TME) can dampen their ability to control tumor progression.

226 on for how low levels of Beclin 1 facilitate tumor proliferation and contribute to poor cancer outcom

227 (LSC) retention and growth in the remodeled tumor-promoting BM is unclear.

228 T) (58.1%), catenin beta 1 (CTNNB1) (30.7%), tumor protein 53 (TP53; 18.7%), AT-rich interaction doma

229 rance and subsequent full protection against tumor rechallenge in 33% of nanoformulated CCL21-treated

230 ttributed to metastatic spread of disease or tumor recurrence after initial treatment.

231 echanisms by which the Western diet promotes tumor recurrence, including changes in the microbiome, i

232 The Warburg effect is a tumor-related phenomenon that could potentially be targe

233 S lesion endothelial cells to neuroendocrine tumors remains unknown.

234 veral studies, focused on different types of tumors, report a promising anticancer activity induced b

235 en receptor (CAR)-modified T cells, to solid tumors requires combinatorial strategies to overcome imm

236 nary function in lung cancer patients before tumor resection is essential for patient selection for s

237 serve as a therapeutic strategy to overcome tumor resistance to osimertinib.

238 Neuro-Oncology, Oncology, Treatment Effects, Tumor Response Supplemental material is available for th

239 light several emerging approaches to promote tumor retention and limit systemic exposure of potent in

240 One quarter of all tumor samples contain somatic integrations of telomeric

241 titatively imaged PD-1/PD-L1 interactions in tumor samples from patients, employing an assay that rea

242 Correlative studies on blood and tumor samples were performed to investigate potential bi

243 article design parameters for enhancement of tumor selectivity to achieve improved in vivo therapeuti

244 In contrast, only a minority of sporadic tumors show alterations in these genes.

245 iculty in specific targeting/delivery to the tumor site.

246 However, the role of cDC1s in expansion of tumor-specific CD8(+) T cells remains unclear.

247 ate identification of hundreds of shared and tumor-specific non-canonical HLA peptides, including an

248 niformly seropositive to ChHV5 regardless of tumor status.

249 hemselves but also impact other cells of the tumor stroma.

250 ematically assess methods for reconstructing tumor subclonality.

251 ing sCNAs in the NAT tissue and the adjacent tumor, suggesting a shared clonal origin, as well as ins

252 s, down-regulation of adhesion molecules and tumor suppressing phosphatases, and alteration in immune

253 owever, the contribution of this function to tumor suppression is poorly understood.

254 nical evidence reveal dual roles for GJs, in tumor suppression, generally referred to as dormancy, an

255 nt of underlying basal cells, constituting a tumor-suppressive effect.

256 = 0.0028), which has been reported as both a tumor suppressor and an oncogene.

257 In addition, Klotho is also a tumor suppressor and has beneficial roles in multiple or

258 These findings indicate that KMT2D is a lung tumor suppressor and that KMT2D deficiency confers a the

259 These findings demonstrate that BRCA2 tumor suppressor function tolerates substantial reductio

260 ations in the neurofibromatosis type 1 (NF1) tumor suppressor gene.

261 mutations can be exploited to identify novel tumor suppressor genes and to obtain a deeper characteri

262 sponse, as concomitant deletion of the Trp53 tumor suppressor or Chek2 DNA damage checkpoint kinase r

263 h cell cycle arrest at G2/M, upregulation of tumor suppressor p53 and p21 protein.

264 SMARCB1 has also been recognized to be a tumor suppressor protein which controls many tumorigenic

265 monstrate for the first time that p190A is a tumor suppressor using a xenograft mouse model with carc

266 olism rendered checkpoint blockade-resistant tumors susceptible to immunotherapy.

267 es from unaggressive and usually noninvasive tumors that recur and commit patients to long-term invas

268 In one pancreatic tumor, there were many more L1 insertions in aneuploid t

269 ll as instances in which both NAT tissue and tumor tissue harbor a gain of the same oncogene arising

270 s and adjuvant therapies to ablate remaining tumor tissues are needed during surgical resection of pr

271 D163(+) TAMs in glioblastoma patient-derived tumor tissues.

272 t increased the sensitivity of HR(+) 59-2-HI tumor to PD-L1 blockade, suggesting that antiprogestins

273 ith DZNep strongly sensitizes SCLC cells and tumors to cisplatin.

274 diagnosis of suspicious margins of dissected tumors to declare more precise intraoperative diagnosis

275 Disseminated tumors to the bone and lung are easily detected by micro

276 WT PTEN LN-229 tumors, and sensitized LN-229 tumors to TMZ therapy.

277 % and 33.4% when based on SUV(mean) and mean tumor-to-blood ratio, respectively.

278 ion data showed the highest tumor uptake and tumor-to-blood ratios for [(89)Zr]Zr-DFO-scFv-Fc-CD44 be

279 FET PET parameters were obtained (i.e., mean tumor-to-brain ratios [TBR], time-to-peak values).

280 expression distributions in three different tumor types from the Cancer Genome Atlas (TCGA).

281 sequencing data from 2,658 cancers across 38 tumor types, we analyzed 288,457 somatic structural vari

282 genes that are commonly de-regulated in PDAC tumors upon activation of KRAS and inactivation of TP53.

283 vivo biodistribution data showed the highest tumor uptake and tumor-to-blood ratios for [(89)Zr]Zr-DF

284 High-risk features were defined by bulky tumors, variant histology, lymphovascular invasion, hydr

285 to engineer human cell lines expressing POLE tumor variants, with and without mismatch repair (MMR).

286 trasound provides real-time visualization of tumor vasculature and perfusion.

287 he LAC/PYR was significantly correlated with tumor volume (R = 0.903, P = 0.005) and MCT 1 (R = 0.85,

288 l response trends for logarithmically scaled tumor volume are estimated as regression splines in a ge

289 implications of PSMA PET-derived whole-body tumor volume for overall survival are poorly elucidated

290 ith matching transcriptome sequencing for 63 tumors was performed.

291 live time-lapse imaging of primary resected tumors, we discover that tumor-derived oRG-like cells un

292 Single-time-point dose factors for tumor were determined to be 11.0, 12.1, 13.6, and 15.2 G

293 Most tumors were primary sarcomas (88.5%), the majority of wh

294 ntroduces truncated CD19 expression in solid tumors, which are then eradicated by CD19-specific CAR-T

295 4 high-grade; 9 primary tumors, 34 recurrent tumors) who had preoperative (time before surgery: media

296 rtion of proliferating CD8(+) T cells in the tumor with enhanced cytolytic potential and requires T c

297 hat scientists gained the ability to profile tumors with a resolution that allowed for granular asses

298 Human tumors with exonuclease domain mutations in the gene enc

299 ive surveillance, to aggressive and invasive tumors with high disease-specific mortality.

300 or nail beds, whole genome sequencing of 87 tumors with matching transcriptome sequencing for 63 tum