ライフサイエンスコーパス: cancer cell

1 bit numerous oncogenic signaling pathways in cancer cells.

2 and epithelial-to-mesenchymal transition of cancer cells.

3 e invadopodial maturation in invasive breast cancer cells.

4 s and overexpressed in response to stress in cancer cells.

5 squamous cell carcinoma and breast carcinoma cancer cells.

6 rowth, or stimulate the death, of developing cancer cells.

7 has been observed for other BAF subunits in cancer cells.

8 were internalized slowly by HER2-expressing cancer cells.

9 regulating the survival and proliferation of cancer cells.

10 in addition has already been demonstrated in cancer cells.

11 n the density and behaviour of the remaining cancer cells.

12 n-activated protein kinase (MAPK) pathway in cancer cells.

13 taking three tissues with varying levels of cancer cells.

14 autophagy, as well as by polyploidization of cancer cells.

15 1 in the Philadelphia chromosome of leukemia cancer cells.

16 el of PAK4 protein in triple negative breast cancer cells.

17 evention and Orai1-SOCE signaling pathway in cancer cells.

18 nusoidal infiltration of the liver by breast cancer cells.

19 ndrogen regulation of DNA repair in prostate cancer cells.

20 chymal transition, motility, and invasion by cancer cells.

21 n impairs the metastatic potential of breast cancer cells.

22 otent stem cells with trisomy 21, as well as cancer cells.

23 , contributes to PARPi sensitivity in breast cancer cells.

24 9), the SIRT1 gene was removed from cervical cancer cells.

25 esistance to cisplatin and olaparib in human cancer cells.

26 tion of DNA damage via Ku70/Ku80 in prostate cancer cells.

27 ct), a metabolic adaptation also observed in cancer cells.

28 promote cell survival and drug resistance in cancer cells.

29 ssion of p27 are frequent characteristics of cancer cells.

30 hich is essential for membrane biogenesis in cancer cells.

31 apoptosis, senescence and autophagy in many cancer cells.

32 critical for sustained EMT traits of ovarian cancer cells.

33 supports the energy-demanding metabolism of cancer cells.

34 lication decision and in its deregulation in cancer cells.

35 rgeted siRNA delivery to EFGR-overexpressing cancer cells.

36 mutated peptides presented on the surface of cancer cells.

37 Ambra1 binds to both FAK and Src in cancer cells.

38 ro against both multiple myeloma and ovarian cancer cells.

39 n increased accumulation of sorafenib in the cancer cells.

40 on of NF-kappaB-dependent MMP1 expression in cancer cells.

41 R2-containing OV vaccinia infected and lysed cancer cells.

42 33, which is located on the surface of liver cancer cells.

43 somes, a condition that occurs frequently in cancer cells.

44 microenvironment, and interactions with non-cancer cells.

45 levels of Glut1 and inhibited glycolysis in cancer cells.

46 expression of which is often dysregulated in cancer cells.

47 activity with leucovorin against colorectal cancer cells.

48 n normal mammary epithelial cells and breast cancer cells.

49 ncreased cisplatin-induced apoptosis in lung cancer cells.

50 ulation of invasion and metastasis in breast cancer cells.

51 lso inhibit endothelial phenotypes of breast cancer cells adopted in response to a nutrient-deficient

52 ylation and signaling pathways in pancreatic cancer cells after gemcitabine treatment using iTRAQ lab

53 we show that MENs can distinguish different cancer cells among themselves as well as from their norm

54 lycolytic flux leads to glucose addiction in cancer cells and a corresponding increase in pyrimidine

55 Natural killer (NK) cells recognize and kill cancer cells and infected cells by engaging cell surface

56 and triggered apoptosis in KRAS-mutant lung cancer cells and inhibited tumor growth in murine models

57 ll-length mutant proteins that accumulate in cancer cells and may confer unique gain-of-function (GOF

58 LIP technology may prove useful in targeting cancer cells and metastases for tumor diagnosis, imaging

59 um-sensitive and platinum- resistant ovarian cancer cells and ovarian cancer stem cells and (ii) down

60 Here, we first demonstrated that breast cancer cells and pancreatic adenocarcinoma cells generat

61 ed naive and enzalutamide-resistant prostate cancer cells and reduced AR and AR-V7 levels to mitigate

62 cancer allograft model, co-injection of PDAC cancer cells and SerpinB2(-/-) mouse embryonic fibroblas

63 ) spatiotemporal interactions between breast cancer cells and stromal cells, and iii) cancer-regulate

64 Communication between cancer cells and the tumor microenvironment results in t

65 ives on the relationship between KRAS-mutant cancer cells and their microenvironment components.

66 man genome, are overexpressed in some breast cancer cells and tissues but without regard to cancer su

67 cells, as well as in KRAS mutated pancreatic cancer cells and was essential for ER homoeostasis.

68 s essential for mitochondrial maintenance in cancer cells and whether this contributes to therapy res

69 in both a nematode in vivo model and breast cancer cells, and could potentially be utilized as an ad

70 mor models, in primary human breast and lung cancer cells, and in deposited expression data.

71 loited to impair NRF2-mediated signalling in cancer cells, and thus sensitise them to chemotherapeuti

72 human cell lines, including both normal and cancer cells, appear to converge to a state that contain

73 ve growth and apoptosis resistance of breast cancer cells are associated with metastasis and disease

74 governing responses to targeted therapies in cancer cells are complex dynamic systems that demonstrat

75 e interactions between the immune system and cancer cells are continuous, dynamic, and evolving from

76 that, during metastatic dissemination (when cancer cells are exposed to periods of ECM detachment),

77 ntext of a matrigel-segregation effect where cancer cells are transiently isolated from host tissue.

78 It is widely assumed that HPV-positive cancer cells are under selection pressure to continuousl

79 cular signatures of coordinated behaviors of cancer cells as a population - in turn may become a dete

80 ased ROS production and apoptosis in hypoxic cancer cells as well as impaired growth of tumor xenogra

81 seen with EGF, provoking responses in breast cancer cells associated with differentiation rather than

82 ronectin (Fn) assembled by CAFs mediates CAF-cancer cell association and directional migration.

83 and promote oncogenic transcription to which cancer cells become highly addicted.

84 nzenesulfonates (PIB-SOs) in CYP1A1-positive cancer cells, both in vitro and in vivo.

85 cancer cell killing in cultured human colon cancer cells, but also improved antitumor activity in vi

86 osis can be a nutrient source for pancreatic cancer cells, but it is not fully understood how the tum

87 b-AP15 induces apoptosis in cancer cells, but the underlying mechanisms are largely

88 tional MMAE warhead destroyed CD276-positive cancer cells, but were ineffective against tumor vascula

89 zation might also affect the antigenicity of cancer cells by altering the immunopeptidome.

90 bearing mice improved paclitaxel delivery to cancer cells by decreasing intratumoral microvessel leak

91 lial-to-mesenchymal transition (EMT) of lung cancer cells by directly repressing the expression of tr

92 egulation alters cell proliferation in human cancer cells by inducing both apoptosis and cell cycle a

93 to produce chromosome segregation defects in cancer cells by inhibiting the correction of erroneous K

94 to suppress the KRAS oncogene in pancreatic cancer cells by means of small molecules binding to RG4s

95 ively inhibits endothelial cells rather than cancer cells by targeting multiple pathways including he

96 nd to what extent TRAIL/TRAIL-R signaling in cancer cells can affect the immune microenvironment.

97 establish a unique gene regulatory axis that cancer cells can exploit to circumvent the immune system

98 oncept that immunisation of devils with DFTD cancer cells can successfully induce humoral responses a

99 STAG1 represents a vulnerability of cancer cells carrying mutations in the major emerging tu

100 In this issue of Cancer Cell, Chen et al. describe complementary approach

101 KRAS-mutated lung cancer cell clones were stably silenced for LSD1 express

102 -kappaB, Bcl-2 and p53) in these NPs-treated cancer cells compared to 5-fluorouracil (5-FU) treated c

103 models and enhances the chemosensitivity of cancer cells, consistent with the role of hPXR in drug r

104 In vitro treatment of breast and ovarian cancer cell cultures in aqueous media by tamoxifen and B

105 P NPs are able to induce efficient apoptotic cancer cell death both in vitro and in vivo through tumo

106 The silencing of SALL4 in cancer cells decreased the expression levels of Glut1 an

107 ration typical of most tissues, we find that cancer cells depend on high levels of the iron-sulfur cl

108 Previously, we found that in cancer cells derived from pancreatic ductal adenocarcino

109 ed extremely good analytical performances in cancer cell detection with linear range of 1x10(2) to 1x

110 Cancer cells differ from normal cells in both gain of fu

111 reveal that enhancers transcribed in breast cancer cells direct critical gene regulatory networks th

112 ar mechanisms that are suggested to underlie cancer cell dissemination are specific to the metastatic

113 tively causes cell cycle arrest and death in cancer cells due to depletion of intracellular GSH and e

114 HIF-1alpha protein accumulated in pancreatic cancer cells even though hypoxic response was decreased

115 Cancer cells exert mastery over the local tumor-associat

116 Cancer cells exploit Spy1 to stimulate proliferation thr

117 r growth and migratory phenotypes of ovarian cancer cells expressing SHMT1 shRNAs.

118 ese data suggest a novel cooperation between cancer cell-extrinsic TGFbeta signaling and cancer cell-

119 Current attempts to culture these primary cancer cells focus on long-term maintenance under growth

120 carcinoma cells, which caused cell death of cancer cells followed by phagocytosis of cell debris by

121 report clonal shifts (change >0.1 in clonal cancer cell fraction, Q < 0.1) in 31% of patients during

122 Cancer cells frequently possess extra amplified centroso

123 omic and histological signatures of residual cancer cells from neoadjuvant-treated breast cancer pati

124 ntly reduce the clonogenicity of bone marrow cancer cells from patients with acute myeloid leukaemia

125 for exercise-dependent suppression of breast cancer cell growth.

126 erases that function in pathways critical to cancer cell growth.

127 e dynamics and that the embryonal theory for cancer cell growth/proliferation is overly simplistic, a

128 The effect of the G4-ligands on Panc-1 cancer cells has also been examined.

129 o contract the matrix and induce invasion of cancer cells has been well documented.

130 pithelial-to-mesenchymal transition (EMT) in cancer cells has been widely considered as an approach t

131 Pancreatic cancer cells have extensively reprogrammed metabolism, w

132 ers (SEs), are central to the maintenance of cancer cell identity and promote oncogenic transcription

133 We previously found that cancer cells in a high mesenchymal therapy-resistant cel

134 AC to reduce the viability of luminal breast cancer cells in in vitro assays.

135 nnels mediate the efflux of ATP and AMP from cancer cells in response to induction of extrinsic apopt

136 consumption and Kyn production controlled by cancer cells in response to the activated T-lymphocytes.

137 reted peptide by epithelial ovarian and lung cancer cells in situ This finding prompted us to study t

138 activity blocked dissemination of colorectal cancer cells in the bone marrow and tumor-driven osteoly

139 bpopulation of mesenchymal stromal cells and cancer cells in the bone marrow.

140 and metastatic states) as well as normal and cancer cells in tissue slices with high accuracy.

141 viability, colony formation, and invasion of cancer cells in vitro and in vivo, which were confirmed

142 and activated apoptosis in MDA-MB-231 breast cancer cells in vitro and in vivo.

143 migratory and invasive capabilities of lung cancer cells in vitro and in vivo.

144 n activate immune effector functions to kill cancer cells in vitroIn vivo, the antibody targets p5365

145 l-to-mesenchymal transition (EMT) of ovarian cancer cells in vivo, STAT4 failed to induce EMT directl

146 evealed that IL-1beta is highly expressed in cancer cells in which the androgen receptor (AR) is not

147 studies with orthotopically injected breast cancer cells in wild-type and RAGE-knockout C57BL6 mice.

148 highly cytocidal toward several human breast cancer cells, including hormone-independent and chemores

149 Accordingly, E+P treatment of breast cancer cells increased ER binding to the NEMO promoter,

150 Invasive cancer cells interact with the surrounding extracellular

151 ity mostly (if not only) as a consequence of cancer cell-intrinsic effects.

152 cancer cell-extrinsic TGFbeta signaling and cancer cell-intrinsic RUNX3 inactivation as aggravating

153 importance of the tumor microenvironment and cancer cell-intrinsic signaling in the regulation of PD-

154 sphorylation-mediated LDHA activity promotes cancer cell invasion and anoikis resistance through redo

155 methylase KDM3A played a dual role in breast cancer cell invasion and apoptosis by demethylating hist

156 Cancer cell invasion from primary tumors is mediated by

157 ial for transcriptional regulation promoting cancer cell invasive phenotypes in lung adenocarcinoma,

158 In cell culture, it opposed increased cancer cell invasiveness driven by upregulated ppGalNAc-

159 e a mechanism by which they are activated in cancer cells, involving release of the I(-) ligand in th

160 The metabolic phenotype of a cancer cell is determined by its genetic makeup and micr

161 term effects, but the emergence of resistant cancer cells is a major barrier to full cures.

162 an also traffic into solid tumors and engulf cancer cells is questionable, given the well-known limit

163 A hallmark of cancer cells is the ability to survive and proliferate w

164 ression by DSS-BEN/miR-34a not only enhanced cancer cell killing in cultured human colon cancer cells

165 livery results in 10-fold improvement of its cancer cell-killing efficacy.

166 In cancer cells, kinases of the Clk family control the supp

167 strates that sFRP1 overexpression in gastric cancer cells leads to increased cell proliferation and a

168 For in vivo studies, a human breast cancer cell line (MDA-231) was implanted in five mice pe

169 tosolic Ca(2+) concentration of HCT116 colon cancer cell line and modified the cytosolic Ca(2+) oscil

170 is across all major types of cancer from the Cancer Cell Line Encyclopedia, which provides genetic an

171 Reducing NAPRT levels in a BRCA2-deficient cancer cell line exacerbated DNA damage in response to c

172 By continuously exposing the gastric cancer cell line MKN45 to 5-FU for >100 passages, we est

173 Experiments involving a human cancer cell line panel and mouse xenografts revealed tha

174 537, in the estrogen-responsive MCF7 breast cancer cell line.

175 d with mice bearing LNCaP and PC-3 (prostate cancer cell line; PSMA-negative) tumors.

176 discriminate between normal and human breast cancer cell lines (fibrocystic and metastatic states) as

177 re potent at inhibiting the growth of breast cancer cell lines (MCF7, MCF7/VP16, BT474, T47D, ZR-75-1

178 th and DNA damage was studied in two ovarian cancer cell lines (OVCAR3 and A2780), normal hamster ova

179 iNVICT on simulated data as well as prostate cancer cell lines and cfDNA obtained from castration-res

180 ls constitutively in a panel of basal breast cancer cell lines and in more than one third of basal tu

181 MICU1 is overexpressed in a panel of ovarian cancer cell lines and that MICU1 overexpression correlat

182 d4 This signature drove clustering of breast cancer cell lines and tumors into the common subtypes an

183 Here we demonstrate, using a variety of cancer cell lines as well as activated primary T cells,

184 noxide (CO) reduced GSH/GSSG in three breast cancer cell lines by inhibiting CBS.

185 ld and reduces the toxicity of Taxol towards cancer cell lines by over 200-fold.

186 Cancer cell lines carrying genetic aberrations that impa

187 have analyzed a panel of 17 KRAS mutant lung cancer cell lines classified as K-Ras-dependent or -inde

188 Prostate cancer cell lines derived from HiMyc tumors (HMVP2 and d

189 as found to be over-expressed in all ovarian cancer cell lines examined and upregulated by mutated TP

190 vestigate this question, we developed breast cancer cell lines expressing an inducible, constitutivel

191 filaments, reduced the invasion of prostate cancer cell lines in 3D in vitro assays.

192 y in primary cancer specimens in vivo and in cancer cell lines in vitro.

193 pounds (9b-9n, 10) were evaluated on various cancer cell lines including, MCF-7 breast, HL-60 leukemi

194 The utility of cancer cell lines is affected by the similarity to endog

195 ited the growth of multiple RAS-mutant human cancer cell lines of diverse tissue origin by blockade o

196 ds compared to monolayer cultures of ovarian cancer cell lines or primary cells.

197 Biological investigation of 2-5 on human cancer cell lines showed enhancement of antiproliferativ

198 s to suppress let-7 target genes in multiple cancer cell lines such as HMGA2 and MYC.

199 nalyzed the proteomes of 10 human pancreatic cancer cell lines to a depth of >8,700 quantified protei

200 s by direct and indirect assays in 12 breast cancer cell lines to estimate the spontaneous occurrence

201 16790A reduced viability of two basal breast cancer cell lines with pronounced endogenous overexpress

202 cellular metabolic profiles of four prostate cancer cell lines with varying degrees of aggressiveness

203 ial-mesenchymal transition in human prostate cancer cell lines, and stable overexpression of miR-194

204 tal RNA extracted from human lung and breast cancer cell lines, discriminating between the cancer-pos

205 50 of 3.3 nM) against a large number (93) of cancer cell lines.

206 -refractory papillary and follicular thyroid cancer cell lines.

207 cer tissues as well as pancreatic and breast cancer cell lines.

208 designed conjugate was studied in normal and cancer cell lines.

209 We also measured expression by 15 human cancer cell lines.

210 wound closing in three types of immortalized cancer cell lines.

211 etic control of oncofetal gene expression in cancer cells may offer novel insights into the onset and

212 olated proteins and from receptors in intact cancer cell membranes.

213 understanding of hypoxia-induced changes in cancer cell metabolism, with an initial focus on HIF-med

214 al new insights into how macrophages enhance cancer cell metastasis, and they identify TNFalpha and T

215 nvironment has been implicated in modulating cancer cell migration and independently predicts progres

216 ive tool for exploring the thermodynamics of cancer cell migration and invasion.

217 1 inhibition did not modulate MCT1-dependent cancer cell migration, silencing or genetic deletion of

218 In this issue of Cancer Cell, Mina et al. systematically characterize pat

219 nd polyploidy increase the immunogenicity of cancer cells mostly by affecting their adjuvanticity rat

220 3-stromal interactions and production of the cancer cell motile factor RANKL.

221 This also induced PC3 cancer cell motility and increased colony size in 2D cul

222 To grow faster cancer cells must activate aerobic glycolysis for energy

223 s are exposed to periods of ECM detachment), cancer cells must alter their metabolism in a fashion th

224 screening of an shRNA library on a panel of cancer cells of different origins as well as normal cell

225 Breast cancer cells often develop resistance to endocrine thera

226 Cancer cells often trigger an inflammatory process, whic

227 s show that LOX overexpression in colorectal cancer cells or systemic delivery of the conditioned med

228 ctively delivering therapeutic reagents into cancer cells or tumor tissues while simultaneously gener

229 ent perplexing findings that polyploid giant cancer cells (PGCCs) acquired embryonic-like stemness an

230 teraction with the microenvironment modulate cancer cell phenotypes and properties, and shape tumor a

231 These data reveal heterogeneity in cancer cell phenotypes, including angiogenesis, prolifer

232 Increasing evidence supports the idea that cancer cell plasticity promotes metastasis and tumor rec

233 ems, MFs secreted high levels of IL-6, while cancer cells produced high levels of TGF-beta.

234 ium-binding A4 (S100A4), a protein linked to cancer cell proliferation and invasiveness.

235 ore precisely assign therapies counteracting cancer cell proliferation and metastatic spread.

236 gram; however, the GLI2 targets that promote cancer cell proliferation are unknown.

237 Rapid cancer cell proliferation promotes the production of red

238 ead and neck and lung) significantly promote cancer cell proliferation, migration and invasion.

239 nd its expression level is critical for lung cancer cell proliferation, which may serve as a prognost

240 ed medium from LOX-overexpressing colorectal cancer cells promoted tumor cell dissemination in the bo

241 l conditions, maintained mTORC1 signaling in cancer cells promotes survival by suppressing endogenous

242 al determinants of the growth of human liver cancer cells, providing a strong rationale to elucidate

243 luripotency, suggesting a mechanism by which cancer cells reacquire properties that are characteristi

244 mple separations: live and dead yeast; human cancer cells/red blood cells; and rodent fibroblasts/red

245 ) was lower in CAFs but elevated in prostate cancer cells relative to their normal counterparts.

246 However, how BRD4 is regulated in cancer cells remains largely unknown.

247 hile overexpression of USP13 renders ovarian cancer cells resistant to chemotherapy.

248 vides a better understanding of how prostate cancer cells respond heterogeneously to androgen depriva

249 tumorigenesis, the high metabolic demand of cancer cells results in increased production of reactive

250 is extensively studied in carcinogenesis and cancer cell's response to chemotherapy and radiotherapy,

251 polyubiquitin gene UBB, which renders these cancer cells sensitive to further decreases in ubiquitin

252 he stroma conditioned by IL-1beta-expressing cancer cells served as a supportive niche also for coexi

253 Cancer cells share several metabolic traits, including a

254 comprised either melanoma cells or prostate cancer cells stably adorned with Toll-like receptor-9 li

255 ir and cell survival, resulting in increased cancer cell survival during DNA damage.

256 ation and ROS generation, thereby sustaining cancer cell survival in hypoxia.

257 e the unique transhesive profiles for breast cancer cells that are adapted to colonize different meta

258 of metastasis-associated behaviors, ovarian cancer cells that express low endogenous levels of MT1-M

259 rtially permissive for the majority of human cancer cells that harbor defects in antiviral signaling,

260 f AURKA is regulated by androgen in prostate cancer cells that highly express AR, emphasizing its pot

261 Herein we show in a diverse array of human cancer cells that IMP2 overexpression stimulates and IMP

262 Consequently, we observed that cancer cells that reside in a CD44+/CD24- state are char

263 Most troublesome is the observation that cancer cells that survive treatment still will have suff

264 Here, we characterize, in breast cancer cells, the molecular effects of a recently develo

265 Indeed, when CXCR7 was silenced in breast cancer cells, their metastatic ability was inhibited.

266 h the efficacy of a molecule process against cancer cells, this work provides an important insight fo

267 may inhibit cell proliferation of esophageal cancer cells through Orai1-mediated intracellular Ca(2+)

268 evolving from the initial establishment of a cancer cell to the development of metastatic disease, wh

269 ontributes to metabolic plasticity, allowing cancer cells to adapt to various microenvironments.

270 f phospho-deficient LDHA Y10F sensitized the cancer cells to anoikis induction and resulted in attenu

271 eting or inhibiting USP13 sensitizes ovarian cancer cells to cisplatin and PARP inhibitor (olaparib)

272 B and Akt signaling pathways sensitizes lung cancer cells to cisplatin-induced apoptosis, we for the

273 gradient concentration, allowing exposure of cancer cells to different doses, and the immunolabeling

274 r while elevated levels can sensitize breast cancer cells to doxorubicin leading to apoptotic cell de

275 lammatory properties, which acts directly on cancer cells to promote their survival and proliferation

276 and consequently reduces the sensitivity of cancer cells to the chemotherapeutic agent 5-fluorouraci

277 Non-invasive in vivo cancer cell tracking in spontaneously metastasizing tumo

278 ptome profiling of 144 single LNCaP prostate cancer cells treated or untreated with androgen after ce

279 sequencing (RIP-seq) analyses of HuR in oral cancer cells treated with ionizing radiation (IR), deter

280 stresses in mediating cellular senescence in cancer cells treated with RSV.

281 Herein, we report that in various cancer cells upon oxygen deprivation, HIF-1 activation d

282 While some cancer cells upregulate de novo serine synthesis, many o

283 or imaging extracellular lactate produced by cancer cells using CEST imaging.

284 nt of MRP1 functional activity in individual cancer cells using scanning electrochemical microscopy (

285 ion, induced a phenotypic switch in prostate cancer cells via mechanotransduction.

286 IPK2 can elicit a cytoprotective response in cancer cells via NRF2.

287 lar nanostructures that selectively inhibits cancer cells via simultaneously targeting multiple hallm

288 ction-mediated phenotypic switch in prostate cancer cells was accompanied by decreased sensitivity of

289 articles that target HER2 and CD44 in breast cancer cells, we demonstrate labeling of fixed cells wit

290 tumor construct, MCF7 and MDA-MB-231 breast cancer cells were coinjected into the mammary fat pad of

291 hown to be also expressed in endothelial and cancer cells where it was shown to modulate vascular end

292 e niche also for coexisting IL-1beta-lacking cancer cells, which are otherwise unable to generate tum

293 mplex virus (oHSV) selectively replicates in cancer cells while inducing anti-tumor immunity.

294 ression and potentiated apoptosis in thyroid cancer cells while not affecting survival in normal thyr

295 or suppressor p53 (encoded by TP53) provides cancer cells with a selective advantage under conditions

296 Treatment of CAFs but not prostate cancer cells with hydrogen peroxide directly inhibited m

297 nstrate that treatment of human MCF-7 breast cancer cells with pro-inflammatory cytokines results in

298 the plasticity and heterogeneity of prostate cancer cells with regard to androgen dependence, definin

299 ns in free iron and iron-related proteins in cancer cells without affecting the oxidative stress resp

300 pecific ligand allows a widespread "net" for cancer cells, without a priori knowledge of the cancer t