ライフサイエンスコーパス: tumor cell

1 fication of cell-intrinsic properties of the tumor cell.

2 ced in stroma following alpha3 deletion from tumor cells.

3 t surround, protect, and promote survival of tumor cells.

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

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

6 aseline, indicating the presence of residual tumor cells.

7 as well as increased antigen presentation in tumor cells.

8 at are uniquely essential to the survival of tumor cells.

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

10 antly reduced intracranial growth of mammary tumor cells.

11 lls and validation in KB2P1.21 mouse mammary tumor cells.

12 as well as increased antigen presentation in tumor cells.

13 proliferation and inducing autophagy of the tumor cells.

14 f-art approach to heterogeneity profiling in tumor cells.

15 g CTLs pre-cultured with TMPs from untreated tumor cells.

16 an important role in determining the fate of tumor cells.

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

18 NKA inhibition to their cytotoxic effects on tumor cells.

19 selectively releases alkylating agents into tumor cells.

20 c niche that captures aggressive circulating tumor cells.

21 ssays, circulating tumor DNA and circulating tumor cells.

22 mmed death-ligand 1 (PD-L1) on KSHV-carrying tumor cells.

23 ated from mouse brain tumors kill cocultured tumor cells.

24 consumption and cell migration rates in non-tumor cells.

25 ism, shaping a maladapted survival niche for tumor cells.

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

27 nipulation, increasing capture efficiency of tumor cells.

28 in-3 as the major counterreceptor of GPVI on tumor cells.

29 d integration sites in subpopulations of the tumor cells.

30 the growth and transformation of epithelial tumor cells.

31 ated to the bone microenvironment as well as tumor cells.

32 MTV-PyMT mice and orthotopically grafted 4T1 tumor cells.

33 lls with the potential to differentiate into tumor cells.

34 macrophage colony-stimulating factor CSF1 by tumor cells.

35 ing the ability of cytotoxic T cells to kill tumor cells.

36 affect alloreactive immune responses against tumor cells.

37 iates epigenetic reprogramming of metastatic tumor cells.

38 have a high affinity for galectin-expressing tumor cells.

39 higher in tissues with a high MD as well as tumor cells.

40 in platelets and favors the extravasation of tumor cells.

41 bility in homologous recombination-deficient tumor cells.

42 ing myeloperoxidase-containing granules into tumor cells.

43 lung metastasis model, we found that primary tumor cells activated vimentin and N-cadherin in situ, b

44 from FAK-null CAFs contribute to the reduced tumor cell activities and metastasis.

45 Wnt5a promoted ovarian tumor cell adhesion to peritoneal mesothelial cells as w

46 Knockdown of GM-CSF in tumor cells also delays tumor progression with decreased

47 )DODA-Me showed antiproliferative effects on tumor cells, altered cellular bioenergetics, suppressed

48 ts as a chemotherapeutic drug efflux pump in tumor cells, although its physiological functions remain

49 al-time in vivo monitoring of PD-L1 positive tumor cells and CTLs with cellular resolution by non-inv

50 DMR had higher degrees of clustering between tumor cells and CTLs, and between tumor cells and HLA-DR

51 an update on metabolic communication between tumor cells and heterogeneous stromal components in prim

52 ng between tumor cells and CTLs, and between tumor cells and HLA-DR(+) macrophages, but not HLA-DR(-)

53 PD-L1 is expressed in tumor cells and its interaction with PD-1 plays an impor

54 bles a more immediate study of fresh primary tumor cells and minimizes adaptive changes that occur wi

55 NETs wrap and coat tumor cells and shield them from cytotoxicity, as mediat

56 mpounds are cytotoxic to apoptosis-resistant tumor cells and show activity in animal tumor models.

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

58 of infiltrative nature via crosstalk between tumor cells and their microenvironment.

59 s a result of an evolving cross-talk between tumor cells and their surrounding nontransformed stroma.

60 immune evasion, collective dissemination of tumor cells, and emergence of cancer cell subpopulations

61 imary tumors, elevated levels of circulating tumor cells, and increased spontaneous metastasis to the

62 differences among the parental, circulating tumor cells, and lung metastatic cells.

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

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

65 immune-effector functions of the underlying tumor cell are insufficiently characterized.

66 target nucleic acid delivery specifically to tumor cells are discussed.

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

68 Circulating tumor cells are tumor-derived pioneers responsible for t

69 e tumor cell engagement during mitosis, when tumor cells are vulnerable, for efficacy.

70 T-cells and PD-L1 + macrophages and PD-L1 + tumor cells as mechanistic determinants of response.

71 Tumor cells at tumor/brain-interface often exist behind

72 Expression of Tn and STn in tumor cells attenuates their sensitivity to TRAIL treatm

73 A gene signature reflecting tumor cell-autonomous PADI4 inhibition was associated wi

74 ation, we sought to study how YAP influences tumor cell behavior within the circulatory system.

75 crease the invasiveness of pancreatic cancer tumor cells, but the mechanisms by which Dyn2 regulates

76 ted cellular and membrane levels of PD-L1 in tumor cells by 50% as measured by Western blotting and f

77 multilayering, APC(-/-) tumors induce rho in tumor cells by autonomous downregulation of E-cadherin (

78 y for the robust and specific elimination of tumor cells by cellular immunotherapy.

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

80 the stem-like properties of KRAS-expressing tumor cells by targeting SOX9.

81 ndent accumulation of lipid peroxides within tumor cells by transferring myeloperoxidase-containing g

82 Despite the apparent destruction of most tumor cells by VSV-EBOVDeltaMLD, the virus remained acti

83 The FAM122A expression level in a tumor cell can serve as a useful biomarker for predictin

84 difficulty in distinguishing tumor from non-tumor cells can lead to inaccurate Ki-67 indices and pos

85 ls, as only a small fraction of disseminated tumor cells can overcome the numerous hurdles they encou

86 ed it to investigate how and to which extent tumor cells can survive in adverse micro-environments ch

87 571K), eIF4E-transporter was mislocalized in tumor cells carrying CRM1(E571K).

88 to identify a collective signal generated by tumor cell clusters supporting metastatic colonization.

89 r results suggest that m(6)A demethylases in tumor cells contribute to the efficacy of immunotherapy

90 1's involvement in vascular endothelial cell tumor cell cross-talk.

91 Circulating tumor cells (CTC) disseminating is an important cause of

92 Circulating tumor cells (CTCs) derived from a primary tumor can be d

93 Isolation of circulating tumor cells (CTCs) from blood samples has important prog

94 More recently, detection of circulating tumor cells (CTCs) has been considered as an appealing p

95 For example, circulating tumor cells (CTCs) have been demonstrated as useful biom

96 s in metastatic lung nodules and circulating tumor cells (CTCs) in two mouse models of mammary cancer

97 tDs NPs could target the in vivo circulating tumor cells (CTCs) to suppress TNBC lung metastasis.

98 yeloperoxidase suppresses neutrophil-induced tumor cell cytotoxicity.

99 echanisms through which PMNs directly induce tumor cell death and proliferation in vivo and suggest t

100 e demonstrate that in vitro, hMGL-4.0 causes tumor cell death, associated with increased reactive oxy

101 or-mediated feedforward circuit triggered by tumor cell death, which enforces the CD73-checkpoint.

102 enomenon in which the growth and survival of tumor cells depend on the activity of a particular prote

103 N-gly-positive subclones is evidence of the tumor cells' dependence on sites, despite the changing g

104 Abolishing cGAMP production in Cgas(-/-) tumor cells, depletion of extracellular ATP, or inactiva

105 lowing ovarian cancer cell detachment and in tumor cells derived from malignant ascites of high-grade

106 These findings suggest that tumor cell-derived lactate activates GPR81 in dendritic

107 an autocrine role to promote tumor growth by tumor cell-derived lactate.

108 During cancer progression, tumor cells develop a variety of mechanisms to cope with

109 Cancer therapies aim to kill tumor cells directly or engage the immune system to figh

110 The tumor cells displayed morphological and immunophenotypic

111 How tumor cells disseminate within the lymphatic network rem

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

113 tant YAP expression is sufficient to enhance tumor cell dissemination in zebrafish and mice.

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

115 their potential for sterilizing disseminated tumor cells (DTCs), it is critical to determine the cont

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

117 tential to improve in vivo identification of tumor cells during colposcopy examination, allowing a ra

118 ition, the phagocytic clearance of apoptotic tumor cells (efferocytosis) enhances the immunosuppressi

119 Here, we report that tumor cells embedded in a 3-dimensional collagen gel, ho

120 osures of ispinesib is critical for adequate tumor cell engagement during mitosis, when tumor cells a

121 The conditioned medium of GEM-treated tumor cells enhances differentiation of mouse bone marro

122 pecifically study a population of long-lived tumor cells enriched in CSCs, which show stem-like chara

123 steps of metastasis are known to occur while tumor cells enter, travel through, or exit circulation,

124 ength suggests an alternative method whereby tumor cells escape the critical shortening of telomeres.

125 hromosomal alterations, a mechanism by which tumor cells evolve, adapt, and resist therapeutics.

126 elicits a subpopulation of otherwise luminal tumor cells exhibiting basal differentiation traits, whi

127 that the interplay between platelet GPVI and tumor cell-expressed galectin-3 uses ITAM-signaling comp

128 H-based detection of ANGPT2, we found strong tumor cell expression of ANGPT2 in a subset of patients

129 Tumor cell expression of IL1beta in vivo was driven by m

130 losamide and forskolin significantly reduced tumor cell extravasation in zebrafish, and niclosamide d

131 Thus, this study analyzed the effect of tumor cell-free DNA, isolated from the blood of prostate

132 iptome, mutation, and phenotypic features of tumor cells from 35 MYD88-mutated WM patients in relatio

133 nd sorting highly tumorigenic and metastatic tumor cells from a heterogeneous cell population is a da

134 Cancer metastasis, i.e., the spreading of tumor cells from the primary tumor to distant organs, is

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

136 eletion of RUNX1 in ccRCC cell lines reduced tumor cell growth and viability in vitro and in vivo.

137 te in modulating Hippo signaling to suppress tumor cell growth.

138 sed NRP1 expression and ablated FGF-mediated tumor cell growth.

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

140 the vascular tree, which depends on whether tumor cells have gone through epithelial-mesenchymal tra

141 and cancer cell fusion is a direct route to tumor cell heterogeneity.

142 nd activation of STING(S162A/G230I/Q266I) in tumor cells holds great therapeutic promise for the trea

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

144 ching in the mouse lungs prior to arrival of tumor cells (i.e., in the premetastatic niche) in the mo

145 ants, we show that when mixed with wild-type tumor cells, IFN-gamma-insensitive tumor cells indeed gr

146 bitor SerpinB9 (Sb9) results in the death of tumor cells in a granzyme B (GrB)-dependent manner.

147 ferential contributions of pre- and post-EMT tumor cells in breast cancer metastasis.See related comm

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

149 lymphoid cells being explored as they engage tumor cells in different mechanisms compared with T cell

150 ealed a higher fraction of ANGPT2-expressing tumor cells in metastatic versus primary sites.

151 nctional activity of E-cadherin expressed on tumor cells in response to environmental factors is an i

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

153 MEK1/2, and demonstrate its efficacy toward tumor cells in vivo.

154 Coinjection of Th9/Th17 cells with tumor cells in WT, Rag1-/-, Il9r-/-, and Il17ra-/- mice

155 potent cGAS-dependent type-I IFN response in tumor cells, increased IFNgamma-producing CD8(+) T cells

156 In turn, ectopic Zeb1 in tumor cells increases VEGFA production and reciprocally

157 wild-type tumor cells, IFN-gamma-insensitive tumor cells indeed grow out, which depends upon PD-L1 ex

158 Bacteria-tumor cell interactions and metabolic crosstalk were ext

159 reflect the effects of hypoxia on direct PMN-tumor cell interactions.

160 g anti-CD8alpha mAb or by transplantation of tumor cells into B6.CB17-Prkdc SCID mice.

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

162 These findings indicate that in addition to tumor cell-intrinsic mechanisms that cause constitutive

163 with alpha-actinin 4 is required to promote tumor cell invasion.

164 fibroblasts (CAF) that facilitate epithelial tumor cell invasion.

165 hallenges, and future trends for circulating tumor cell investigations, arguing that the time is comi

166 We conclude that DNA sensing within tumor cells is essential for dMMR-triggered anti-tumor i

167 vasive growth pattern of mesenchymal subtype tumor cells is responsible for its poor outcome.

168 wever, the regulation of PD-L1 expression on tumor cells is still poorly understood.

169 lpha-radiation in tissues, resulting in high tumor cell killing and low toxicity to surrounding tissu

170 of LAYN in human CD8+ T cells reduced direct tumor cell killing ex vivo.

171 lentiviral vectors encoding CAR that direct tumor cell killing.

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

173 Moreover, loss of CASP9 signaling in tumor cells led to adaptive resistance by upregulating p

174 er, thus highlighting an instructive role of tumor cell lineage in reprogramming the stromal microenv

175 ids containing versatile clinically relevant tumor cell lineages with regard to the expression of AR

176 We found that a subset of brain tumor cell lines and BTICs expressed high constitutive l

177 treatment increased PD-L1 expression in the tumor cell lines and caused up to a 12-fold increase in

178 Tumor cell lines exhibited a marked increase in sensitiv

179 Here, we use tumor cell lines harboring mutations in Cosmc, and there

180 In human tumor cell lines, ABCC4 knockdown and inhibition reduced

181 ease in sensitivity to ubidecarenone vs. non-tumor cell lines.

182 assessed their cytotoxicity in various human tumor cell lines.

183 of 1-3 muM against proliferation of several tumor cell lines.

184 bserved experimentally in 11 patient-derived tumor cell lines.

185 /5 pathological response, indicating 90-100% tumor-cell loss, is more likely to occur in patients usi

186 The isolated soft tumor cells (< 400 Pa) but not the stiff ones (> 700 Pa)

187 estimate the underlying distribution of the tumor cell marker pan-cytokeratin (panCK).

188 n secondary organs or secretion from primary tumor cells may be promising therapeutic strategies to s

189 osity events is an attractive concept, since tumor cells may lack enzymatic activities present in nor

190 f genetic drivers promoting dissemination of tumor cells may provide opportunities for novel therapeu

191 Tumor cells metabolically coordinate or compete with the

192 Oncogene-driven changes in tumor cell metabolism can impact the TME to limit immune

193 ing the mechanisms of how autophagy supports tumor cell metabolism is essential.

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

195 Further, silencing furin reduced tumor cell migration and invasion in vitro and tumor gro

196 6 regulates cytoskeletal dynamics to promote tumor cell migration and invasion.

197 Tumor cell migration to LECs was inhibited by blocking C

198 several human cancer cell lines and inhibits tumor cell migration, contains an unusual 2-acyl-4-hydro

199 feration, invasion, and migration in thyroid tumor cell models.

200 ier stability while concurrently suppressing tumor cell motility.

201 Tumor cells must alter their antioxidant capacity for ma

202 DDX21 was detected mostly in the tumor cell nuclei, with high expression in some mitotic

203 mples, we found high expression of MHC-II in tumor cells of AT-II cellular origin, which was correlat

204 ese in turn skew differentiation towards the tumor cell-of-origin and alter interactions between lymp

205 Tumor cells often exhibit augmented capacity to maintain

206 a previously underappreciated dependency of tumor cells on HR signaling for anchorage-independent gr

207 box binding homeobox 1 (ZEB1) in claudin-low tumor cells or forced expression of ZEB1 in basal-like t

208 ing the ability of cytotoxic T cells to kill tumor cells or the reframing of their receptor to elimin

209 tive YAP increased the number of circulating tumor cells over time.

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

211 gly, epigenetic effects of PADI4 on the bulk tumor cell population did not explain the CSC phenotype.

212 However, in sorted tumor cell populations, PADI4 downregulated expression o

213 tection and tracking of clonal and subclonal tumor cell populations.

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

215 No changes in tumor cell proliferation (primary endpoint) or other sec

216 these factors in cuSCC cell lines suppressed tumor cell proliferation and induced apoptosis.

217 ce growth factors and cytokines that enhance tumor cell proliferation and migration.

218 demonstrates a role for the satellite RNA in tumor cell proliferation and movement.

219 nation with osimertinib, potently suppressed tumor cell proliferation in vitro and caused tumor regre

220 Knockdown of GULP1 in UCB cells promoted tumor cell proliferation in vitro and enhanced tumor gro

221 of these inflammatory genes, as well as EMT, tumor cell proliferation, and migration in vitro and tum

222 lating miR-21 via miRzip extensively targets tumor cell proliferation, migration and invasion in vitr

223 y to downregulate c-MYC and directly inhibit tumor cell proliferation, NHWD-870 blocks the proliferat

224 Simultaneously, their ability to promote tumor cell proliferation, which appeared to be mediated

225 atients with the highest MDK levels promoted tumor cell proliferation, which was attenuated after the

226 pacity to downregulate MET and inhibit human tumor cell proliferation.

227 ells, MYC activates Notch to dedifferentiate tumor cells, promoting a temporal shift in SCLC from ASC

228 uced epithelial-to-mesenchymal transition of tumor cells, promoting metastasis.

229 Expression of activated AKT in tumor cells recapitulates the effects of fibroblasts res

230 unctionally, enhanced ROS in Angpt2-silenced tumor cells reduced colonization potential in vitro and

231 esent a biophysical model that describes how tumor cells regulate intracellular and extracellular aci

232 enriched in embryonic stem cells (ESCs) and tumor cells relative to the ubiquitously expressed POLR3

233 Pancreatic tumor cells release small extracellular vesicles (sEVs,

234 osuppressive factors induced by radiation on tumor cells remain to be identified.

235 Darwinian evolution of tumor cells remains underexplored in childhood cancer.

236 Tumor cells require nominal increases in protein synthes

237 ble CRC patients, we here determined whether tumor cells retaining also other NAT2 low activity varia

238 Chromosomal instability (CIN) increases a tumor cell's ability to acquire chromosomal alterations,

239 Additionally, HOXA9-transfected tumor cells showed significantly increased soft-agar clo

240 tases that occur frequently provide sites of tumor cell spread, whereas tumor antigen transfer into a

241 exists within collectively invading packs of tumor cells, suggesting that cellular subtypes cooperate

242 chemokine production by macrophages and B16 tumor cells, suggesting that the major role for STING ac

243 Tumor cell-surface markers are usually overexpressed or

244 i, suggesting expression of Tn/STn may offer tumor cell survival advantages through altering DR4 and/

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

246 ressing cells deposit fibronectin to promote tumor cell survival.

247 esting a mechanism for prolonged epithelioid tumor cell survival.

248 ceptor (CAR) to mediate recognition of mouse tumor cells that bear its cognate Tn-glycopeptide epitop

249 ntial immune evasion mechanisms in recurrent tumor cells that dampen DC antigen presentation and recr

250 heterogeneous and contain subpopulations of tumor cells that exhibit stem-like features.

251 ensitivity was not altered by fibroblasts in tumor cells that exhibited sustained MTOR signaling due

252 all samples but only phosphorylated in TNBC tumor cells that expressed SFK_pY416.

253 shape, which might be a defining feature of tumor cells that is harnessed by E4orf4.

254 The tumor cells that survived exhibited stemness markers, sp

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

256 bitor can overcome CHK1i resistance of these tumor cells, thereby enhancing anti-cancer activity.

257 C4S and C6S increased the numbers of viable tumor cells, thereby promoting glioma cell proliferation

258 ysfunctional mitochondria in Angpt2-silenced tumor cells, thereby resulting in enhanced reactive oxyg

259 tosis were observed in alpha3beta1-deficient tumor cells, these changes followed a robust increase in

260 ng neutrophils are transported to metastatic tumor cells through a macropinocytosis-lysosome pathway,

261 ated secretory phenotype (SASP) of senescent tumor cells through activation of matrix metalloproteina

262 in PDA that depends on IL1beta production by tumor cells through TLR4-NLRP3 inflammasome activation.

263 when transfected with wild-type Cosmc, these tumor cells thus express normal extended O-glycans and b

264 This coupling mechanism is exploited by tumor cells to aberrantly sustain transcriptional progra

265 nd that shRNA silencing of SPINK1 sensitizes tumor cells to anoikis and inhibits proliferation.

266 human cells boosted p53 activity and allowed tumor cells to be killed more efficiently.

267 teractions between macrophages, T cells, and tumor cells to determine how the immune response changes

268 avorable transcriptional program employed by tumor cells to escape apoptosis, hence developing more a

269 important determinant of the ability of the tumor cells to metastasize.

270 blunted the selective advantage of ER-mutant tumor cells to survive estrogen deprivation, anchorage i

271 involves the dedifferentiation of epithelial tumor cells towards a motile, metastatic, and mesenchyma

272 in the TME of medulloblastoma: a fraction of tumor cells trans-differentiate into TuAstrocytes, which

273 In many tumors, cells transition reversibly between slow-prolife

274 s or forced expression of ZEB1 in basal-like tumor cells, two triple-negative breast cancer (TNBC) su

275 Tumor cell-type heterogeneity, defined as the proportion

276 c-Myc depletion occurred in a wide range of tumor cell types, including lymphoma, lung, glioblastoma

277 How the numerous mutations in tumor cells ultimately achieve this aberrant production

278 The rest of the tumor cells undergo an irreversible loss of their biosyn

279 that at 0.5% peptide density, enhancement of tumor cell uptake over non-targeted nanoparticles was ~2

280 Most tumor cells use aerobic glycolysis (the Warburg effect)

281 mammalian cell growth beyond Ras-transformed tumor cells via sustained mTORC1 activation.

282 SFK phosphorylated at Y416 (SFK_pY416(+)) in tumor cells was strongly associated with phosphorylation

283 Functional analysis of tumor cells was successfully used in a clinical setting

284 e.g., IL1B) from immune infiltrates, ELF3 in tumor cells was upregulated to trigger the activation of

285 homing of AnxA5 to the TME enriched with PS+ tumor cells, we demonstrate in vivo that fusing tumor-an

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

287 Tumor cells were divided into sensitive and resistant po

288 w level of androgen receptor expression, the tumor cells were resistant to androgen receptor inhibiti

289 tastatic tumors and found that the nuclei of tumor cells were significantly larger in metastases.

290 ps to defective PD-L1 upregulation on mutant tumor cells, which improves anti-tumor efficacy of CD8(+

291 oinflammatory M1 macrophages can phagocytose tumor cells, while anti-inflammatory M2 macrophages such

292 macropinocytosis-lysosome pathway, endowing tumor cells with augmented survival and proliferative ca

293 Concordantly, tumor cells with high CXorf67 expression levels show inc

294 ) can sequentially target BBB/BBTB and brain tumor cells with surface maltobionic acid (MA) and 4-car

295 CD3 bispecifics can redirect T cells to kill tumor cells with target HLA/peptide on their surfaces in

296 number of Ki-67-positive and Ki-67-negative tumor cells within a subjectively picked hot-spot.

297 specific gene can affect the distribution of tumor cells within an animal, thereby influencing the gl

298 llows the selective elimination of malignant tumor cells without affecting healthy tissue.

299 al-mesenchymal transition (EMT) phenotype in tumor cells without affecting tumor-intrinsic Wnt signal

300 rved small extrachromosomal DNA fragments in tumor cells, yet comprehensive examination of their stru