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1 tive stress responses, tumor progression and chemoresistance.
2 ar fitness' that may be also associated with chemoresistance.
3 crophages was found to reverse their natural chemoresistance.
4 ith active Notch signaling, known to mediate chemoresistance.
5 rstudied phenomenon known as hypoxia-induced chemoresistance.
6 on that contributes to tumor maintenance and chemoresistance.
7 (AML) patient samples, indicating a role in chemoresistance.
8 hey drive tumor progression, metastasis, and chemoresistance.
9 sidered responsible for tumor initiation and chemoresistance.
10 t, is limited by its severe side effects and chemoresistance.
11 nt EMT and CSC functions, thereby conferring chemoresistance.
12 y in general, plays an important role in AML chemoresistance.
13 cells, thereby supporting tumour growth and chemoresistance.
14 ited therapeutic efficacy is achieved due to chemoresistance.
15 henotype, as well as the rare progression to chemoresistance.
16 auses uncontrolled lethality, in part due to chemoresistance.
17 ctor T cells: they abrogate stromal-mediated chemoresistance.
18 but instead acutely secrete IL-6, promoting chemoresistance.
19 ggesting a novel mechanism to overcome tumor chemoresistance.
20 but that loss of HMGA2 did not give rise to chemoresistance.
21 OCC spheroids, as well as cell migration and chemoresistance.
22 roliferation, migration, transformation, and chemoresistance.
23 r in breast cancer patients who had acquired chemoresistance.
24 dual disease, underscoring their role in AML chemoresistance.
25 racteristic of melanoma progression and also chemoresistance.
26 s for 'edgotype' analysis in a cell model of chemoresistance.
27 te carrier SLC7A11, previously implicated in chemoresistance.
28 totic effect, both of which contribute to NB chemoresistance.
29 al of leukemic cells and also tackling their chemoresistance.
30 g their ability to promote cancer growth and chemoresistance.
31 p57Kip2 suppresses tumorigenesis and causes chemoresistance.
32 a potential therapeutic target for reversing chemoresistance.
33 cers and is implicated in the development of chemoresistance.
34 own reduced CSC numbers, in vivo growth, and chemoresistance.
35 arrow mesenchymal stromal cell (MSC)-induced chemoresistance.
36 feration rate of MCL cells as a mechanism of chemoresistance.
37 ignant progression, invasion, metastasis and chemoresistance.
38 ion delays apoptosis and might contribute to chemoresistance.
39 ated with tumor initiation, progression, and chemoresistance.
40 suggest p53 aggregation as a new marker for chemoresistance.
41 member expression are frequently involved in chemoresistance.
42 Ca prevention, tumorigenesis, metastasis and chemoresistance.
43 ir antitumour effects, a phenomenon known as chemoresistance.
44 mal clodronate protects against PIFA-induced chemoresistance.
45 that may contribute to its pathogenesis and chemoresistance.
46 ptosis, which may be employed for overcoming chemoresistance.
47 t, and specifically for NRAS/KRAS mutations, chemoresistance.
48 inhibition of IL6-induced proliferation and chemoresistance.
49 regulate breast CSC (BCSC) self-renewal and chemoresistance.
50 henotypes, including extranodal invasion and chemoresistance.
51 pathways is one of the key determinants for chemoresistance.
52 ly associated with poor clinical outcome and chemoresistance.
53 ntaining 1B (GRAMD1B), a protein involved in chemoresistance.
54 munity, that controls senescence evasion and chemoresistance.
55 acquired apoptosis resistance, resulting in chemoresistance.
56 emotherapeutic drugs may facilitate cellular chemoresistance.
57 f diabetic ss-cell apoptosis and cancer cell chemoresistance.
58 esponsible for their aggressive behavior and chemoresistance.
59 hought to drive tumor growth, metastasis and chemoresistance.
60 cross-complementing 1 (ERCC1), a marker for chemoresistance.
61 al modes of control and limiting the risk of chemoresistance.
62 interfering with CLL cell proliferation and chemoresistance.
63 as ET-1, enhancing the network that sustains chemoresistance.
64 n Mcl-1 stabilization and an exacerbation of chemoresistance.
65 hich may contribute to tumor progression and chemoresistance.
66 is associated with poor cancer outcomes and chemoresistance.
67 malignancy, characterized by a high rate of chemoresistance.
68 2 contributes to both intrinsic and acquired chemoresistance.
69 tion (EMT) is associated with metastasis and chemoresistance.
70 ced drug uptake is an important mechanism of chemoresistance.
71 nail-induced cancer stem cell enrichment and chemoresistance.
72 to reduce toxicities and prevent or overcome chemoresistance.
73 crophages may form an indirect mechanism for chemoresistance.
74 ise and the associated mechanisms leading to chemoresistance.
75 contributing to tumor cell proliferation and chemoresistance.
76 own that miR-125b plays an important role in chemoresistance.
77 on is limited by both intrinsic and acquired chemoresistance.
78 g that miR-125b is critical in Snail-induced chemoresistance.
79 iated traits such as migration, invasion and chemoresistance.
80 rvival, and their potential as modulators of chemoresistance.
81 s alongside chemotherapy for overcoming PDAC chemoresistance.
82 o identify novel mechanisms involved in SCLC chemoresistance.
83 of high-risk neuroblastomas recur because of chemoresistance.
84 lution, tumorigenesis, and the phenomenon of chemoresistance.
85 owth inhibition, apoptosis, G0/G1 arrest and chemoresistance.
86 sponsible for tumor relapse, metastasis, and chemoresistance.
87 carcinoma, contributing to poor survival and chemoresistance.
88 limited efficacy due to de novo or acquired chemoresistance.
89 stance differs from that underlying acquired chemoresistance.
90 en a high metabolically active phenotype and chemoresistance.
91 nd mechanistically control colorectal cancer chemoresistance.
92 emosensitive but then relapses with acquired chemoresistance.
93 utations are linked to tumor progression and chemoresistance.
94 of self-renewal, cell cycle quiescence, and chemoresistance.
95 nown about the role of histone expression in chemoresistance.
96 pression promoted xenograft tumor growth and chemoresistance against cisplatin in an animal model res
97 geting sCLU via miR-378 may help disable the chemoresistance against cisplatin in lung adenocarcinoma
98 ed repeated chemotherapy and correlates with chemoresistance, aggressiveness and poor prognosis in NS
99 a major role for cancer stem cells (CSC) in chemoresistance, although their involvement in acquired
100 nocarcinoma (PDA) is attributed to intrinsic chemoresistance and a growth-permissive tumor microenvir
103 hat elevated HE4 serum levels correlate with chemoresistance and decreased survival rates in EOC pati
104 dothelial cell crosstalk signaling in cancer chemoresistance and demonstrate the improved efficacy of
105 apeutic target to prevent and treat acquired chemoresistance and disease recurrence in OC and enhance
107 ed gene expression associated with stemness, chemoresistance and epithelial-mesenchymal transition an
108 c phenotype such as migration, invasiveness, chemoresistance and expression of cancer stem-cell marke
109 all-molecule modulator of miR-34a to reverse chemoresistance and further enhance the therapeutic effi
110 le for DNMT3A(R882) mutations in driving AML chemoresistance and highlight the importance of chromati
111 acute need to decipher mechanisms underlying chemoresistance and identify new targets to improve pati
112 ical agent, AS101, to degrade VLA-4-mediated chemoresistance and improve clinical responses in patien
113 y be a highly effective approach to overcome chemoresistance and improve the outcome of advanced BC.
116 expression correlated strongly with acquired chemoresistance and malignant behavior of OC cells, expr
118 128-3p) is key to concomitant development of chemoresistance and metastasis in residual NSCLC cells h
119 ession and show that NO production regulates chemoresistance and metastasis of breast cancer cells.
120 Tumor-infiltrating immune cells can promote chemoresistance and metastatic spread in aggressive tumo
121 (ASCT) may provide an alternative to address chemoresistance and overcome the blood-brain barrier.
123 te that cancer stem-like cells contribute to chemoresistance and poor clinical outcomes in many cance
126 for INPP4B gain of function as a mediator of chemoresistance and poor survival outcome in AML indepen
127 tumor cells may yield insights into clinical chemoresistance and potentially improve therapeutic outc
128 docrine marker expression is associated with chemoresistance and reducing MYC levels decreases gemcit
131 lammation has a crucial role in induction of chemoresistance and results, in part, from the induction
132 f the proinflammatory cytokine IL-6 promotes chemoresistance and show that the chemotherapeutic doxor
133 ent-derived samples was also associated with chemoresistance and strongly correlates with bcl-xL expr
134 are poor and have remained stagnant owing to chemoresistance and the high propensity to form lung met
136 M3A promotes ovarian CSCs, proliferation and chemoresistance and thus, highlights the significance of
137 thereby providing a new strategy to overcome chemoresistance and to improve the treatment and surviva
139 This study explores the role of PKM2 in chemoresistance and whether inhibiting PKM2 augments the
140 by virtue of its Y5 receptor (Y5R)-mediated chemoresistance and Y2 receptor (Y2R)-mediated prolifera
142 gressive with extensive tissue infiltration, chemoresistance, and expressed genes related to epitheli
143 dels the progressive development of clinical chemoresistance, and implicate an adjunctive therapy to
144 tly suppress GRP78 levels and GRP78-mediated chemoresistance, and suggest that this strategy holds th
145 of TAMs as tumor drivers and as mediators of chemoresistance, and the potential effectiveness of targ
146 ll proliferation, stem cell differentiation, chemoresistance, and tissue organization, the ubiquitous
147 oid formation, ALDH expression and activity, chemoresistance, and tumorigenesis in subcutaneous and i
148 ells (CSCs) with enhanced tumorigenicity and chemoresistance are believed to be responsible for treat
149 LL), short-term and long-term toxicities and chemoresistance are shortcomings of standard chemotherap
150 eaturing unlimited self-renewal capacity and chemoresistance, are critical cellular targets for new t
151 cts, we also found SOX9 to mediate cisplatin chemoresistance associated with reduced disease-free sur
153 -transitioned prostate cancer, abrogated the chemoresistance both in cell culture and in animal model
154 strated tissue repair response can result in chemoresistance, but in other circumstances, TAMs are es
155 requires neutralization of self-renewal and chemoresistance, but these phenotypes are often regulate
156 e may represent a unique model to understand chemoresistance, but to our knowledge, the phenotypic an
157 our prognostic marker, has a pivotal role in chemoresistance by a direct targeting of the actin-bindi
158 presses ovarian cancer apoptosis and confers chemoresistance by binding to its direct novel target, A
160 o chemotherapy suppressed the acquisition of chemoresistance by perturbing the nuclear translocation
161 ibroblasts played the most important role in chemoresistance by upregulating C-X-C motif chemokine re
162 itaxel often fails due to the development of chemoresistance caused by downregulation of the tumor su
163 cancer stem cell by augmenting self-renewal, chemoresistance, cell-cycle progression, proliferation,
164 suggests that the genetic basis for initial chemoresistance differs from that underlying acquired ch
165 l mediators of breast cancer oncogenesis and chemoresistance driven by Foxq1, with potential implicat
166 cancer progression, relapse, metastasis, and chemoresistance due to functional differences in genetic
168 found that loss of miR-424(322)/503 promotes chemoresistance due to the up-regulation of two of its t
172 pathways that promote cancer cell survival, chemoresistance, growth, and crosstalk with the immune s
174 gulators have been proposed as modulators of chemoresistance, here, we sequence genes encoding epigen
176 red metabolism, neoplasticity, invasiveness, chemoresistance, immune evasion, and ultimately to poor
178 vel microRNA-mediated pathway that regulates chemoresistance in breast cancer will facilitate the dev
180 hypothesis that high GSN expression confers chemoresistance in cancer cells by altering the GSN-FLIP
181 Significantly, we found that O-ASC-mediated chemoresistance in cancer cells can be deregulated by al
185 h genomic instability, clonal evolution, and chemoresistance in chronic lymphocytic leukaemia (CLL).
186 h genomic instability, clonal evolution, and chemoresistance in chronic lymphocytic leukemia (CLL).
189 with the Wnt/beta-catenin pathway to sustain chemoresistance in EOC, and they offer a solid rationale
190 r and that its downregulation contributes to chemoresistance in esophageal cancer cells by targeting
194 on to the association of p53 aggregation and chemoresistance in HGSOC cells, we further demonstrated
195 autophagy plays a role in the development of chemoresistance in HNSCC and how autophagy is initiated
197 tively inhibits proliferation, survival, and chemoresistance in leukemia cell lines and primary sampl
198 d its elevated expression is associated with chemoresistance in malignancy, its in vivo role is large
202 ore effective treatments that can circumvent chemoresistance in Multiple Myeloma (MM) is a priority.
204 (EMT) has been linked to the development of chemoresistance in other cancers, yet little is known re
205 ative PCK3145 as potential target to reverse chemoresistance in ovarian cancer and have begun to iden
206 cancer-associated fibroblasts (CAFs) confer chemoresistance in ovarian cancer is poorly understood.
207 igated the contribution of gut microbiota to chemoresistance in patients with colorectal cancer.
208 factors and molecular mechanisms involved in chemoresistance in patients with esophageal squamous cel
213 re, we show that the development of adaptive chemoresistance in the A549 non-small-cell lung cancer c
214 s with stromal cells increased autophagy and chemoresistance in the AML cells exposed to chemotherape
215 nd leukemia cells is essential for promoting chemoresistance in the transformed cells, and targeting
218 promotes tumor growth as well as radio- and chemoresistance in various human malignancies including
220 by splenic macrophages that induces systemic chemoresistance in vivo via an altered DNA damage respon
221 and attenuates progressive manifestation of chemoresistance in xenograft tumours, including primary
225 ism by which NF-kappaB and Akt contribute to chemoresistance involving a signaling pathway consisting
230 mall molecules that can overcome dox-induced chemoresistance is a promising strategy in cancer therap
236 in tumor initiation, growth, metastasis, and chemoresistance is well recognized and is encouraging th
239 for Snail-induced stem cell propagation and chemoresistance may have important implications in the d
242 vide insight into the MDSC exosomal-mediated chemoresistance mechanism, which will be useful for the
245 progress in understanding the niche-imposed chemoresistance mechanisms will likely contribute to the
246 cular mechanism of prostate cancer docetaxel chemoresistance mediated by the mammalian target of rapa
247 erium nucleatum as a previously unrecognized chemoresistance mediator in colorectal cancer, thereby e
248 mic stem cell properties have been linked to chemoresistance, metastatic dissemination, and the induc
250 they might improve safety and delay onset of chemoresistance, no anti-ligand antibodies have been cli
254 ppression of EZH2 protein expression induced chemoresistance of AML cell lines and primary cells in v
255 homolog (KRAS) underlie the pathogenesis and chemoresistance of approximately 30% of all human tumors
256 de evidence that chemotherapy itself induces chemoresistance of bone metastases, mediated by osteobla
257 tigated the contribution of CSCs to acquired chemoresistance of breast cancer and the avenues for rev
263 derscore the role of a pro-oxidant milieu in chemoresistance of hematopoietic and other cancers via s
264 olecular circuit regulating the stemness and chemoresistance of hepatic Lgr5(+) CICs and provide pote
265 miR-128-3p potently reverses metastasis and chemoresistance of highly malignant NSCLC cells, which c
270 that TAM and myofibroblasts directly support chemoresistance of pancreatic cancer cells by secreting
271 in deoxyribonucleotide synthesis, drives the chemoresistance of pancreatic cancer to nucleoside analo
272 for the first time that TAMs can also induce chemoresistance of PDA by reducing gemcitabine-induced a
275 in CD44 and CXCR4 expression, which mediate chemoresistance often observed after multicycle chemothe
276 d leukemia (AML) suffer relapse arising from chemoresistance, often involving upregulation of the onc
277 act as oncosuppressors or oncogenes, induce chemoresistance or chemosensitivity, and are major postt
278 or as these tumors often display generalized chemoresistance, particularly for carcinomas that derive
281 ugh the use of targeted therapy, relapse and chemoresistance remain a major hindrance to the fight to
282 arization, diffuse invasion, and significant chemoresistance, resulting in a recurrent phenotype that
283 A and DeltaNp63) were demonstrated to confer chemoresistance, revealing a novel oncogenic role for p6
284 totic proteins may play an important role in chemoresistance, suggesting a promising role for targeti
285 em/progenitor cells are known to have higher chemoresistance than non-stem/progenitor cells, but the
286 s Nrf2 is strongly associated with aging and chemoresistance, these findings will provide a novel app
287 and functional interaction between PD-L1 and chemoresistance through the microRNA regulatory cascade.
288 hese findings suggest that ADAM12-L mediates chemoresistance to 5-FU and 5-FU-induced recurrence of B
289 ding histone deacetylase inhibitors, confers chemoresistance to cancer, thereby contributing to tumor
291 k of an efficient therapy and development of chemoresistance to the current standard therapy, gemcita
292 els of breast cancer has shown that acquired chemoresistance to the widely used drug paclitaxel can b
294 ent cells decreased leukemic cell growth and chemoresistance via downregulation of prosurvival factor
295 motherapy in cell-autonomous assays, but CIC chemoresistance was also increased by cancer-associated
297 tably, enforcing expression of IKBKE induces chemoresistance, whereas knockdown of IKBKE not only sen
298 toration of miR-424(322) expression reverses chemoresistance, which is accompanied by blockage of the
299 bicin, suggesting that p57Kip2 has a role in chemoresistance, which is consistent with its pro-surviv
300 ING-less BRCA1 was shown to directly mediate chemoresistance, while maintaining some homologous recom
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