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1  could promote cancer mutations and expedite chemoresistance.
2 (hPXR) has been associated with induction of chemoresistance.
3 ibutes to their epigenetic reprogramming and chemoresistance.
4 RB signaling regulates leukemic survival and chemoresistance.
5 nt obstacles to successful OvCa treatment is chemoresistance.
6 ion of Snail1-dependent tumoral invasion and chemoresistance.
7 w poor efficacy due to intrinsic or acquired chemoresistance.
8 stem cell (CSC) expansion and CSC-associated chemoresistance.
9 tive stress responses, tumor progression and chemoresistance.
10 iated traits such as migration, invasion and chemoresistance.
11 o identify novel mechanisms involved in SCLC chemoresistance.
12 of high-risk neuroblastomas recur because of chemoresistance.
13 nown about the role of histone expression in chemoresistance.
14 ar fitness' that may be also associated with chemoresistance.
15 ited therapeutic efficacy is achieved due to chemoresistance.
16 al of leukemic cells and also tackling their chemoresistance.
17  SOX9/2/17 are involved in MRP3-mediated CCA chemoresistance.
18  inhibition of IL6-induced proliferation and chemoresistance.
19 contributing to tumor cell proliferation and chemoresistance.
20 rvival, and their potential as modulators of chemoresistance.
21 s alongside chemotherapy for overcoming PDAC chemoresistance.
22 lution, tumorigenesis, and the phenomenon of chemoresistance.
23 owth inhibition, apoptosis, G0/G1 arrest and chemoresistance.
24 sponsible for tumor relapse, metastasis, and chemoresistance.
25 carcinoma, contributing to poor survival and chemoresistance.
26  limited efficacy due to de novo or acquired chemoresistance.
27 stance differs from that underlying acquired chemoresistance.
28 r the development of MDR-based predictors of chemoresistance.
29 en a high metabolically active phenotype and chemoresistance.
30 nd mechanistically control colorectal cancer chemoresistance.
31 emosensitive but then relapses with acquired chemoresistance.
32 utations are linked to tumor progression and chemoresistance.
33  of self-renewal, cell cycle quiescence, and chemoresistance.
34 ch correlates with poor overall survival and chemoresistance.
35 crophages was found to reverse their natural chemoresistance.
36 ith active Notch signaling, known to mediate chemoresistance.
37 rstudied phenomenon known as hypoxia-induced chemoresistance.
38 on that contributes to tumor maintenance and chemoresistance.
39  (AML) patient samples, indicating a role in chemoresistance.
40 hey drive tumor progression, metastasis, and chemoresistance.
41 sidered responsible for tumor initiation and chemoresistance.
42 t, is limited by its severe side effects and chemoresistance.
43 nt EMT and CSC functions, thereby conferring chemoresistance.
44 y in general, plays an important role in AML chemoresistance.
45  cells, thereby supporting tumour growth and chemoresistance.
46 henotype, as well as the rare progression to chemoresistance.
47 auses uncontrolled lethality, in part due to chemoresistance.
48 ctor T cells: they abrogate stromal-mediated chemoresistance.
49  but instead acutely secrete IL-6, promoting chemoresistance.
50 ggesting a novel mechanism to overcome tumor chemoresistance.
51  but that loss of HMGA2 did not give rise to chemoresistance.
52 OCC spheroids, as well as cell migration and chemoresistance.
53 roliferation, migration, transformation, and chemoresistance.
54 r in breast cancer patients who had acquired chemoresistance.
55 dual disease, underscoring their role in AML chemoresistance.
56 racteristic of melanoma progression and also chemoresistance.
57 ported that karyopherins are associated with chemoresistance.
58  uncovering new opportunities for addressing chemoresistance.
59 agents whose efficacy is often attenuated by chemoresistance.
60 ltiple overlapping effects that characterize chemoresistance.
61 ther MYCN or MYCL also conferred a switch to chemoresistance.
62 assembly of stress granules, an indicator of chemoresistance.
63 h little susceptible to transporter-mediated chemoresistance.
64 fied to be the key mechanism of SOX9-induced chemoresistance.
65 hieve a synergistic effect and a decrease in chemoresistance.
66 permits expression of ARE mRNAs that promote chemoresistance.
67  to promote synthetic lethality and overcome chemoresistance.
68 butor in pancreatic cancer tumorigenesis and chemoresistance.
69 expression of ARE-bearing mRNAs that promote chemoresistance.
70 ffecting downstream pathways involved in AML chemoresistance.
71 ize hPXR agonist-induced gene expression and chemoresistance.
72 that BEL could suppress hPXR agonist-induced chemoresistance.
73 , little is known about their impact on OvCa chemoresistance.
74 that are implicated in cancer metastasis and chemoresistance.
75 r secreted AA as important mediators of OvCa chemoresistance.
76  SOX9/2/17 are involved in MRP3-mediated CCA chemoresistance.
77 at secreted lipids mediate adipocyte-induced chemoresistance.
78 eta signaling to drive tumor progression and chemoresistance.
79 geting sCLU via miR-378 may help disable the chemoresistance against cisplatin in lung adenocarcinoma
80 ed repeated chemotherapy and correlates with chemoresistance, aggressiveness and poor prognosis in NS
81  a major role for cancer stem cells (CSC) in chemoresistance, although their involvement in acquired
82 ffluxion from liver cancer cells, leading to chemoresistance and a diminished chemotherapeutic effect
83 ple-negative breast cancer (TNBC) are due to chemoresistance and aggressive metastases, with high pre
84 C regulator as a prognostic marker of cancer chemoresistance and as a potential drug target for CSC t
85                 Paradoxically, by increasing chemoresistance and cancer metastasis, it is also procan
86           In turn, deletion of OCT4 reverses chemoresistance and delays the relapse.
87 dothelial cell crosstalk signaling in cancer chemoresistance and demonstrate the improved efficacy of
88 apeutic target to prevent and treat acquired chemoresistance and disease recurrence in OC and enhance
89 ignancies due to the development of acquired chemoresistance and disease relapse.
90 , anchorage independence, cell survival, and chemoresistance and efficiently inhibited tumorigenesis
91 ed gene expression associated with stemness, chemoresistance and epithelial-mesenchymal transition an
92 all-molecule modulator of miR-34a to reverse chemoresistance and further enhance the therapeutic effi
93 le for DNMT3A(R882) mutations in driving AML chemoresistance and highlight the importance of chromati
94 acute need to decipher mechanisms underlying chemoresistance and identify new targets to improve pati
95 y be a highly effective approach to overcome chemoresistance and improve the outcome of advanced BC.
96  challenging due to diverse genetic make-up, chemoresistance and inefficient drug transport across th
97 e, we investigated the role of ASC in cancer chemoresistance and invasiveness, the attributes of tumo
98  over-expressed in EOC and play key roles in chemoresistance and invasiveness.
99 ions of leukemia stem cells (LSC) that drive chemoresistance and leukemia relapse.
100 tivation of growth factor receptors leads to chemoresistance and limits the clinical impact of sorafe
101 expression correlated strongly with acquired chemoresistance and malignant behavior of OC cells, expr
102                                       Cancer chemoresistance and metastasis are tightly associated fe
103 128-3p) is key to concomitant development of chemoresistance and metastasis in residual NSCLC cells h
104                               Development of chemoresistance and peritoneal dissemination of EOC cell
105  activated in human tumours correlating with chemoresistance and poor prognosis.
106 tumor cells may yield insights into clinical chemoresistance and potentially improve therapeutic outc
107  lesions, particularly those associated with chemoresistance and progression to highly aggressive for
108 te the mechanistic features of KRAS-mediated chemoresistance and provide a rationale for exploiting m
109 gs show that MYCN overexpression drives SCLC chemoresistance and provide a therapeutic strategy to re
110 docrine marker expression is associated with chemoresistance and reducing MYC levels decreases gemcit
111 ic cancer by overcoming transporter-mediated chemoresistance and reducing systemic toxicity.
112 f treatment including non-specific toxicity, chemoresistance and relapse.
113 get for CSC therapy that may overcome cancer chemoresistance and relapse.
114 lammation has a crucial role in induction of chemoresistance and results, in part, from the induction
115 tion of most chemotherapeutic drugs develops chemoresistance and severe systemic toxicities, herein w
116 f the proinflammatory cytokine IL-6 promotes chemoresistance and show that the chemotherapeutic doxor
117                         These mice developed chemoresistance and spontaneous bone marrow metastases.
118  is critical for glioblastoma initiation and chemoresistance and that inhibition of ID1 enhances the
119 are poor and have remained stagnant owing to chemoresistance and the high propensity to form lung met
120                    Given the role of NRF2 in chemoresistance and the surging interest in p97 inhibito
121 M3A promotes ovarian CSCs, proliferation and chemoresistance and thus, highlights the significance of
122 thereby providing a new strategy to overcome chemoresistance and to improve the treatment and surviva
123 ve been suggested as a mechanism for driving chemoresistance and tumor recurrence in human cancers in
124       Here, we show that NRF2 contributed to chemoresistance and was associated with a poor prognosis
125      This study explores the role of PKM2 in chemoresistance and whether inhibiting PKM2 augments the
126 arcomatoid subtype is associated with higher chemoresistance and worst survival.
127  by virtue of its Y5 receptor (Y5R)-mediated chemoresistance and Y2 receptor (Y2R)-mediated prolifera
128 ce causes increased lung cancer development, chemoresistance, and complete resistance to anti-PD-1 an
129 les of CAFs in modulating tumor vasculature, chemoresistance, and disease progression.
130 gressive with extensive tissue infiltration, chemoresistance, and expressed genes related to epitheli
131 CLX downregulation drives metastatic spread, chemoresistance, and expression of epithelial-to-mesench
132 he drug efflux pump ABCB1 is a key driver of chemoresistance, and high expression predicts treatment
133  detail mechanisms that drive metastasis and chemoresistance, and highlights dysregulation of signali
134 decreases their ability to promote invasion, chemoresistance, and in vivo tumor growth, indicating th
135 fectors that induce metabolic reprogramming, chemoresistance, and invasiveness of retrodifferentiated
136 er cell death, immune activity, emergence of chemoresistance, and metastatic dissemination.
137  known to promote proliferation, metastasis, chemoresistance, and suppression of cytotoxic lymphocyte
138 challenge due to desmoplasia, development of chemoresistance, and systemic toxicity.
139 of TAMs as tumor drivers and as mediators of chemoresistance, and the potential effectiveness of targ
140 ll proliferation, stem cell differentiation, chemoresistance, and tissue organization, the ubiquitous
141 oid formation, ALDH expression and activity, chemoresistance, and tumorigenesis in subcutaneous and i
142  the crosstalk impinges on OC aggression and chemoresistance are not well-characterized.
143 ent epithelial-to-mesenchymal transition and chemoresistance, arguing strongly against the use of dru
144 c translesion synthesis (TLS) contributes to chemoresistance as well as treatment-induced mutations,
145 cts, we also found SOX9 to mediate cisplatin chemoresistance associated with reduced disease-free sur
146 -transitioned prostate cancer, abrogated the chemoresistance both in cell culture and in animal model
147  enhancing colorectal cancer progression and chemoresistance both in vitro and in vivo.
148  requires neutralization of self-renewal and chemoresistance, but these phenotypes are often regulate
149 e may represent a unique model to understand chemoresistance, but to our knowledge, the phenotypic an
150 presses ovarian cancer apoptosis and confers chemoresistance by binding to its direct novel target, A
151 tone H3 lysine 9 methylation, KDM3A promotes chemoresistance by demethylating p53.
152 ler, lysyl oxidase (LOX) as a key inducer of chemoresistance by developing chemoresistant TNBC tumors
153 data propose a mechanism where CD82 promotes chemoresistance by increasing PKCalpha activation and do
154 y, therapy-induced senescence contributes to chemoresistance by inducing cancer stem-like cells (CSC)
155 o chemotherapy suppressed the acquisition of chemoresistance by perturbing the nuclear translocation
156 ibroblasts played the most important role in chemoresistance by upregulating C-X-C motif chemokine re
157 itaxel often fails due to the development of chemoresistance caused by downregulation of the tumor su
158 re used only when a patient has demonstrated chemoresistance clinically.
159 i combination to suppress stemness-dependent chemoresistance development in xenotransplantation model
160 sociated molecular determinants underpinning chemoresistance development.
161  self-renewal, tumorigenicity, pluripotency, chemoresistance, differentiation, invasive ability, and
162  suggests that the genetic basis for initial chemoresistance differs from that underlying acquired ch
163 MB (SHH-MB), but their repeated use develops chemoresistance due to mutations in smoothened (SMO).
164 found that loss of miR-424(322)/503 promotes chemoresistance due to the up-regulation of two of its t
165 nowledge on how CRPC progresses and acquires chemoresistance during tumor progression.
166           The study used a siRNA against the chemoresistance gene survivin and two model polyanion dr
167 xhibited elevated expression of stemness and chemoresistance genes and demonstrated increased clonoge
168        Whether SOX17 is also involved in CCA chemoresistance has been investigated.
169                                     Acquired chemoresistance has curtailed cancer survival since the
170 tanding of the driving mechanisms underlying chemoresistance hinders the development of effective the
171                                              Chemoresistance, i.e., tumor insensitivity to chemothera
172 ome profiling of multiple cellular models of chemoresistance identified unique sets of distal enhance
173 red metabolism, neoplasticity, invasiveness, chemoresistance, immune evasion, and ultimately to poor
174                    Among other mechanisms of chemoresistance, impaired uptake through human organic c
175 a-catenin, which regulated ARC and augmented chemoresistance in AML cells; inhibition of beta-catenin
176 croenvironment and microenvironment-mediated chemoresistance in AML.Significance: The antiapoptotic p
177 is a potential strategy to overcome acquired chemoresistance in breast cancer.
178  strategy for reversing transporter-mediated chemoresistance in cancer cells.
179 ling system, has shown to be associated with chemoresistance in cancer cells.
180                                   Overcoming chemoresistance in cancer, understanding drug-drug inter
181 potential basis for predictive biomarkers of chemoresistance in cancer.
182 nction of FOXO1 can be harnessed to overcome chemoresistance in cancer.
183 ams could identify targetable key drivers of chemoresistance in cancers.
184 h genomic instability, clonal evolution, and chemoresistance in chronic lymphocytic leukemia (CLL).
185 r and that its downregulation contributes to chemoresistance in esophageal cancer cells by targeting
186 er cells, leading to enhanced metastasis and chemoresistance in experimental models.
187 nistic understanding of DNA repair-supported chemoresistance in glioblastoma cells.
188 asticity drives aberrant vascularization and chemoresistance in glioblastoma multiforme (GBM).
189 gest that decreases in MAF1 protein underlie chemoresistance in HCC and perhaps other cancers and poi
190  a previously poorly understood mechanism of chemoresistance in HCC.
191 autophagy plays a role in the development of chemoresistance in HNSCC and how autophagy is initiated
192 ibition of these signaling proteins reversed chemoresistance in in vitro and in vivo models.
193                                  This curbed chemoresistance in KRAS-mutant pancreatic cancers.
194 r post-transcriptional regulation underlying chemoresistance in leukemia.
195 rapeutic regimens; however, it also leads to chemoresistance in many cancer types including NB.
196 ty, reducing or even inhibiting the acquired chemoresistance in melanoma patients.
197 rvival across human cancers and demonstrates chemoresistance in mice.
198 ore effective treatments that can circumvent chemoresistance in Multiple Myeloma (MM) is a priority.
199 , but its contributions to tumorigenesis and chemoresistance in nasopharyngeal carcinoma (NPC) are no
200 r SOX9 is an important regulator of acquired chemoresistance in non-small-cell lung cancer (NSCLC).
201 potential target against both metastasis and chemoresistance in NSCLC.
202  (EMT) has been linked to the development of chemoresistance in other cancers, yet little is known re
203  cancer-associated fibroblasts (CAFs) confer chemoresistance in ovarian cancer is poorly understood.
204 a potential therapeutic strategy to overcome chemoresistance in ovarian cancer.
205 i-apoptotic function may potentially inhibit chemoresistance in OvCa patients.
206 igated the contribution of gut microbiota to chemoresistance in patients with colorectal cancer.
207 factors and molecular mechanisms involved in chemoresistance in patients with esophageal squamous cel
208 tratumoral MECs correlated with survival and chemoresistance in patients with ovarian cancer.
209 merged as a key regulator of hypoxia-induced chemoresistance in PDA and other cancers.
210  with cisplatin and effectively reverses NAC-chemoresistance in PDXs from NAC-resistant breast cancer
211 long with chemotherapy substantially reduces chemoresistance in primary leukemic cells ex vivo and in
212 based chemotherapy, including acquisition of chemoresistance in recurrent disease.
213 ve as a novel therapeutic target to overcome chemoresistance in SCLC.
214 s with stromal cells increased autophagy and chemoresistance in the AML cells exposed to chemotherape
215 e to chemotherapy, yet markers predictive of chemoresistance in this disease are lacking.
216  enhanced antioxidant defense as a driver of chemoresistance in this setting.
217 oping and testing LOX inhibitors to overcome chemoresistance in TNBC patients.
218 sphere-forming potential, cell motility, and chemoresistance in vitro, and was sufficient to attenuat
219                          We modeled acquired chemoresistance in vivo using a series of patient-derive
220                      Mechanisms that mediate chemoresistance include drug export, increased metabolis
221                     These exosomes increased chemoresistance-inducing factor, Snail, in recipient epi
222  with colorectal cancer (CRC) proliferation, chemoresistance, inflammation, metastasis, and now DNA d
223 n has been associated to cancer progression, chemoresistance, invasiveness, and metastasis.
224 ism by which NF-kappaB and Akt contribute to chemoresistance involving a signaling pathway consisting
225                                              Chemoresistance is a major barrier to effective chemothe
226                                              Chemoresistance is a major obstacle in triple negative b
227 ently used chemotherapy for glioma; however, chemoresistance is a major problem limiting its effectiv
228 mall molecules that can overcome dox-induced chemoresistance is a promising strategy in cancer therap
229 lso demonstrate that this co-culture-induced chemoresistance is abrogated by inhibition of the CXCR4
230       Understanding the molecules regulating chemoresistance is critical in order to combat chemoresi
231                                              Chemoresistance is driven by unique regulatory networks
232        Whether SOX17 is also involved in CCA chemoresistance is investigated in this study.
233                                              Chemoresistance is one of the leading causes of mortalit
234                                           As chemoresistance is the leading cause of cancer spread, p
235 ugh which these cellular interactions affect chemoresistance is unclear.
236 s by which TAM and fibroblasts contribute to chemoresistance is unclear.
237 in tumor initiation, growth, metastasis, and chemoresistance is well recognized and is encouraging th
238          Our results identify ABCB5 as a GBM chemoresistance marker and point to the potential utilit
239             Our results establish ABCB5 as a chemoresistance mechanism in MCC and suggest utility of
240                       Here we report a novel chemoresistance mechanism involving histone H4 expressio
241 vide insight into the MDSC exosomal-mediated chemoresistance mechanism, which will be useful for the
242 y, pointing to clinical significance of this chemoresistance mechanism.
243 o and in vivo, thus abrogating any potential chemoresistance mechanisms involving DNA repair.
244  progress in understanding the niche-imposed chemoresistance mechanisms will likely contribute to the
245 lenge because of its intrinsic and extrinsic chemoresistance mechanisms.
246 camptothecin (SN22) designed to overcome key chemoresistance mechanisms.
247 cular mechanism of prostate cancer docetaxel chemoresistance mediated by the mammalian target of rapa
248 erium nucleatum as a previously unrecognized chemoresistance mediator in colorectal cancer, thereby e
249 n in children, could be repurposed to reduce chemoresistance, migration and invasion in paediatric ep
250 they might improve safety and delay onset of chemoresistance, no anti-ligand antibodies have been cli
251 y nonseminomas may explain the more frequent chemoresistance observed with this tumor subtype.
252 at PKM2 overexpression is a key mechanism of chemoresistance of advanced BC to cisplatin.
253 ppression of EZH2 protein expression induced chemoresistance of AML cell lines and primary cells in v
254 de evidence that chemotherapy itself induces chemoresistance of bone metastases, mediated by osteobla
255 ng of perturbed forks has been associated to chemoresistance of BRCA-deficient cancer cells.
256 tigated the contribution of CSCs to acquired chemoresistance of breast cancer and the avenues for rev
257            However, the role of ADAMs in the chemoresistance of cancer cells has rarely been reported
258 cogenic changes in the growth, survival, and chemoresistance of cancer cells.
259             Moreover, GREB1 loss may predict chemoresistance of endometrial cancer.
260 luence of non-neoplastic cells and matrix on chemoresistance of GBM cells to three agents with differ
261 ed the potential role of ABCB5 in growth and chemoresistance of GBM.
262 ng an important role in the pathogenesis and chemoresistance of haematological malignancies.
263  miR-128-3p potently reverses metastasis and chemoresistance of highly malignant NSCLC cells, which c
264 tion of KDM3 inhibits tumorigenic growth and chemoresistance of human colorectal CSCs.
265 nhibition would suppress both metastasis and chemoresistance of melanoma.
266 and HSPA2 gene expression reduced growth and chemoresistance of NSCLC cells.
267 that TAM and myofibroblasts directly support chemoresistance of pancreatic cancer cells by secreting
268 s an important role in tumor progression and chemoresistance of PDAC.
269  in CD44 and CXCR4 expression, which mediate chemoresistance often observed after multicycle chemothe
270              In addition to known drivers of chemoresistance, our findings identified SOX9 as a criti
271 or as these tumors often display generalized chemoresistance, particularly for carcinomas that derive
272 blem is compounded by near-universal primary chemoresistance; patients with advanced stage OCCC thus
273               Here we describe principles of chemoresistance predictor development via correlating a
274 udy was to identify analytical challenges in chemoresistance-predictor development and suggest ways t
275                                              Chemoresistance predictors use laboratory parameters mea
276 espite thousands of publications on putative chemoresistance predictors, there are only about a dozen
277                                     Although chemoresistance remains a primary challenge in the treat
278 nscriptional regulation contributes to their chemoresistance remains unknown.
279 potential therapeutic target for attenuating chemoresistance signaling in AML.
280 s Nrf2 is strongly associated with aging and chemoresistance, these findings will provide a novel app
281  to sustain tumor pathogenesis and to confer chemoresistance through a noncanonical mechanism.
282 and functional interaction between PD-L1 and chemoresistance through the microRNA regulatory cascade.
283 aclitaxel to overcome the drug effluxion and chemoresistance thus, synergistically treating HCC.
284           Genetic deletion of Bok results in chemoresistance to 5-fluorouracil (5-FU) in different ce
285 hese findings suggest that ADAM12-L mediates chemoresistance to 5-FU and 5-FU-induced recurrence of B
286                                              Chemoresistance to cisplatin is a principal cause of tre
287       A critical clinical problem of PSCC is chemoresistance to cisplatin, which is induced by Pten d
288 linical use of a predictor of ovarian cancer chemoresistance to its frontline therapy is presented.
289  the PDK4 inhibitor dichloroacetate reversed chemoresistance to sorafenib or cisplatin in HCC stem ce
290  these cells was sufficient to fully restore chemoresistance under low nutrient conditions.
291 CXCR4) and hedgehog pathways cooperate in PC chemoresistance via bidirectional tumor-stromal crosstal
292               It has been proposed that such chemoresistance via cytochrome P450/drug transporters ca
293 ent cells decreased leukemic cell growth and chemoresistance via downregulation of prosurvival factor
294 MUC) glycoproteins has been shown to enhance chemoresistance via increased cell stemness.
295          The correlation between miR-378 and chemoresistance was tested in patient samples.
296 r MYCN amplification in SCLC progression and chemoresistance, we developed a genetically engineered m
297 anced cell invasion, PD-L1 upregulation, and chemoresistance, were sustained in the absence of contin
298 toration of miR-424(322) expression reverses chemoresistance, which is accompanied by blockage of the
299 fferentiation, metastatic dissemination, and chemoresistance, which is associated with elevated TGF-b
300 ING-less BRCA1 was shown to directly mediate chemoresistance, while maintaining some homologous recom

 
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