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1 In this article, we describe the molecular rationale for 5 distinct approaches to inhibiting polyme
2 ves resistance to ibrutinib and provides the rationale for a combination strategy that includes ibrut
4 he MYC G-quadruplex and i-motif, providing a rationale for a molecular switch mechanism driven by SP1
5 This rapidly changing scenario provides a rationale for a more systematic collection of patient-re
9 in alcohol-seeking and relapse and present a rationale for a novel pharmacological intervention that
10 a broad spectrum of data, constitutes a neat rationale for a numerically effective and theoretically
13 blocks metastatic spread, thus providing the rationale for a therapeutic strategy based on PIN1 inhib
17 e antitumor immunity, as well as support the rationale for administering immunotherapy in early-stage
20 stable 2HB state and offers a tension-based rationale for an optimal NL length to ensure processivit
21 ly used survivorship programmes, discuss the rationale for and potential benefits of expanded types o
22 ere provide the pre-clinical and mechanistic rationale for assessing ARID1A defects as a biomarker of
26 B cell lymphomagenesis and provides a strong rationale for blocking the IL-6 pathway in patients with
29 he core pharmacophore for MC4R and provide a rationale for careful assay selection for agonist screen
31 fined, followed by sections on epidemiology, rationale for changes from prior criteria, clinical eval
32 y associated with poor outcomes, providing a rationale for chromosomal loss patterns in neuroblastoma
34 TTEs as well as the appropriate use criteria rationale for classifying studies as rarely appropriate.
35 ibition in vitro and in vivo, establishing a rationale for clinical investigation and further motivat
42 ficance: These results provide a mechanistic rationale for combination therapy of CXCR4 and BCL-2 inh
44 fects on cell growth inhibition, providing a rationale for combination therapy with inhibitors of the
45 Furthermore, our results provide a strong rationale for combination treatment strategies targeting
46 tance mechanism to gemcitabine and provide a rationale for combining chemo/radiotherapy with TIMP1 in
49 intratumoral T cell infiltration, provide a rationale for combining these targeted therapies with im
53 s in the context of cells, which provide the rationale for designing approaches to control the assemb
55 ase function and regulation has provided the rationale for developing E3-targeting therapeutics for t
56 ntial to prevent these sequelae, providing a rationale for developing strategies aimed at acceleratin
59 in acute leukaemia and suggest a mechanistic rationale for disrupting the YEATS domain in disease.
61 ha in inflammatory atherogenesis and provide rationale for dual cytokine antagonism in future studies
63 cation of epigenetic regulators, providing a rationale for epigenetic therapy in ER-positive breast c
64 helping nutrition researchers to clarify the rationale for examining mediation, avoid common pitfalls
67 n this Personal View, we explain further the rationale for expanding the genetic database of NIRVs an
69 iral production during ART, thus providing a rationale for exploring immunotherapeutic approaches in
70 additional evidence has emerged to suggest a rationale for extending statin consideration to an even
71 is of ER-positive breast cancer and provides rationale for FDA-approved use of mTORC1 inhibitors in c
72 tion from ADP to rigor provides a structural rationale for force sensitivity in this step of the mech
76 ption for locally advanced cSCC and provides rationale for further investigation in future clinical t
77 elated pleural fibrosis and provide a strong rationale for further investigation of GSK-3beta signali
81 ve or treatment-resistant NSCLC, providing a rationale for further studies of avelumab in this diseas
82 traperitoneal seeding of EOC and provide the rationale for future studies targeting Ncad in preclinic
83 troke or transient ischemic attack provide a rationale for future trials of improved thrombus aspirat
86 life-threatening infections provides a clear rationale for hematopoetic stem cell transplantation (HS
87 GR genomic binding and provide a biophysical rationale for how promiscuous binding by GR allows funct
88 TP-hydrolysis mechanism, provide a molecular rationale for how the Rho ATPase domains distinguishes b
90 pendent of BCR-ABL for survival, providing a rationale for identifying and targeting kinase-independe
91 In summary, our work offers a mechanistic rationale for IDH1 inhibition as a metabolic strategy to
93 y homogeneous phenotype of LTBI, providing a rationale for immunological risk stratification to impro
95 ollectively, the data call into question the rationale for increasingly widespread self-medication wi
96 essor of metastasis and provide a compelling rationale for inhibition of ECT2 as a therapeutic approa
97 terminant of TNBC aggressiveness and provide rationale for investigating age-stratified therapies des
99 ing LCFA metabolism and therefore provides a rationale for investigating its role in LCFA-utilizing p
101 tor in their genome sequences, providing the rationale for investigating these receptors to understan
103 vides the basis to evaluate a new biological rationale for its activity when used clinically to initi
104 tive effects during inflammation; however, a rationale for its apical expression has been lacking.
105 initiation involving IMP3 and they provide a rationale for its association with aggressive disease an
106 agonalized with long Ni-C bonds, providing a rationale for its current synthetic inaccessibility.
107 d stoichiometry for A116V moPrP, providing a rationale for its increased channel-forming capability.
108 ubset, and provide a systems-based molecular rationale for its key functions downstream of IL-15.
109 survival of mature T cells, which provides a rationale for its potential use as an immunotherapeutic
111 ng drives CRPC, and they offer a mechanistic rationale for its therapeutic targeting in this disease.
112 ctrum therapeutic use of GC, the biochemical rationale for locally treating inflammatory skin conditi
113 These data provide the fundamental basis and rationale for management of the axilla in clinical trial
115 rate in myeloid transformation and provide a rationale for mechanism-based therapy in CMML patients w
116 mbursement pending demonstration of clinical rationale for Medicaid patients with inappropriate PCIs.
118 s of molecular data were combined, providing rationale for microsatellite instability for 8 of the 9
119 re-test survey that ascertained the clinical rationale for MR imaging, the clinical management plan i
121 increase tumour immunogenicity and provide a rationale for new combination regimens comprising CDK4/6
125 in exocrine gland development and support a rationale for performing exocrine functional tests for p
130 m of breast cancer metastasis and provides a rationale for potential therapeutic interventions in the
131 ls of decision making could provide a strong rationale for precommitment strategies and that interdis
134 argets both the liver and the eye provides a rationale for protecting the severely premature infant f
135 The proposed regulatory strategy suggests a rationale for quorum-sensing-dependent stimulation of th
138 The report describes the consensus process, rationale for selecting data elements to be reported, de
141 e numerous coordination complexes provides a rationale for some of the spectacular contributions that
142 ly dangerous plaques and offer a mechanistic rationale for SPM therapy to promote plaque stability.
143 nalyses provide an intuitive and mechanistic rationale for strategic delay, which contrasts with the
145 ics: pathophysiology, clinical presentation, rationale for stratification, imaging, massive PE manage
148 basis for the TNM staging system and is the rationale for surgical resection of tumor-draining lymph
149 or influenza vaccine responses and provide a rationale for targeted, ex vivo Ag-driven molecular prof
150 Overall, our preclinical data provide the rationale for targeting DUB enzyme Rpn11 upstream of 20S
151 YC in malignant transformation and provide a rationale for targeting EBV's roles in cell cycle modula
153 oxylmethylation on RAB GTPases and provide a rationale for targeting ICMT in the treatment of metasta
154 This regulatory loop provides a mechanistic rationale for targeting ILK to suppress oncogenic KRAS s
157 s HNSCC invasion and metastasis, providing a rationale for targeting PI3K/PDK1 and TGFbeta signaling
160 naling axis in tumorigenesis, and provides a rationale for targeting Snail to improve mTOR-targeted t
164 In this focused review, we highlight the rationale for targeting the pathway in lymphomas, provid
165 ne responses in different cell types and the rationale for targeting Tim-3 for effective cancer immun
166 role in KRAS-driven resistance and provide a rationale for targeting translation to overcome resistan
167 aken together, our findings provide a strong rationale for testing combinations of panPI3K, PI3Kbeta
168 ety profile, our results will provide with a rationale for testing NSAIDs as potential chemoadjuvants
170 e a foundation for preclinical studies and a rationale for testing whether NMDAR antagonists might be
171 ridoxal 5'-phosphate cofactor and provides a rationale for the allosteric activator function of FXN i
173 ormally fleeting in hydroxylases, provides a rationale for the carbon-carbon scission reaction cataly
175 results establish a preclinical mechanistic rationale for the clinical development of Axl inhibitors
176 results establish a preclinical mechanistic rationale for the clinical development of AXL inhibitors
177 Overall, our findings provide a preclinical rationale for the clinical development of MALT1 inhibito
179 K4 as an oncogene in myeloma and provide the rationale for the clinical evaluation of PAK4 modulator
180 trate for USP6, and they offer a mechanistic rationale for the clinical investigation of Jak and STAT
182 ation and inhibition, our study delivers the rationale for the clinically observed phenomenon of resi
183 erent immune checkpoint modulators, form the rationale for the design of immune checkpoint-based immu
184 nigmatic phenomenon of protean agonism and a rationale for the design of such compounds for a G prote
185 ple levels in prostate cancer and provides a rationale for the design of therapies that restore NK ce
186 de a novel drug target that may serve as the rationale for the development of a new therapeutic appro
187 into the role of IL1RAP in CML and a strong rationale for the development of an IL1RAP antibody ther
188 ll carcinoma (RCC), providing a pre-clinical rationale for the development of Axl and Met inhibitors
189 T cell leukemia, establish a mechanism-based rationale for the development of BET bromodomain degrada
190 ral ventromedial medulla provides additional rationale for the development of CB2 receptor-selective
191 popolysaccharides (LPS) interactions provide rationale for the development of non-cytotoxic antibioti
192 totic APC/C by phosphorylation and provide a rationale for the development of selective inhibitors of
193 perties of proNGF and NGF and help provide a rationale for the diverse biological effects of NGF and
194 arding Abeta oligomers, and provide a strong rationale for the evaluation of crenezumab as a potentia
195 mented safety profile of this drug provide a rationale for the evaluation of niclosamide in the manag
197 source of diverse magnetic phenomena, and a rationale for the existence of intermetallics with giant
199 preclinical proof of concept and mechanistic rationale for the exploration of SSTNIGF1R as an experim
203 pha PtdIns/PtdCho exchange cycle and offer a rationale for the high conservation of particular sets o
205 beta interaction results suggest a molecular rationale for the higher AD prevalence among smokers, an
206 ng the nuclear export sequence), providing a rationale for the increased cytoplasmic aggregation of R
210 ructure in the protein provides a structural rationale for the observation that unfolding is hierarch
212 he binding site, thus providing a structural rationale for the observed disruption of the transition
213 ts, supported by DFT calculations, suggest a rationale for the observed photophysical properties that
215 hts into enzyme-inhibitor interactions and a rationale for the observed selectivity and potency.
218 us anaplastic T-cell lymphoma, and provide a rationale for the pharmacologic inhibition of EZH2 activ
219 reasons why this project was initiated, the rationale for the planned work, and the expected benefit
221 structure and spectroscopic investigations a rationale for the positive impact of acetonitrile is pro
225 which phages circumvent them, and provide a rationale for the prevalence of pilus glycosylation in n
226 is, Leu, and Asp, respectively), providing a rationale for the purine base specificity of S. venezuel
228 uring information transmission, suggesting a rationale for the regulation of these information proces
229 proposal is intriguing, as it offers both a rationale for the relatively high hydrogen-atom-transfer
230 DNA-binding domain and provide a biophysical rationale for the reported functional regulation of the
232 ansporter NRAMP1 to the vacuole, providing a rationale for the reversion of nramp3nramp4 phenotypes.
233 ism of AEP and DOT1L and suggest a molecular rationale for the simultaneous inhibition of the MLL fus
234 lasma membrane versus endosomes, providing a rationale for the spatial encoding of cAMP signaling.
236 ther, this structural information provides a rationale for the stimulation of MalK ATPase activity by
239 gnalling pathway, thereby providing a simple rationale for the upregulation of ARHGAP36 in medullobla
241 ase revascularization exist, and much of the rationale for the use of antiplatelet agents after endov
244 ic BCR signaling, thus providing a molecular rationale for the use of HSP90 inhibitors in the treatme
245 olangiocarcinoma and establish a mechanistic rationale for the use of low-dose paclitaxel in blocking
246 together, our results provide a preclinical rationale for the use of NR4A1 small-molecule antagonist
247 ur results offered a preclinical mechanistic rationale for the use of PARP and ATR inhibitors to impr
250 ess, the efficacy of buparlisib supports the rationale for the use of PI3K inhibitors plus endocrine
251 s and the clinical evidence that support the rationale for the use of SGLT2 inhibitors in patients wi
253 ation of inflammatory response and provide a rationale for the use of Wnt11 to manipulate human disea
256 Uch37 in cell cycle progression, providing a rationale for their function in cellular proliferation a
258 eemingly clear mechanism of action and solid rationale for their use in cancer therapy, mTORis have m
260 hat promotes OSC tumor growth, and provide a rationale for therapeutic targeting of this pathway for
263 and FTD by acting on autophagy, providing a rationale for therapeutic use of DBS and synaptic stimul
264 n and to foster exercise tolerance provide a rationale for therapeutic use of IL-37 in the treatment
266 this cancer-relevant function has provided a rationale for therapeutically targeting proteostasis reg
276 of pancreatic beta-cells and underscore the rationale for transient beta-cell rest as a treatment st
278 slation-related pathways offer a mechanistic rationale for treatment of osteosarcomas and other cance
279 iolet-radiation-induced mutations, providing rationale for treatment with immunotherapy antibodies th
284 IFNAR1 suppressed tumor growth providing the rationale for upregulating IFNAR1 to improve anti-cancer
285 Information was sought on study design, rationale for using deceased controls, application of th
286 s and neuronal activity remains unclear, the rationale for using diffusion MRI to monitor neuronal ac
288 file as an antibiotic, our results provide a rationale for using minocycline as a therapeutic agent f
292 Our findings provide further support to the rationale for using n-3 PUFAs as a treatment option for
294 injection, our findings provide a promising rationale for validation of (18)F-DCFPyL in future prosp
296 city of the Amy13K CBMs provides a molecular rationale for why E. rectale is able to only use certain
297 ly tested for binding to PDEdelta provides a rationale for why some prenylated proteins, such as KRAS
298 interest in anti-TH2 biologics, we propose a rationale for why they are particularly successful in co
299 ommunication by the Rag GTPases, providing a rationale for why they exist as a dimer and revealing a
300 f adaptive deep brain stimulation provides a rationale for why this approach could be more efficaciou
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