ライフサイエンスコーパス: cancer cell

1 e in metabolic routes preferentially used by cancer cells.

2 l biomarker overexpressed in primary ovarian cancer cells.

3 videos of labeled EVs uptake by living lung cancer cells.

4 s of ciliogenesis in normal and basal breast cancer cells.

5 and increases migratory propensity in renal cancer cells.

6 ith EGFR surface expression in head and neck cancer cells.

7 otype that supports the metastatic spread of cancer cells.

8 creates enhanced cytotoxicity in pancreatic cancer cells.

9 todynamic therapy (PDT) to resect and ablate cancer cells.

10 ely described as potent cytotoxic agents for cancer cells.

11 cessing 7.5 mL blood samples spiked with 100 cancer cells.

12 ony formation and cell proliferation of skin cancer cells.

13 in the H&E specimen into stromal, immune, or cancer cells.

14 and changing DNA repair capacity in prostate cancer cells.

15 acid to inhibit lung, brain, and soft-tissue cancer cells.

16 is, and unleashed T cell-mediated killing of cancer cells.

17 sociated molecular patterns (DAMPs) by dying cancer cells.

18 athway, which is often altered in colorectal cancer cells.

19 nsulin and to abrogate insulin signalling in cancer cells.

20 photoreceptor-specific exons in HepG2 liver cancer cells.

21 could also enhance matriglycan expression in cancer cells.

22 roach for combinatorial genetic screening in cancer cells.

23 s in normal prostate epithelial and prostate cancer cells.

24 nd inhibits the aggressiveness of colorectal cancer cells.

25 ng in reduced EGF receptor activation in the cancer cells.

26 effects on cervical (HeLa) and colon (HT-29) cancer cells.

27 cruited more T cells compared with dispersed cancer cells.

28 m parental MDA-MB-231 triple-negative breast cancer cells.

29 stress underlies many genomic alterations in cancer cells.

30 gaging the extracellular space in normal and cancer cells.

31 formation in liver, but also breast and lung cancer cells.

32 he transactivation of EGFR by LPA in ovarian cancer cells.

33 GFP hepatoma cells or AHR-deficient LLC lung cancer cells.

34 pt peritoneal spread and adhesion of ovarian cancer cells.

35 lated in leading edges of certain classes of cancer cells.

36 tabolism independent of genetic mutations in cancer cells.

37 induced by femoral inoculation of Lewis lung cancer cells.

38 ferentially upregulated surface molecules on cancer cells.

39 by the low number of antigens restricted to cancer cells.

40 e of E-cadherin in B16F10 melanoma and other cancer cells.

41 ulation of checkpoint regulator PD-L1 on the cancer cells.

42 for inducing immune-mediated destruction of cancer cells.

43 d FBXO44 as an essential repressor of REs in cancer cells.

44 ell cycle regulators were examined in breast cancer cells.

45 es growth retardation in a panel of prostate cancer cells.

46 mutations, we report that human HCT116 colon cancer cells also survive when ORC5 protein expression i

47 SPR-mediated knockout of FN3K in human liver cancer cells altered the abundance of redox metabolites,

48 e subcellular enrichment of glycogen in live cancer cells and achieved specific glycogen mapping thro

49 Various cancer cells and actively dividing tumor-endothelial cel

50 acterized cellular reference samples (breast cancer cells and B cells), captured either separately or

51 THDF3 in controlling the interaction between cancer cells and brain microenvironment, thereby inducin

52 nucleosomes that are known to exist in human cancer cells and contain H3 histone variants CENP-A and

53 BCAA metabolic reprogramming is regulated in cancer cells and how it influences cancer progression.

54 Here we find that, in colorectal cancer cells and in developing mouse forelimbs, BCL9 pro

55 ts into how GLI1 controls gene expression in cancer cells and may inform approaches targeting this on

56 nate inhibitor for TMPRSS2 in human prostate cancer cells and may serve as a potential factor to supp

57 ing them to the respective CM induced EMT in cancer cells and modulated the expression profile of gen

58 The epigenetic traits of cancer cells and of associated tumor microenvironment co

59 ous studies, the biological effect of CAP on cancer cells and other mammalian cells has been based so

60 rotein amounts in human Ishikawa endometrial cancer cells and patient-derived cell lines because we h

61 thelial-mesenchymal transition (EMT) in lung cancer cells and promoted metastatic spreading.

62 P372-1 sensitizes NQO1-expressing pancreatic cancer cells and spares immortalized normal pancreatic d

63 nts that target transcriptional addiction in cancer cells and suggest combination treatments that tar

64 s promote the metastasis of colon and breast cancer cells and suggests that GPVI represents a promisi

65 pered by the difficulty to deliver them into cancer cells and susceptibility to nuclease degradation.

66 anded gamma9delta2T cells was active against cancer cells and that activity of the parental clone, or

67 enchymal phenotype of triple-negative breast cancer cells and that CBFbeta-depleted cells undergo a m

68 nd UBR5 are co-amplified in more than 40% of cancer cells and that MYC copy number amplification corr

69 s adopt MAPK-dependent circuitries in breast cancer cells and that the kinase TTK is important in acu

70 therapy due to their high overexpression on cancer cells and their ability to internalize together w

71 es, we characterised a range of human breast cancer cells and their protein-level responses to two cl

72 lectron carrier coenzyme Q, both in cultured cancer cells and tumors.

73 t cell fitness in cancer cell lines, primary cancer cells, and fibroblasts under unhindered growth co

74 the caspase-9/3 cascade and thereby suppress cancer cell apoptosis, and highlight the role of Trx/Trx

75 Thus, cancer cells appear to survive in the CSF by outcompetin

76 ERBB2) and overexpression of HER2 protein on cancer cells are found in 10-26% of gastric cancer (GC)

77 tment approach to deliver toxins directly to cancer cells are one of the fastest growing classes of o

78 ealing more effective cell killing when more cancer cells are present.

79 e report that, shortly after treatment, some cancer cells are sequestered in a quiescent state with l

80 ERK1/2 signaling in KRAS-mutated colorectal cancer cells as a driver of tumor-stroma interactions th

81 iven cancer cells, such as Lats1/2-deficient cancer cells as well as Galpha(q/11) mutated uveal melan

82 ed a panel of human and murine head and neck cancer cells at low effector-to-target ratios in a PD-L1

83 ssociated fibroblasts (CAFs) cooperates with cancer cell-autonomous signals to increase MYC level, pr

84 , HR+, CARM1-high, high-grade serous ovarian cancer cells become PARPi sensitive, undergo mitotic cat

85 In summary, aggressive cancer cell behaviour and reduced drug responsiveness wa

86 equently, capsaicin induced apoptosis in the cancer cells, but not in the less glycosylated benign ur

87 ay of long noncoding RNAs (lncRNA) in breast cancer cells, but their biological functions remain larg

88 Autophagy can protect stressed cancer cell by degradation of damaged proteins and organ

89 y, our data show that NVS-CECR2-1 also kills cancer cells by CECR2-independent mechanism.

90 er agent in phase III clinical trials, kills cancer cells by destabilizing microtubules.

91 well as cleaved caspase-3 and -PARP in colon cancer cells by downregulating RSK1 and MSK2 downstream

92 We developed neratinib-resistant HER2-mutant cancer cells by gradual dose escalation.

93 PYCR1 knockdown in MCF10A H-RAS(V12) breast cancer cells by inhibiting de novo proline biosynthesis

94 tic exerts many STAT3-independent effects on cancer cells, calling for reassessment of results previo

95 qualitative assessment of surface markers on cancer cells can allow for point-of-care prediction of p

96 Here, we show that cancer cells can be selectively deprived of self-renewal

97 ifferentiation of human and mouse pancreatic cancer cells can influence the phenotype of non-neoplast

98 Furthermore, intravasation of cancer cell clusters was observed following the formatio

99 ical regulator of lipid responses in ovarian cancer cells cocultured with adipocytes.

100 complex interactions between infections and cancer cell communities in order to develop innovative c

101 owed that DeltaPsim is more heterogeneous in cancer cells compared to fibroblasts, and it is maintain

102 Defining traits of platinum-tolerant cancer cells could expose new treatment vulnerabilities.

103 Complementary studies using human breast cancer cell culture models revealed that siRNA-mediated

104 presents a different characteristic level of cancer cell de-differentiation.

105 hat are used chemotherapeutically to promote cancer cell death can have the opposite effect on wild-t

106 nal cancer and lung metastasis by triggering cancer cell death when netrin-1 is lowly expressed.

107 rize effects of unacylated ghrelin on breast cancer cells, define its mechanism of action, and explor

108 Cancer cells deform as they move through while blood cel

109 tems, uncovering a vulnerability of spheroid cancer cells deprived of extracellular matrix to undergo

110 red across an isogenic panel of human breast cancer cells derived from MDA-MB-231 cells.

111 Yet, the contribution of cancer cell-derived ECM and tumor mechanics to drug adap

112 Consequently, COX6B2-expressing cancer cells display a proliferative advantage, particul

113 hibited neutrophil- and macrophage-dependent cancer cell dissemination more effectively than tamoxife

114 oliferation, provides a selective benefit to cancer cells during chemotherapy treatment.

115 ironment restores this malignant property of cancer cells during hormone therapy.

116 Breast cancer cells 'educate' lymphatic endothelial cells (LECs

117 g miR122 and PTX were delivered to the liver cancer cells efficiently due to their rubber-like proper

118 MUC1 knockdown in pancreatic cancer cells enhanced unfolded protein response (UPR) si

119 It is incompletely understood how cancer cells escape NK cell surveillance.

120 In both C. elegans and human cancer cells, ether-lipid synthesis protects against fer

121 Clonal diversity is a consequence of cancer cell evolution driven by Darwinian selection.

122 , we found that melanoma and lung and breast cancer cells experiencing stress from oncogene inhibitio

123 Methods: ER+, PR+ T47D breast cancer cells expressing wild-type (WT) ER or an activati

124 g validated epitopes with well-characterized cancer cell expression and processing, enhancing TCR-T e

125 120-catenin isoform switching in SW480 colon cancer cells: fl-APC increased the expression of genes i

126 In colorectal cancer cells, FL3 treatment blocked phosphorylation of P

127 een tumor-infiltrating lymphocytes (TIL) and cancer cells for metabolic resources often renders T cel

128 X), one of the major acid/base regulators in cancer cells, forms a protein complex with MCT1 and MCT4

129 -mutation (kataegis) event in a group of ~30 cancer cells from a recurrent ovarian carcinoma.

130 Also, cancer cells from different tissue origins have a lower

131 the presence of DPP, resulting in attenuated cancer cell growth and eventually cell death.

132 -metabolizing enzyme that also has a role in cancer cell growth and metabolism.

133 ith LARGE overexpression is shown to inhibit cancer cell growth and tumorigenicity.

134 in an enzymatic assay, while also inhibiting cancer cell growth and viability and activating p53-depe

135 inhibitor of PTP4A3 and human A2780 ovarian cancer cell growth was reduced.

136 modifications important to tumorigenesis and cancer cell growth, here we report a chemoproteomic anal

137 breast cancer cells, selectively suppresses cancer cell growth.

138 stem-like mechanisms aberrantly acquired by cancer cells has been challenging.

139 the reframing of their receptor to eliminate cancer cells has revolutionized cancer treatment.

140 We determined that cancer cells have a high ratio of SmgGDS-607:SmgGDS-558

141 use tumor antigens and DNA released by dying cancer cells have the potential to amplify innate immune

142 al transition (EMT) has been associated with cancer cell heterogeneity, plasticity, and metastasis.

143 In cervical cancer cells, human papilloma virus (HPV) protein E7 bin

144 emodelling of the blood vasculature, causing cancer cell hypoxia and death in distant avascular regio

145 complex interactions among various types of cancer cells, immune cells, stroma, angiogenic molecules

146 ormed a cell tracking experiment of prostate cancer cells in a PLA device for advanced cell culture.

147 T3 expression has few deleterious effects on cancer cells in attached conditions, SIRT3 upregulation

148 ded electrodes that can detect and enumerate cancer cells in blood.

149 inst both BRCA-deficient and BRCA-proficient cancer cells in cellular assays.

150 ed with doxorubicin, selectively kills liver cancer cells in culture, as the selectivity of the aptam

151 ne rejection and allows growth of human lung cancer cells in lal(-/-) mice.

152 rious human cancer cells, killing SW48 colon cancer cells in particular with a submicromolar half max

153 efficiently promoted apoptosis in colorectal cancer cells in response to Nutlin-3A, which otherwise p

154 es a technology for noninvasive isolation of cancer cells in sufficient numbers for multiple clinical

155 AZP-531 also suppresses the growth of breast cancer cells in vitro and in xenografts, and may be a no

156 When cocultured with breast cancer cells in vitro, MCs hindered activation of cMET,

157 delta T-cell-mediated eradication of bladder cancer cells in vitro.

158 migration and invasion of 4T1 murine breast cancer cells in vitro.

159 i) that targets multiple compartments in the cancer cell, including mitochondria.

160 -dependent growth inhibition of a variety of cancer cells, including human triple-negative breast can

161 matically assessed in vivo growth of ovarian cancer cells, including six validated HGSC cell lines, i

162 Upregulation of GLS2 in cancer cells induced an antiproliferative response with

163 beta MAPK inhibitor, SB202190, and abrogated cancer cell-induced muscle protein loss in C2C12 myotube

164 we explore the role of pro-survival genes in cancer cell integrity during clonal evolution in non-sma

165 as an important regulator of cell migration, cancer cell invasion, and vesicular content release, we

166 cking protein with roles in neurogenesis and cancer cell invasion.

167 ofiling the heterogeneous phenotypes of live cancer cells is a key capability that requires single-ce

168 romote therapeutic immune cells to recognize cancer cells is important for the success of cell-based

169 of CXL146 as a novel therapy in treating MDR cancer cells is warranted.

170 In this issue of Cancer Cell, it is shown that, when EZH2 is functionally

171 rriers and leveraging on several synergistic cancer cell killing mechanisms.

172 its cytotoxic activity against various human cancer cells, killing SW48 colon cancer cells in particu

173 pression of the catalytic domain of PDE3A in cancer cells lacking PDE3A is sufficient to confer sensi

174 generate inflammatory cytokines that induce cancer cell LCN2 expression but do not generate LCN2 the

175 s which cause high drug effluxion from liver cancer cells, leading to chemoresistance and a diminishe

176 inct features to ER-negative DCIS.com breast cancer cells, leading to populations enriched with highl

177 tate cancer), and one kind of EpCAM negative cancer cell line (293T kidney cancer).

178 We performed Protect-seq on the human colon cancer cell line HCT-116 and observed overlap with previ

179 uracil pattern upon drug treatments in human cancer cell line models derived from HCT116.

180 cally investigate this, we performed robotic cancer cell line screens and discovered a marked sensiti

181 spheroids formed from two established human cancer cell lines (HCT116 and CAL27) to single and combi

182 trated to test three kinds of EpCAM positive cancer cell lines (MCF-7 breast cancer, SW480 colon canc

183 In human breast cancer cell lines and 4T1 mouse mammary tumor cells, PD-

184 rgeted therapy in a subset of HER2(+) breast cancer cell lines and allow cancer cells to proliferate

185 g with its promoter region in luminal breast cancer cell lines and indirectly through a distal estrog

186 In studies of pancreatic cancer cell lines and mice, we found that ZIP4 increases

187 epresent a measure of Ras dependency in both cancer cell lines and patient samples.

188 Compound 1 was cytotoxic for both breast cancer cell lines and the majority of cells died by trea

189 In cancer cell lines and xenograft models, mRNA and protein

190 In vivo, SHH interference in colon cancer cell lines decreased primary tumor growth and met

191 ltiplexed single-cell RNA-seq to profile 198 cancer cell lines from 22 cancer types.

192 In this study, we cultured ovarian cancer cell lines in adherent and nonadherent conditions

193 etermining the metastatic potential of human cancer cell lines in mouse xenografts at scale.

194 odulation of SASH1 levels in a panel of lung cancer cell lines mediated changes in cellular prolifera

195 A549, DU 145, HeLa, HCT 116, and MCF7 human cancer cell lines provide insights into the impact of st

196 antibody or CRISPR knockout of IL37 in lung cancer cell lines repolarized TAMs, resulting in recover

197 ow sub-micromolar range among various tested cancer cell lines such as A2780 (0.23 muM), PC3 (0.48 mu

198 Finally, 45 inhibited proliferation of two cancer cell lines that are resistant to cancer drugs and

199 across a panel of genetically diverse mouse cancer cell lines that were cultured in the presence of

200 On average, the sensitivity of human cancer cell lines to DNMDP is correlated with PDE3A expr

201 an lung cancer tissues and immortalized lung cancer cell lines via indirect immunofluorescence and im

202 ncer, particularly because a large number of cancer cell lines with characteristic mesenchymal featur

203 model, we not only predict drug responses in cancer cell lines with high accuracy but also identify f

204 ntly enhanced AKT sensitivity in a subset of cancer cell lines, and a far richer array of PARP inhibi

205 overed a marked sensitivity of hematological cancer cell lines, including B-cell lymphomas, to the po

206 rmance was characterized using four prostate cancer cell lines, including PC-3, VCaP, DU-145, and LNC

207 DynaFit revealed that cell fitness in cancer cell lines, primary cancer cells, and fibroblasts

208 overexpressed in SW480 and HCT116 colorectal cancer cell lines, which were analyzed by immunoblotting

209 luation of their activity against five human cancer cell lines.

210 rials on the cell cycle of PANC-1 and AsPC-1 cancer cell lines.

211 n from the extracted protein mixtures of the cancer cell lines.

212 for in vitro cytotoxicity against a panel of cancer cell lines.

213 lates and validated with DNA from two breast cancer cell-lines and two patient tumour tissue samples

214 0.024 wt % of the total protein from breast cancer cell lysates.

215 markers snail and MMP14 were upregulated in cancer cells maintained in 3D (P < 0.001), cadherin-11 w

216 Here, we show that breast cancer cells maintained in hypoxia release small extrace

217 herent or induced mitochondrial dysfunction, cancer cells manifest overlapping metabolic phenotypes,

218 nto understanding miRNA signaling underlying cancer cell metabolism and development of new strategies

219 hanisms whereby stromal fibroblasts regulate cancer cell metabolism independent of genetic mutations

220 ave emerged as key components in determining cancer cell metabolism.

221 g miRNAs and examine their effects on breast cancer cell migration through exosome-mediated delivery.

222 Here, using human breast cancer cell models, we identified a pathway in which cha

223 otype can facilitate metabolic plasticity of cancer cells more specifically in metastasis and therapy

224 For metastasis to occur, cancer cells must exocytose proteases, like matrix metal

225 ve any effect on the growth and migration of cancer cells nor did it induce receptor downregulation.

226 For efficient and safe delivery to cancer cells, nucleic acids must generally be packaged i

227 Indeed, Rac1-null PC3 prostate cancer cells or cancer models with low levels of Rac1 ac

228 designed to enable preferential labelling of cancer cells, or specifically delivered to cancerous tis

229 Besides, the liver cancer cells overexpress the drug exporters which cause

230 y a proteotype associated with an aggressive cancer cell phenotype.

231 ht on microenvironmental signals controlling cancer cell plasticity along EMT and suggests that hybri

232 Cancer cells progressively adopt alternate lineage ident

233 reduces HDL-associated increases in prostate cancer cell proliferation and disease progression.

234 our results demonstrate that RBM10 inhibits cancer cell proliferation and induces apoptosis in part

235 , Aurora B and RepoMan independently promote cancer cell proliferation by reducing checkpoint--induce

236 However, the mechanism of CYP24A1-mediated cancer cell proliferation remains unclear.

237 so simultaneously inhibits the STAT3-induced cancer cell proliferation, demonstrating a novel approac

238 regulates alternative splicing and controls cancer cell proliferation.

239 ence with platelet binding to PD-L1 negative cancer cells promotes T cell-induced cancer cytotoxicity

240 uadruplex ligand that, when studied in human cancer cells, proved to be able to stabilize both G-quad

241 ed between anti-CD20 antibodies and lymphoma cancer cell receptors.

242 g proinflammatory cytokines, chemokines, and cancer cell-recruited neutrophils result in enhanced met

243 selective if this pathway is overactive in a cancer cell relative to a nontransformed cell.

244 Cancer cells rely on the enzyme telomerase (EC 2.7.7.49)

245 Deletion of Ccr2 in cancer cells resulted in multiple alterations associated

246 In this issue of Cancer Cell, Ruhland et al. demonstrate that transport a

247 Furthermore, this poisoning may be cancer cell selective if this pathway is overactive in a

248 plant Arabidopsis thaliana with human breast cancer cells, selectively suppresses cancer cell growth.

249 Yet our understanding of how cancer cells sense and convert mechanical stimuli into b

250 ceptor signaling as an important mediator of cancer cell sensitivity to CAR T-cell cytotoxicity, with

251 ssemination of tumor cells, and emergence of cancer cell subpopulations with stem cell-like propertie

252 tion of AP-1 suppresses growth of YAP-driven cancer cells, such as Lats1/2-deficient cancer cells as

253 rom retained introns can be presented on the cancer cell surface, the development of personalized can

254 ively targets tumors in vivo by anchoring to cancer cell surfaces in a pH-dependent manner.

255 differentiation between cell states promotes cancer cell survival under stress and fosters non-geneti

256 ld abrogate ROS-induced ER stress to promote cancer cell survival.

257 By entering G0, cancer cells survive unfavorable conditions such as chem

258 l cycle progression and proliferation of the cancer cells tested, the novel substrate-mediated treatm

259 ed primary/metastatic melanoma or colorectal cancer cells than those that are not.

260 e intrinsic and extrinsic vulnerabilities of cancer cells that can be therapeutically exploited.

261 anscription or DNA-damage repair in prostate cancer cells that co-express AR-V7 and AR-FL.

262 lsed magnetic field exposure of human breast cancer cells that express a sialic-acid rich glycocalyx

263 he metabolic heterogeneity and plasticity of cancer cells that had until recently remained unapprecia

264 In human cancer cells that harbor mutant KRAS and WT p53 (p53), K

265 letion of HIRA elicits systemic death of ALT cancer cells that is mitigated by re-expression of ATRX,

266 of cell lines derived from MDA-MB-231 breast cancer cells that vary in their metastatic potential, we

267 Here we show, in prostate cancer cells, that LSD1 associates with FOXA1 and active

268 Cancer cells then become very dependent on the proper fu

269 d arrays was also demonstrated by performing cancer cell-therapeutic response studies.

270 In cancer cells, this "metabolon disruption" results in a d

271 omologous recombination (HR) repair arise in cancer cells through inherited or acquired mutations in

272 al DNA glycosylase, NEIL2, sensitizes breast cancer cells to A3B-mediated mutations and double-strand

273 d performed experiments with suspended human cancer cells to characterize the performance of the sens

274 r function changes the metabolic activity of cancer cells to drive unrestricted proliferation.

275 t core set of genes and pathways that enable cancer cells to evade killing mediated by cytotoxic T ly

276 employed varying EMT models of murine breast cancer cells to identify the key players establishing ep

277 but not catalytic AURKA inhibitors sensitize cancer cells to inhibition of the CDC7 kinase subunit of

278 ovarian cancer and depleting BRD9 sensitizes cancer cells to olaparib and cisplatin.

279 non-canonical role of caspase-8 exploited by cancer cells to override the p53-dependent G2/M cell-cyc

280 f HER2(+) breast cancer cell lines and allow cancer cells to proliferate in the presence of the HER2

281 A 10-min exposure of A549 human lung cancer cells to sequential 50- and 385-Hz oscillating ma

282 veral phenotypes that impact the capacity of cancer cells to survive and proliferate are dynamic.

283 wed by sequencing (ChIP-seq) in MCF-7 breast cancer cells treated with the proteasome inhibitor MG132

284 In breast cancer cells under normoxia, CHD4 enrichment at HIF targ

285 Cancer cells undergo metabolic adaptation to sustain unc

286 covered that a subset of non-small cell lung cancer cells underwent a gradually progressing epithelia

287 Investigating the behavior of breast cancer cells via reaction kinetics may help unravel the

288 ted that 8a decreases triple-negative breast cancer cell viability, and immunoblotting revealed that

289 hat 5-FU resistance in DLD-1/5-FU colorectal cancer cells was mainly associated with SM increase and

290 drug responsiveness was observed when breast cancer cells were maintained in 3D under fluid flow and

291 ents reminiscent of metastatic sites, breast cancer cells were more resistant to the estrogen recepto

292 vern multiple pro-tumoural attributes in the cancer cell while dynamically reprogramming the function

293 nomolar cytotoxicity against HER2-expressing cancer cells, while showing no activity against antigen-

294 all molecule, CXL146, selectively eliminates cancer cells with GRP78 overexpression via activating un

295 3A-SLFN12 complex formation, thereby killing cancer cells with high levels of PDE3A and SLFN12 expres

296 and concomitant drug release, when in breast cancer cells with increased levels of reducing agents.

297 lves the interaction of genetically abnormal cancer cells with normal stromal cells.

298 Coculturing lung cancer cells with Th9/Th17 cells or exposing them to the

299 MYC-mediated apoptosis in p53-mutant breast cancer cells with UBR5/MYC coamplification.

300 proteins which inhibits metastatic spread of cancer cells without impact on growth of the primary tum

301 Furthermore, inhibiting force generation in cancer cells would increase the T cell activating capaci