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1 ids colonization and renders the tumor cells chemoresistant.
2 ion effects, and patients bearing Mt p53 are chemoresistant.
3 ial to mediate tumor regrowth are relatively chemoresistant.
4 which are frequently radiation-resistant and chemoresistant.
5 n aggressive B cell lymphoma that is largely chemoresistant.
6 an self-renew and are highly tumorigenic and chemoresistant.
7  with either chemosensitive (50 patients) or chemoresistant (44 patients) relapse, including 22 who f
8 ci at 4092 genes becoming hypermethylated in chemoresistant A2780/cp70 compared with the parental-sen
9 erS5/6 activities (approximately twofold) in chemoresistant ABCB1(high) (A498, Caki-1) compared with
10          In this study, we demonstrated that chemoresistant acute myeloid leukemia (AML) cells had a
11 apoptotic death and selective eradication of chemoresistant AML cells in vitro and in vivo.
12 ses the outgrowth of a pre-determined set of chemoresistant AML clones with stemness properties, inst
13                            Importantly, more chemoresistant AML LSCs appeared to be retained in Lama4
14 etic stem cells, leukemic blasts, as well as chemoresistant AML were all consistently hallmarked by i
15 potential importance of WIT-1 methylation in chemoresistant AML.
16     Apaf-1-negative melanomas are invariably chemoresistant and are unable to execute a typical apopt
17 ease progression at 1 year for patients with chemoresistant and chemosensitive disease were 75% and 2
18 on and illustrate a therapeutic strategy for chemoresistant and desmoplastic CRCs.
19 -arr1, ARRB1) links Wnt signaling to acquire chemoresistant and EMT phenotype.
20                                    We induce chemoresistant and G0 leukemic cells by serum starvation
21  cancer cells endowed with high tumorigenic, chemoresistant and metastatic potential.
22 isolated from ovarian cancer cell lines were chemoresistant and preferentially grew tumors, compared
23 r Notch, but these cells are also relatively chemoresistant and provide trophic support to neuroendoc
24 erexpressed in many human cancers, including chemoresistant and radioresistant breast cancer cells, b
25 herapies may be missing the subpopulation of chemoresistant and radioresistant cancer stem cells (CSC
26 ed a chemosensitive SCLC PDX model to become chemoresistant and resulted in sensitivity to inhibition
27      Adult T-cell leukemia (ATL) is a highly chemoresistant and usually fatal T-cell malignancy due t
28 irst 3 years for the chemosensitive relapse, chemoresistant, and induction failure groups were 61%, 4
29 tiple stem cell characteristics, were highly chemoresistant, and were enriched in xenografts residual
30                      CK5-positive cells were chemoresistant as determined by fourfold reduced rate of
31  of DNA-PKcs in vivo resensitizes inherently chemoresistant ATM-deficient tumors to genotoxic chemoth
32 e emerged as effective treatment options for chemoresistant B cell acute lymphoblastic leukemia (B-AL
33                     ROR1 is overexpressed in chemoresistant BC where it correlates with poor therapy
34 emoresistance is critical in order to combat chemoresistant BC.
35 growth in both the chemosensitive BL0440 and chemoresistant BL0269 models.
36 llagen type III is enriched in patients with chemoresistant bladder cancer after neoadjuvant chemothe
37 timal tri-drug combination in eight distinct chemoresistant bladder cancer cell lines.
38 se findings provide a rationale for treating chemoresistant bone metastasis of PCa with inhibitors of
39    Malignant gliomas are highly invasive and chemoresistant brain tumors with extremely poor prognosi
40 restoration of PARP inhibitor sensitivity in chemoresistant BRCA1/2-deficient cells.
41 with olaparib can restore the sensitivity of chemoresistant BRCA1/2-deficient cells.
42 ful predictive biomarker for a population of chemoresistant breast cancer patients.
43 (TNBC), contributing to the maintenance of a chemoresistant breast cancer stem cell (BCSC) population
44 eatures, and may arise from an earlier, more chemoresistant breast epithelial precursor than basal-li
45 splantation (NMAT) infrequently cures active chemoresistant, bulky, or aggressive B-cell lymphoma (B-
46   Low-grade serous carcinoma of the ovary is chemoresistant but mutations in the MAPK pathway could b
47  PSP94 peptide derivative PCK3145 suppresses chemoresistant cancer cell and tumor growth in vitro and
48 TT and cellular HDAC assays on sensitive and chemoresistant cancer cell lines as well as HDAC profili
49 acious therapeutics against solid tumors and chemoresistant cancer cell lines.
50 e protein, ABCG2, is up-regulated in certain chemoresistant cancer cells and in the mammary gland dur
51 iant cancer cells (PGCCs) are multinucleated chemoresistant cancer cells found in heterogeneous solid
52 eased expression of miR-9-3p and miR-9-5p in chemoresistant cancer cells may support their validation
53 dentification of medicinal compounds against chemoresistant cancer cells via new mechanism of action
54 the critical role of PGCCs as aggressive and chemoresistant cancer cells, as well as their ability to
55 in rapid loss of this prosurvival protein in chemoresistant cancer cells.
56  signaling, amplifying the TRIM37 network in chemoresistant cancer cells.
57  incurable due to the inability to eradicate chemoresistant cancer stem-like cells (sCSC) that are li
58 lanoma is a highly aggressive and frequently chemoresistant cancer, the incidence of which continues
59  rationally designed therapy for metastatic, chemoresistant cancers and might overcome the problems a
60                                 In contrast, chemoresistant cancers and normal tissues were poorly pr
61  p53 mutations often occur in aggressive and chemoresistant cancers but are rarely observed in melano
62 e other hand, kinase inhibitor-resistant and chemoresistant cancers have increased cilia and increase
63  have potential therapeutic implications for chemoresistant cancers, especially of brain tumours wher
64 n D1 is observed in many aggressive forms of chemoresistant cancers, these findings provide insight i
65 lanoma represent biologically aggressive and chemoresistant cancers.
66 ts of targeting RAD6 with SMI#9 for managing chemoresistant cancers.
67 grafts to generate paired chemosensitive and chemoresistant cancers.
68 ce that this agent can preferentially target chemoresistant CD133(+) cells with CSC character in SCLC
69 es and c-MYC protein were upregulated in the chemoresistant CDX model, while MYC/MAX dimerization blo
70 al inhibition of NO synthase re-sensitizes a chemoresistant CDX progression model in vivo, revealing
71 tumours at relapse following chemotherapy or chemoresistant cell lines derived at the time of patient
72 NA rescue functional assays on 12 strains of chemoresistant cell lines each against cisplatin, 5-fluo
73 tients, and alternative approaches to target chemoresistant cells are needed.
74    Our results show that drugs resensitizing chemoresistant cells are superior to those aimed at trig
75 ling cells with those that target quiescent, chemoresistant cells associated with nutrient and oxygen
76 ature myeloid blast cells with stem-like and chemoresistant cells being retained in the bone marrow t
77 oma bulk populations and indicate that these chemoresistant cells can be specifically targeted via AB
78 restingly, direct delivery of ATP into cross-chemoresistant cells destabilized HIF-1alpha and inhibit
79 d not survive glucose deprivation, while the chemoresistant cells displayed adaptability.
80                                        These chemoresistant cells exhibited a corresponding upregulat
81 d it represents hematopoietic stem cells and chemoresistant cells from several solid tumors.
82            Recent studies have reported that chemoresistant cells have an increased oxidative state i
83 tic approach to mitigate the impact of these chemoresistant cells in cancer progression and to improv
84 genotoxic drug treatment favors selection of chemoresistant cells in genetically heterogeneous tumors
85 de evidence that SP is an enriched source of chemoresistant cells in human melanomas, and suggest tha
86 3K activation can lead to the development of chemoresistant cells in prostatic carcinomas through the
87  <30% due to the persisting dissemination of chemoresistant cells in the peritoneal fluid and the imm
88  oxygen species (ROS)-mediated death of even chemoresistant cells independently of p53 status.
89                                              Chemoresistant cells must consume excess resources to ma
90                            MCAM depletion in chemoresistant cells reduced cell proliferation and redu
91                             GPT2 knockout in chemoresistant cells restored the metabolic phenotype to
92 ed that MCAM modulated lactate production in chemoresistant cells that exhibit a distinct metabolic p
93                  In tumours, accumulation of chemoresistant cells that express high levels of anti-ap
94 tion, which serves to maintain slow cycling, chemoresistant cells through an IL1beta/IL8/CXCR1 cytoki
95   Inhibition of Akt is required to sensitize chemoresistant cells to CDDP in a p53-dependent manner,
96 e C-terminal GSN fragment (C-GSN) sensitized chemoresistant cells to CDDP, intact GSN and its N-termi
97 y undergoing clinical evaluation, sensitized chemoresistant cells to cisplatin.
98 t which is known to favor the development of chemoresistant cells.
99 g also facilitated CDDP-induced apoptosis in chemoresistant cells.
100 y proliferate at the expense of the less fit chemoresistant cells.
101 ynergize with chemotherapeutic agents across chemoresistant cellular and mouse models.
102 erapy options, particularly in patients with chemoresistant clones carrying STAT5BN642H.
103                                      Certain chemoresistant colon cancer cells are therefore exquisit
104 c transaminase 2 (GPT2), were upregulated in chemoresistant compared to chemosensitive cells.
105 displayed a glycolytic phenotype while their chemoresistant counterparts (C200 and PEO4) exhibited a
106 vestigated CSC properties in newly developed chemoresistant CRC cell lines and sought to identify tar
107                                              Chemoresistant CRC cells are enriched for CSC markers an
108 ore effective therapy should target both the chemoresistant CSCs and the proliferating epithelial cel
109 nt, indicating that paclitaxel enrichment of chemoresistant CSCs is less dependent on microenvironmen
110 limited toxicity in mice with aggressive and chemoresistant diffuse intrinsic pontine glioma.
111 scription modulator that is overexpressed in chemoresistant, diffuse large B-cell lymphomas (DLBCLs).
112 eous blocks in both pathways correlated with chemoresistant disease (92% of patients with chemoresist
113               Adverse OS was associated with chemoresistant disease (relative risk [RR], 2.9), more t
114                                Resurgence of chemoresistant disease after primary therapy typifies ep
115 ith high-grade NHL, mantle cell lymphoma, or chemoresistant disease had a poor outcome.
116                                     However, chemoresistant disease is still problematic.
117 ugh their contribution in development of the chemoresistant disease remains elusive.
118 Developing effective strategies to eradicate chemoresistant disease requires experimental models that
119  OS were 42% and 55%, whereas for those with chemoresistant disease the PFS and OS were 22% and 29%.
120 chemoresistant disease (92% of patients with chemoresistant disease versus 33% of patients with chemo
121 nitial therapy but is prone to relapses with chemoresistant disease, indicating the need for novel th
122 typically followed by recurrence with lethal chemoresistant disease.
123 velop recurrence, which rapidly evolves into chemoresistant disease.
124 nal non-operable patients with recurrent and chemoresistant disease.
125  and that such expression may be a marker of chemoresistant disease.
126 al chemosensitivity followed by emergence of chemoresistant disease.
127 here are no standardized treatments for this chemoresistant disease.
128 disease and the near guaranteed emergence of chemoresistant disease.
129 vanced-stage patients relapse and succumb to chemoresistant disease.
130 l metastasis and about 50% will relapse with chemoresistant disease.
131  lethal gynecological cancer, often leads to chemoresistant diseases.
132                                 We show that chemoresistant DTCs occupy the perivascular niche (PVN)
133 ted strong synergistic antitumor activity in chemoresistant EC cell lines, HEC-1B and ARK-2 cells.
134 to a marked reduction in tumor growth in two chemoresistant EC mouse xenograft models.
135 VEGF receptors, reduced proliferation of the chemoresistant EOC cells through induction of G2/M cell
136      Investigations in clinical specimens of chemoresistant EOC tissues confirmed increased recruitme
137 bitors have demonstrated limited activity in chemoresistant EOC.
138 potential of dacomitinib in treatment of the chemoresistant EOC.
139 nd an increase in endothelial cells whilst a chemoresistant epithelial stem cell population correlate
140 diffuse large B cell lymphoma (ABC-DLBCL), a chemoresistant form of DLBCL.
141 ly chemosensitive, but rapidly relapses in a chemoresistant form with an overall survival of <5%.
142  C/EBPbeta is associated with metastatic and chemoresistant forms of breast cancer.
143 rgeted therapeutic agents for metastatic and chemoresistant gestational trophoblastic neoplasia.
144 ited the proliferation of chemosensitive and chemoresistant glioma cells but did not display toxicity
145  therapy for a poor prognosis and frequently chemoresistant group of patients with MM, for whom thera
146 e, we report higher gelsolin (GSN) levels in chemoresistant gynecological cancer cells compared with
147 d be investigated further as a treatment for chemoresistant HB.
148                                              Chemoresistant hepatoblastoma (HB) is associated with po
149                                           In chemoresistant hepatospheres, CD47 was found to be up-re
150 r values, we infer that most patients harbor chemoresistant HGSC cells at diagnosis and that, if the
151 utic strategy that could improve outcomes in chemoresistant HGSOC.
152 ol with mechanistic rationale against highly chemoresistant human PaC cells.
153  fibroblast (CAF) polarization (p=0.006) and chemoresistant IL-6/STAT-3 signaling in vivo.
154      In part, a lack of natively metastatic, chemoresistant in vivo models has limited our insight in
155                      Because NSCLC is highly chemoresistant, it is, usually not treatable.
156 ilostamide, causes profound growth arrest of chemoresistant KM12C colon cancer cells.
157  in a subset of NB cell lines, including the chemoresistant LA-N-6 cell line.
158 ide but in almost every case becomes rapidly chemoresistant, leading to death within 1 year.
159            Most patients with AML succumb to chemoresistant leukemia stem cells (LSCs), which persist
160 pitulate gene expression profiles of in vivo chemoresistant leukemic and G0 models.
161 a promising strategy to target and eliminate chemoresistant leukemic cells.
162 herapy is a promising strategy for targeting chemoresistant leukemic cells.
163 gulin1-beta1 (HRG1/NRG1), which is higher in chemoresistant lines compared to cisplatin-sensitive cel
164 reduced Akt-activated beta-catenin levels in chemoresistant LSCs and reduced LSC tumorigenic activity
165  agents) could favor elimination of residual chemoresistant lymphoma cells.
166  as an adjuvant therapy for the treatment of chemoresistant malignancies, and highlight the utility o
167 denocarcinoma (PDAC) is a highly metastatic, chemoresistant malignancy and is characterized by a dens
168 eritoneum is a hormonally driven, relatively chemoresistant malignancy with limited treatment options
169 n hormone therapy resistant (MDA-MB-231) and chemoresistant (MCF-7TN-R) breast cancer cells.
170 s P-gp expression and is associated with the chemoresistant mechanisms of metastatic human breast can
171  cancer cell lines (MDA-MB-231) to study the chemoresistant mechanisms regulated by miRNAs.
172 hich points to the existence of a relatively chemoresistant melanoblast-like cell population residing
173 ed for cytotoxic activity against a panel of chemoresistant melanoma cell lines, and it was found tha
174 nd inducer of cell death in otherwise highly chemoresistant melanoma cells.
175 stigating nanoparticle treatment options for chemoresistant melanomas.
176 rapy often fail because of the recurrence of chemoresistant metastases.
177 or, primary (testicular and mediastinal) and chemoresistant metastatic human GCTs, we show that the p
178 res enriched in CR-CSCs, including four from chemoresistant metastatic lesions, were used for in vitr
179                               Persistence of chemoresistant minimal residual disease (MRD) plasma cel
180     Finally, BI extended mouse survival in a chemoresistant model and significantly improved chemothe
181                                     Multiple chemoresistant models demonstrated suppression of SLFN11
182 rapeutic efficacy in both chemosensitive and chemoresistant models of small cell lung cancer.
183  in several types of cancer cells, including chemoresistant multiple myeloma (MM) cells.
184 tic approach to target highly aggressive and chemoresistant MYC-activated cancers.
185 rmacological inhibition of USP7 resensitized chemoresistant MYCN-overexpressing PDX models to chemoth
186 ts, but these are short-lived because of the chemoresistant nature of hormone-refractory prostate can
187 e-independent, and likely contributes to the chemoresistant nature of RCCs.
188                              Blocking Y5R in chemoresistant NB cells rich in this receptor sensitized
189 gue AN-238 provides an effective therapy for chemoresistant neoplasms such as RCC.
190   Drug efflux pump ABCB1 is overexpressed in chemoresistant neoplasms where it effluxes various chemo
191 d 1 mg/kg/day for 28 days) were evaluated in chemoresistant neuroblastoma-bearing mice and compared w
192  of cancer stem cells markers and sensitized chemoresistant OC cells to carboplatin.
193 e CD55 S/T domain is sufficient to sensitize chemoresistant OC cells to cisplatin.
194 rom chemoresistant patients, and enriched in chemoresistant OC cells.
195 ide leverage to treat ovarian cancer that is chemoresistant on the basis of ineffective apoptosis.
196 ival rates remain at ~70%, but patients with chemoresistant or metastatic disease have extremely poor
197 herefore, it would be beneficial to identify chemoresistant or refractory patients early during thera
198 DM2-overexpressing cancer cells are commonly chemoresistant, our findings suggest that this naturally
199 of SYK and EGFR as a promising treatment for chemoresistant ovarian cancer by disrupting DNA synthesi
200           Dual inhibition of SYK and EGFR in chemoresistant ovarian cancer cells elicited a synergist
201                                              Chemoresistant ovarian cancer cells showed increased oxi
202  high abundance from both chemosensitive and chemoresistant ovarian cancer cells via exosomes.
203 C down-regulation in both chemosensitive and chemoresistant ovarian cancer cells.
204 e the therapeutic utility of MePS2 siRNAs in chemoresistant ovarian cancer mouse models via targeting
205 ion exerts synergistic anticancer effects in chemoresistant ovarian cancer, providing a strategy to t
206  to prevent the development of recurrent and chemoresistant ovarian cancer.
207 s the PD-L1/PD-1 and CD80/CTLA-4 pathways in chemoresistant ovarian cancer.
208 of GLS inhibitor and PARP inhibitor to treat chemoresistant ovarian cancers, especially those with hi
209 for the development of effective therapy for chemoresistant ovarian cancers.
210  of neoplasms, but particularly in recurrent chemoresistant ovarian carcinomas, suggesting a biologic
211              Lupeol significantly sensitized chemoresistant PaC cells to undergo apoptosis by recombi
212            Glutaminase inhibitors sensitized chemoresistant pancreatic cancer cells to gemcitabine, t
213 ucine) as an adjuvant treatment to sensitize chemoresistant pancreatic cancer cells.
214 by the selective enrichment of intrinsically chemoresistant pancreatic cancer stem cells that are equ
215 or chemical inhibition of Wnt signaling in a chemoresistant patient-derived xenograft (PDX) model of
216          These miRNAs effectively suppressed chemoresistant patient-derived xenograft growth in vivo,
217 us of a subset of OC specimens, ascites from chemoresistant patients, and enriched in chemoresistant
218 help to avoid application of chemotherapy to chemoresistant patients.
219 tients in chemosensitive relapse, and 7% for chemoresistant patients.
220 ognostically relevant in MM and may identify chemoresistant PCs in vitro.
221 d be already present at the MRD stage, where chemoresistant PCs show a singular phenotypic signature
222 tor in chemoresistant SCLC cell lines and in chemoresistant PDX compared with matched treatment-naive
223  with ORY-1001-induced NOTCH activation in a chemoresistant PDX model.
224 A1-mutated metastatic sample and the derived chemoresistant PDX, but not in the matched docetaxel-sen
225 ment of human ovarian cancer (OVCA), and the chemoresistant phenotype in OVCA cells is associated wit
226  membrane scaffold, CD82, contributes to the chemoresistant phenotype of AML.
227 tyrosine kinase activity is required for the chemoresistant phenotype of HER-2/neu-overexpressing NSC
228 NHL B-cell lines, resulting in reverting the chemoresistant phenotype to a sensitive phenotype.
229 ly modified histones, which correlate with a chemoresistant phenotype.
230 pithelial-mesenchymal transition (EMT) and a chemoresistant phenotype.
231 the inability of Tie2 activation to induce a chemoresistant phenotype.
232 er cell line PA1 leads to an increase in the chemoresistant phenotype.
233 contribute to the development of a radio- or chemoresistant phenotype.
234 oxicity and thereby may contribute to a more chemoresistant phenotype.
235 c stroma, which contribute to the profoundly chemoresistant phenotype.
236  downstream of Dll1 and is associated with a chemoresistant phenotype.
237 creased metabolic activity associated with a chemoresistant phenotype.
238 e case of invasive cancer phenotypes, a more chemoresistant phenotype.
239 tatic samples were characterized as having a chemoresistant phenotype.
240                                          The chemoresistant population in recurrent osteosarcoma is s
241 (Lmo2Tg) mouse model in which we can monitor chemoresistant preleukemia stem cells (pre-LSCs) and leu
242 fer both tumor cell heterogeneity as well as chemoresistant properties.
243  the fallopian tubes that has a high rate of chemoresistant recurrence and low five-year survival rat
244 nt survival, effective treatments addressing chemoresistant recurrences are particularly needed.
245  derived from leukemia patients experiencing chemoresistant relapse that were exposed to these nanopa
246 tors (DNMTi, hypomethylating drugs) prevents chemoresistant relapses.
247                Thus, our results establish a chemoresistant role for RIP1 that maintains inhibitor of
248 iously unexplored therapeutic target in this chemoresistant sarcoma.
249  growth and mitochondrial dysfunction in the chemoresistant SCLC cell line H69AR.
250 s a markedly upregulated surface receptor in chemoresistant SCLC cell lines and in chemoresistant PDX
251 nt mutations was found to be associated with chemoresistant secondary lymphomas.
252 enocarcinoma, and is further enhanced during chemoresistant selection.
253 inhibited the growth of three of five lethal chemoresistant serous adenocarcinoma PDXa models without
254 strategy poised for testing in patients with chemoresistant serous ovarian cancer.
255  that TPCs can reversibly enter a quiescent, chemoresistant state and thereby underscore the need for
256 ke Fusobacterium species induce a quiescent, chemoresistant state in cancer cells in the colon by dis
257 itical role in acquiring and maintaining the chemoresistant state in ovarian cancer.
258 pies; however, essentially all progress to a chemoresistant state.
259 el molecular marker for a distinct subset of chemoresistant, stem cell phenotype-expressing tumor cel
260           Intriguingly, three metastatic and chemoresistant subclones, S2-CP9, S2-LM7AA, and S2-013,
261 , suppress proliferation of the less fit but chemoresistant subpopulations.
262 tial cause of cancer relapse is pretreatment chemoresistant subpopulations.
263 Metaplastic breast cancer (MpBC) is a highly chemoresistant subtype of breast cancer with no standard
264 f pluripotency markers (NANOG and POU5F1) in chemoresistant teratomas or transformed carcinomas.
265 DKK4 and NOTCH signaling levels and are more chemoresistant than paired subcutaneous xenografts.
266 ng actionable targets in treatment-naive and chemoresistant TNBC is a critical unmet medical need.
267 key inducer of chemoresistance by developing chemoresistant TNBC tumors in vivo and characterizing th
268           Leukemias with NT5C2 mutations are chemoresistant to 6-mercaptopurine yet show impaired pro
269                                          The chemoresistant traits of BORG depend upon its robust act
270 ay in TECs and converts naive tumor cells to chemoresistant TSCs, thereby facilitating their invasive
271 rug that, by inhibiting Tim16, may sensitize chemoresistant tumor cell to proapoptotic stimuli.
272  is largely attributed to the development of chemoresistant tumor cells.
273 re generally attributed to subpopulations of chemoresistant tumor cells.
274  cell renal cell cancer (CC-RCC) is a highly chemoresistant tumor characterized by frequent inactivat
275 sophageal adenocarcinoma is a heterogeneous, chemoresistant tumor for which the availability and size
276 s a molecular marker for distinct subsets of chemoresistant tumor-initiating cell populations in dive
277 ial for STI571 in patients afflicted by this chemoresistant tumor.
278 orubicin and cisplatin chemotherapy, and all chemoresistant tumors adopted a p53-like phenotype after
279 JAK2 inhibitor CYT387 reduced progression of chemoresistant tumors and increased survival.
280 plastic breast cancers (MBC) are aggressive, chemoresistant tumors characterized by lineage plasticit
281  patients bear inoperable, locally advanced, chemoresistant tumors demonstrating the urgent need for
282 evance of these findings to the treatment of chemoresistant tumors in vivo has remained unclear.
283 d the superiority of metronomic protocols in chemoresistant tumors in vivoCancer Res; 77(17); 4723-33
284 tection-challenged BRCA1-deficient naive- or chemoresistant tumors require SMARCAD1-mediated active f
285 lpha, the inhibitor of NF-kappaB, sensitizes chemoresistant tumors to the apoptotic potential of TNFa
286                                Patients with chemoresistant tumors were twice as likely to have high
287 making it an attractive anticancer agent for chemoresistant tumors with enhanced antiapoptotic activi
288 ere established from both chemosensitive and chemoresistant tumors, and nearly 30% of the PDX models
289 etastatic JAK-STAT3 pathway was activated in chemoresistant tumors, and treatment with the JAK1/JAK2
290 in tumors are among the most common and most chemoresistant tumors.
291 ognosis and present with more aggressive and chemoresistant tumors.
292 say using live mitochondria from RASAL2-high/chemoresistant tumour cells demonstrated attenuated rele
293 ncy of p53 mutations observed in this highly chemoresistant tumour type.
294 cer cells, including hormone-independent and chemoresistant types.
295 ncer stem cells (CSC) are hypothesized to be chemoresistant, we investigated CSC properties in newly
296 chter transformation (DLBCL-RT) is typically chemoresistant with poor prognosis.
297 onic lymphocytic leukemia (CLL) is typically chemoresistant, with a poor prognosis.
298                                      In vivo chemoresistant xenograft models, an unbiased genome-wide
299  in 3D-cultured cell lines, tumor organoids, chemoresistant xenografts, syngeneic tumors and PDX mode
300 in the more chemosensitive WERI, but not the chemoresistant Y79 line.

 
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