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1 act pathogens, including ones that are multi-drug resistant.
2  better understand how breast cancers become drug-resistant.
3 75.1%) of which are multidrug or extensively drug resistant and 38.2%, 51.9%, and 36.3% of which cont
4             We compared clinical outcomes of drug-resistant and -susceptible TBM treated with either
5 the production of novel antibiotics to treat drug-resistant and Gram-negative infections.
6 both kinases can be significantly rescued by drug-resistant Aurora A alone.
7                                        Multi-drug resistant bacteria are a persistent problem in mode
8                       The emergence of multi-drug resistant bacteria is limiting the effectiveness of
9 bit bacterial growth, especially against the drug-resistant bacteria Salmonella typhimurium.
10 to directly monitor the phenotypic switch in drug-resistant bacteria with temporal resolution.
11 h, especially infection from the extensively drug-resistant bacteria, A. baumannii.
12                         In the fight against drug-resistant bacteria, accurate and high-throughput de
13                           With the advent of drug-resistant bacteria, it is necessary to understand t
14 48 is potently active against pathogenic and drug-resistant bacteria, with minimal inhibitory concent
15 ic with potent activity toward Gram-positive drug-resistant bacteria.
16 ent that responds to cell-wall alteration in drug-resistant bacteria.
17 cterial agents to treat people infected with drug-resistant bacteria.
18 tides, are predominantly active against many drug-resistant bacteria.
19  importance given the alarming growth of pan-drug-resistant bacteria.
20  feasible, for study of infections caused by drug-resistant bacteria.
21 that were directly attributable to extremely drug-resistant bacteria.
22  alleles, which could serve as the source of drug-resistant bacteria.
23                                 The surge in drug-resistant bacterial infections threatens to overbur
24 as a therapeutic target for the treatment of drug-resistant bacterial infections.
25  of pure theranostic nanodrugs for combating drug-resistant bacterial infections.
26           The recent increase in extensively drug-resistant bacterial pathogens and the associated in
27                                              Drug-resistant bacterial pathogens pose an urgent public
28                                The spread of drug-resistant bacterial pathogens poses a major threat
29  and exhibits antibacterial activity against drug-resistant bacterial pathogens: pseudouridimycin (PU
30 ed synthetic technologies and tested against drug-resistant bacterial strains.
31 ed DNMT and HDAC inhibition in refractory or drug-resistant breast cancer.
32 -dependent gene activation and re-sensitizes drug-resistant C. glabrata to azole antifungals in vitro
33 n cell subpopulations of varying potency and drug resistant cancer stem-cell phenotypes, including th
34  avenues to develop potent compounds against drug-resistant cancer cells and CSCs.
35  GCS activities were significantly higher in drug-resistant cancer cells and in tumors overexpressing
36 gs provide evidence that clinically relevant drug-resistant cancer cells can both pre-exist and evolv
37 pies is critical to address the emergence of drug-resistant cancers, but direct screening of all poss
38 ls with greater tumorigenic, metastatic, and drug-resistant capacity.
39 It may also be a valuable drug for targeting drug-resistant carcinomas and cancers of the lungs, panc
40 een proposed as an alternative treatment for drug-resistant cases of epilepsy, current procedures suc
41 y, we have solved the X-ray structure of the drug-resistant catalytic core domain protein, which prov
42 ancer cells, and compared the results with a drug resistant cell line, HCC1954.
43  finding that was attenuated in the acquired drug resistant cell line.
44 d excellent inhibition of cell growth in the drug-resistant cell line H1975, without significantly af
45 EAN was not significantly changed in several drug-resistant cell lines with activated P-glycoprotein
46 tion of localized environmental niches where drug-resistant cell populations can evolve and survive.
47 g drug susceptible cells, drug tolerant, and drug resistant cells in less than 12h.
48  prevents the formation of drug-tolerant and drug-resistant cells in Mtb cultures.
49 loped to hijack the biosynthetic rewiring of drug-resistant cells in response to antibiotics.
50 itive tumor cells causes increased growth of drug-resistant cells in the population through a mechani
51 llowed by proteasomal degradation of EZH2 in drug-resistant cells.
52 rations, with a similar potency observed for drug-resistant cells.
53  results in the differentiation of quiescent drug-resistant chronic myelogenous leukemia-initiating c
54 ds showed antibacterial effect against multi-drug resistant clinical isolates of bacterial pathogens
55      GRL-09510 was also potent against multi-drug-resistant clinical HIV-1 variants and HIV-2ROD.
56 icidal activity against drug-susceptible and drug-resistant clinical isolates of M. tuberculosis.
57                             Alarmingly, this drug-resistant clone appears to have spread quickly to o
58                           Interestingly, all drug resistant clones contained guide RNAs for DCK.
59 pulations and routes for the spread of multi-drug resistant clones.
60 r cells dramatically increases the number of drug-resistant clones and allows the detection of both k
61  therapy ultimately enables the emergence of drug-resistant clones, limiting the long-term effectiven
62 tionary capacity, heralding the emergence of drug-resistant clones.
63 tenin interaction with ICG-001 can eliminate drug-resistant CML LICs without deleterious effects to t
64 nd various variants of protease (including a drug resistant construct) using Carr-Purcell-Meiboom-Gil
65 embly of chimeric capsids from wild-type and drug-resistant core proteins was susceptible to multiple
66 peutic agents that can effectively eliminate drug-resistant CSCs and improve the efficacy of cancer t
67 often develop malignant regrowth of residual drug-resistant dormant tumor cells years after primary t
68 l 7 out of 7 countries, and additionally for drug-resistant (DR) TB-related costs in 1 of the 7 count
69 n allosteric inhibitor that targets selected drug-resistant EGFR mutants but spares the wild-type rec
70 ing, substantiates our approach of targeting drug-resistant EGFR-L858R/T790M with inhibitors incorpor
71 lly less flexible, target gatekeeper mutated drug-resistant EGFR-L858R/T790M, and covalently alkylate
72 l chemical entities that efficiently inhibit drug-resistant EGFR.
73 gation as novel antibacterial agents against drug-resistant enterococci.
74                                              Drug-resistant enzymes must balance catalytic function w
75 idemic of drug-susceptible tuberculosis to a drug-resistant epidemic.
76 -rays for the treatment of brain tumours and drug-resistant epilepsies.
77 mulation is a promising alternative to treat drug-resistant epilepsies.
78 ecordings in a large cohort of patients with drug-resistant epilepsy and to focus on interictal very
79 chanistic biomarkers for epileptogenesis and drug-resistant epilepsy in humans, necessitating evaluat
80 ction of NAbs in this prototype of frequent, drug-resistant epilepsy syndrome.
81 nts who were 18 years of age or younger with drug-resistant epilepsy to undergo brain surgery appropr
82                    Fifty-three children with drug-resistant epilepsy underwent EEG-fMRI.
83                  INTERPRETATION: PMG-related drug-resistant epilepsy warrants a comprehensive presurg
84 -center trial, children and adolescents with drug-resistant epilepsy who had undergone epilepsy surge
85 ve seizures in children and adolescents with drug-resistant epilepsy, but additional data are needed
86      In approximately 20 million people with drug-resistant epilepsy, focal seizures originating in d
87         Optimal seizure control, in cases of drug-resistant epilepsy, often requires neurosurgical in
88  postsurgical seizure outcome in PMG-related drug-resistant epilepsy.
89 neuroinflammation plays a pathogenic role in drug-resistant epilepsy.
90 ients referred for presurgical evaluation of drug-resistant epilepsy.
91 planted in patients undergoing treatment for drug-resistant epilepsy.
92     Here we show that the evolution of multi-drug-resistant Escherichia coli can be manipulated in vi
93                             In patients with drug-resistant focal epilepsy requiring surgery, hippoca
94 lying seizures is valuable for understanding drug-resistant focal epilepsy.
95        Surgery is an effective treatment for drug-resistant focal epilepsy.
96 with frequent seizures and a long history of drug-resistant focal epilepsy.
97 emporal lobe epilepsy is the most common and drug-resistant form of epilepsy in adults.
98 rough direct antagonism of the wild-type and drug-resistant form of the Smoothened receptor.
99 obe epilepsy (TLE) is one of the most common drug-resistant forms of epilepsy in adults and usually o
100                             The emergence of drug-resistant fungi poses a major threat to human healt
101 py facilitates the expansion of pre-existing drug-resistant glioblastoma stem cells.
102  urinary tract infections due to extensively drug-resistant Gram-negative bacilli.
103 rt therapies for infections caused by highly drug-resistant Gram-negative bacteria.
104 nated global action in the fight against pan-drug-resistant Gram-negative bacteria.
105 th activity against a diverse panel of multi-drug-resistant Gram-negative pathogens.
106 f H1 hemagglutinin and was effective against drug-resistant H1 influenza viruses.
107 ) are limited, in particular in advanced and drug resistant HCC.
108 NA-based therapeutic to treat refractory and drug-resistant HCC.
109 files with EC50 values </=5 nM against major drug resistant HCV variants.
110 , suggesting a therapeutic strategy to treat drug-resistant, highly aggressive TNBC tumors.
111 c levels are needed to confront the emerging drug-resistant HIV epidemic.
112 And 33% (95% CI: 24-42%) was infected with a drug-resistant HIV variant.
113 fewer long-term liabilities, efficacy on new drug-resistant HIV-1 strains, and less frequent dosing i
114 hallenges remain because of the emergence of drug-resistant HIV-1 strains, limitations because of saf
115 atients infected with wild-type and/or multi-drug-resistant HIV-1 variants, that the newly generated
116  them revealed impressive activities against drug resistant human cancer cells, making them desirable
117 metallo beta-lactamase) from the extensively drug resistant human pathogen Stenotrophomonas maltophil
118       A 29-year-old woman was suffering from drug-resistant hypertension secondary to RAVM.
119 atient care by providing faster detection of drug-resistant infecting strains and to help inform ther
120 try-level, regional, and global estimates of drug-resistant infection and disease.
121     No work has yet quantified the burden of drug-resistant infection, or accounted for other types o
122 -vivo efficacy or in-vitro potential against drug-resistant infections of fungal, viral, and parasiti
123  the mortality and morbidity rates caused by drug-resistant infections, and several MNP-based anti-in
124 d serve as a ray of light for the therapy of drug-resistant infections.
125 imicrobial approach to treatment of chronic, drug-resistant infections.
126  mechanisms as add-on treatments for serious drug-resistant infections.
127 f the few ways forward through the morass of drug-resistant infectious disease and should be fully ex
128 otential of HMA derivatives as inhibitors of drug-resistant influenza M2 ion channels.
129 e armamentarium of agents available to treat drug-resistant invasive fungal infections.
130 are DS (drug sensitive isolates), MDR (multi-drug resistant isolates) and XDR (extremely drug resista
131 -drug resistant isolates) and XDR (extremely drug resistant isolates).
132 ing to the steadily increasing prevalence of drug resistant isolates.
133 ary 2012 and February 2013, twenty-one multi-drug resistant K. pneumoniae strains, were collected fro
134  the recombinant marker genomes gave rise to drug-resistant keratinocyte colonies and cell lines, whi
135                                      All the drug-resistant lesions we identified activate BRAF V600E
136 ainst certain cancer cell lines, including a drug-resistant line.
137 tion, selection, and linkage have identified drug-resistant loci.
138      Artemisinin is highly effective against drug-resistant malarial parasites, which affects nearly
139 cted role for TG2 in triggering autophagy in drug-resistant MCL cells through induction of IL6.
140 tically ill patients to infection with multi-drug resistant (MDR) bacteria are determined by many com
141                                        Multi-drug resistant (MDR) enteric bacteria are of increasing
142 ly stable quinolones effective against multi drug resistant (MDR) Mtb.
143 treatments increased the proportion of multi-drug resistant (MDR) Salmonella from day 4 through day 2
144                            The rise of multi-drug-resistant (MDR) bacteria has spurred renewed intere
145 nning colistin and the epidemiology of multi-drug-resistant (MDR) Escherichia coli (using blaNDM and
146 apy (LITT) in the treatment of patients with drug-resistant mesial temporal lobe epilepsy (mTLE).
147 eded to combat the rise of infections due to drug-resistant microorganisms.
148 ts, synchronous targeting of survivin, other drug resistant molecules, and survivin regulators.
149 e used to develop new strategies to overcome drug-resistant mRCC.
150 nables detection of a minority population of drug resistant Mtb, a clinically relevant scenario refer
151 erexpression potentiates AG activity against drug-resistant Mtb.
152                                    Whether a drug-resistant mutant grows to high densities, and so si
153 tivity, both against the wild type virus and drug-resistant mutant strains.
154  for Mtb detection and the identification of drug resistant mutants using binary deoxyribozyme sensor
155                           Among a handful of drug-resistant mutants, M2-S31N is the predominant mutat
156 killing by these drugs, and able to generate drug-resistant mutants.
157 es the notion that inhibitors targeting Mps1 drug-resistant mutations can emerge as a feasible interv
158                            Indeed, identical drug-resistant mutations have been also identified in dr
159 ccurately predict the clinical prevalence of drug-resistant mutations is a key step toward generating
160                                           No drug-resistant mutations were detected.
161 quencing can measure of the heterogeneity of drug-resistant mutations within and between hosts and he
162 rganism-wide lipidomic analysis platform for drug-resistant mycobacteria and provide direct evidence
163                                        Multi-drug resistant Mycobacterium abscessus complex (MABSC) i
164                      Primary transmission of drug-resistant Mycobacterium leprae, including a rifampi
165                  The emergence and spread of drug-resistant Mycobacterium tuberculosis (DR-TB) are cr
166                          RATIONALE: Minority drug-resistant Mycobacterium tuberculosis subpopulations
167  to the rapid and specific identification of drug-resistant Mycobacterium tuberculosis using RPA unde
168 in the epidemiological surveillance of multi-drug resistant nosocomial pathogens.
169 disseminated tuberculosis syndromes, whether drug-resistant or -susceptible.
170          Patients on contact precautions for drug-resistant organisms were selected for most activity
171 oliferation of TNBC wild type (p < 0.01) and drug resistant (p < 0.05) TNBC cells.
172 aft tumors in both wild type (p < 0.001) and drug-resistant (p < 0.05) xenografts.
173  has been heightened by the recent news that drug-resistant parasites are developing in some populati
174 asites in elimination settings and spreading drug-resistant parasites widely.
175 nd elimination of malaria and containment of drug-resistant parasites.
176 e to pre-existing resistance or evolution of drug-resistant parasites.
177 nking due to the rapidly increasing of multi-drug-resistant pathogenic bacteria.
178                       With the rise of multi-drug resistant pathogens and the decline in number of po
179 mprove the surveillance and control of multi-drug resistant pathogens in an effort to develop effecti
180 nfections caused by this most intractable of drug resistant pathogens.
181 weak antibiotic pipeline and the increase in drug-resistant pathogens have led to calls for more new
182 tural products that have bioactivity against drug-resistant pathogens in order to assess their drug p
183 lostridium difficile incidence, incidence of drug-resistant pathogens, days of therapy over admission
184 ng 42% of drug-sensitive patients and 83% of drug-resistant patients, it is necessary to develop a be
185 ed treatment for around 17% of estimated new drug-resistant patients.
186 nic as well as the development of trials for drug-resistant patients.
187 s senescence to impose the MITF-low/AXL-high drug-resistant phenotype observed in human tumors.
188  alteration that confers a more invasive and drug-resistant phenotype.
189 e bacteria showing multi-drug or extensively drug resistant phenotypes.
190 RAF inhibition, and before the appearance of drug-resistant phenotypes.
191 he formation of tumors or the development of drug-resistant phenotypes.
192                                 Emergence of drug resistant Plasmodium falciparum including artemisin
193 s heralded a new era in effectively treating drug-resistant Plasmodium falciparum malaria.
194 ccesses in malaria control are threatened by drug-resistant Plasmodium parasites and insecticide-resi
195                                              Drug-resistant Plk4 can enhance Aurora A-mediated rescue
196 l infection in the ICU are now classified as drug resistant, prompting hospital-based screening for m
197 omain-containing protein (PumA) of the multi-drug resistant Pseudomonas aeruginosa PA7 strain.
198 eruginosa is an opportunistic and frequently drug-resistant pulmonary pathogen especially in cystic f
199 y, Dp44mT has greater anti-tumor activity in drug-resistant relative to non-Pgp-expressing tumors.
200 r, the mechanisms that render leukemic cells drug resistant remain largely undefined.
201 od epilepsy disorder that is associated with drug-resistant seizures and a high mortality rate.
202  patients who underwent epilepsy surgery for drug-resistant seizures in 36 centers from 12 European c
203  We studied cannabidiol for the treatment of drug-resistant seizures in the Dravet syndrome.
204 nd young adults with the Dravet syndrome and drug-resistant seizures to receive either cannabidiol or
205 agement by earlier (trace) detection of rare drug-resistant sequence variants.
206 gainst all tested bacteria including a multi-drug resistant Staphylococcus aureus strain Y5 and ampic
207 d GOB-18) and, significantly, an extensively drug-resistant Stenotrophomonas maltophilia clinical iso
208 systemic infection murine model setup with a drug-resistant strain of C. albicans.
209 iple species of bacteria including otherwise drug resistant strains.
210 It is essential to monitor the occurrence of drug-resistant strains and to provide guidance for clini
211 ic antibody, synergistically protect against drug-resistant strains in adjunctive therapy with merope
212  number of multidrug-resistant and extremely drug-resistant strains is a significant reason for conce
213 g-resistant tuberculosis (MDR-TB), caused by drug-resistant strains of Mycobacterium tuberculosis, is
214                                              Drug-resistant strains were detected in 52.7%.
215 nsmission occurs and the transmissibility of drug-resistant strains, and estimates of the effect of H
216                   Invasive disease caused by drug-resistant strains, designated MRSA (methicillin-res
217  cells, potency on clinically relevant HIV-1 drug-resistant strains, lack of cytotoxicity and off-tar
218 s caused by both Gram-negative and -positive drug-resistant strains.
219  to high mortality lies in the appearance of drug-resistant strains.
220 linical isolates, which included extensively drug-resistant strains.
221  assess Mtb treatment responses for emerging drug-resistant strains.
222 e antiviral activity against susceptible and drug-resistant subpopulations.
223 ibition of which promotes tumorigenicity and drug-resistant survival.
224 the binding affinity for oritavancin against drug-resistant targets (70 nM) was found to be 11,000 ti
225 cant differences in mechanical response when drug-resistant targets are challenged with different ant
226 and oritavancin against drug-susceptible and drug-resistant targets on a cantilever and demonstrated
227 for treatment of tuberculosis (TB) and multi-drug resistant TB (MDR-TB), repurposing FDA (U.S. Food a
228 Qs) are commonly prescribed as part of multi-drug resistant TB therapy: moxifloxacin (MXF), levofloxa
229 it coincides with de novo emergence of multi-drug-resistant TB (MDR-TB).
230   Delayed diagnosis of tuberculosis (TB) and drug-resistant TB are major challenges of TB control in
231 ospitals and clinics with high prevalence of drug-resistant TB in India, Moldova, and South Africa.
232 are settings, potentially identifying highly drug-resistant TB more quickly and simply than currently
233 t study of 172 subjects with MDR/extensively drug-resistant TB subjects and sequenced the full gyrA a
234 who were HIV positive and/or at high risk of drug-resistant TB.
235                        Targeted regimens for drug-resistant TBM should be further explored.
236                                              Drug-resistant temporal lobe epilepsy (TLE) often requir
237 sing therapeutic agent to eradicate CSCs for drug-resistant TNBC treatment.
238 nd its significant role for the treatment of drug-resistant TNBC.
239 anid (OPC-67683), an approved drug for multi-drug resistant tuberculosis, is a potent inhibitor of Le
240                         Increasingly complex drug-resistant tuberculosis (DR-TB) is a major global he
241                                        Multi-drug-resistant tuberculosis (MDR-TB) is an increasing pu
242 lity risk and improve treatment outcomes for drug-resistant tuberculosis (TB) patients, including ind
243 ing (DST) to design appropriate regimens for drug-resistant tuberculosis (TB).
244 istant tuberculosis (MDR-TB) and extensively drug-resistant tuberculosis (XDR-TB) (M/XDR-TB).
245 c screens for bactericidal compounds against drug-resistant tuberculosis are beginning to yield novel
246 ical, and genomic data from patient cases of drug-resistant tuberculosis backed by shareable, physica
247 so contribute substantially to the burden of drug-resistant tuberculosis because of their much higher
248 tiative supported programmatic management of drug-resistant tuberculosis in 90 countries.
249 y virus (HIV) coepidemic and rising rates of drug-resistant tuberculosis in parts of the world add fu
250 data suggest that control of the epidemic of drug-resistant tuberculosis requires an increased focus
251 s in 240 multidrug-resistant and extensively drug-resistant tuberculosis strains and quantified their
252                                              Drug-resistant tuberculosis threatens recent gains in th
253 gnosis of 20 downstream cases of extensively drug-resistant tuberculosis with almost identical sequen
254 ogists from countries with a heavy burden of drug-resistant tuberculosis working with data scientists
255 rammatically incurable tuberculosis (totally drug-resistant tuberculosis).
256  273 South African patients with extensively drug-resistant tuberculosis, or resistance beyond extens
257 berculosis, or resistance beyond extensively drug-resistant tuberculosis, were followed up over a per
258 alth Organization to treat leprosy and multi-drug-resistant tuberculosis.
259  of action in order to tackle the scourge of drug-resistant tuberculosis.
260 ting many cases of multidrug and extensively drug-resistant tuberculosis.
261 ns-are likely crucial to the pathogenesis of drug-resistant tuberculosis.
262 is Commission, we examine several aspects of drug-resistant tuberculosis.
263 or, are being evaluated for the treatment of drug-resistant tuberculosis.
264  new therapeutic agents for the treatment of drug-resistant tuberculosis.
265 mmittee-supported programmatic management of drug-resistant tuberculosis.
266 osed a threat of transmission of extensively drug-resistant tuberculosis.
267                                              Drug-resistant tuberculous meningitis (TBM) is difficult
268 re often short-lived due to the emergence of drug-resistant tumor subpopulations.
269 ed to 2D culture where MDA-MB-231 attained a drug-resistant tumor-initiating phenotype indicated by i
270 bly, BET bromodomain inhibition resensitizes drug-resistant tumors to Enz by selectively impairing th
271                           Cells derived from drug-resistant tumors were sensitive to TBP when grown i
272 ed resistance to TPB and inhibited growth of drug-resistant tumors.
273 cell pool constitutes a reservoir from which drug-resistant tumours may emerge.
274 of 301 unique resistance alleles across 1934 drug-resistant tumours.
275 r, concerns exist regarding the emergence of drug -resistant variants and subsequent treatment failur
276  quinoxaline maintain better potency against drug resistant variants, likely due to reduced interacti
277 perspectives to study HCV biology, including drug-resistant variants emerging with new antiviral ther
278 l quasispecies and the pre-existence of some drug-resistant variants in the liver, which are not nece
279                          Replicon levels and drug-resistant variants were quantified at various times
280 operties along with the rapid development of drug-resistant variants.
281 ment, leading to the inevitable emergence of drug-resistant variants.
282 cancer (CRPC), but tumours frequently become drug resistant via multiple mechanisms including AR ampl
283 gnosis, lack of ART access or adherence, and drug-resistant viral strains.
284 ted with NNRTI treatment is the emergence of drug resistant virus, this work focused on optimization
285 h resistance data had documented evidence of drug-resistant virus in plasma.
286            Selection and genetic analysis of drug resistant viruses revealed that substitution of pro
287 al target that may suppress the selection of drug-resistant viruses during core protein-targeting ant
288 ively participating in the SHCS in 2013 with drug-resistant viruses initiated ART before 1999 (59.8%)
289 ted based on the patient's risk of harboring drug-resistant viruses.
290 s in pet dogs with spontaneous chronic multi drug-resistant wound infections demonstrated clearance o
291 of multidrug resistant (MDR) and extensively drug resistant (XDR) Mtb strains that emerge globally as
292                                    Extremely drug-resistant (XDR) Acinetobacter baumannii is one of t
293 , multidrug-resistant (MDR), and extensively drug-resistant (XDR) Mycobacterium tuberculosis strains,
294 ly multidrug-resistant (MDR) and extensively drug-resistant (XDR) TB.
295                                  Extensively drug-resistant (XDR) tuberculosis (TB) cannot be easily
296    Multidrug-resistant (MDR) and extensively drug-resistant (XDR) tuberculosis are emerging worldwide
297         A widespread epidemic of extensively drug-resistant (XDR) tuberculosis is occurring in South
298 pecially likely in patients with extensively drug-resistant (XDR) tuberculosis.
299 of multidrug-resistant (MDR) and extensively drug-resistant (XDR) tuberculosis.
300                                           In drug-resistant xenografts, tumor volume was decreased 2.

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