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1 estinal membrane integrity and contribute to gastrointestinal toxicity.
2 ial applications for predicting drug-induced gastrointestinal toxicity.
3 ical use of GSI is limited due to its severe gastrointestinal toxicity.
4 3 has a protective role in radiation-induced gastrointestinal toxicity.
5 or bladder dose or in acute genitourinary or gastrointestinal toxicity.
6 trations of SN-38, which are associated with gastrointestinal toxicity.
7 or bladder dose or in acute genitourinary or gastrointestinal toxicity.
8 xtensively researched, and radiation-induced gastrointestinal toxicity.
9 s respectively 72% and 25% for mucositis and gastrointestinal toxicity.
10 on to the upper abdomen without unacceptable gastrointestinal toxicity.
11  setting because of platelet dysfunction and gastrointestinal toxicity.
12 omise, but special attention must be paid to gastrointestinal toxicity.
13 tory and clinically, toward reducing NSAIDs' gastrointestinal toxicity.
14  COX inhibition, they also cause significant gastrointestinal toxicity.
15 ducing nonsteroidal anti-inflammatory drugs' gastrointestinal toxicity.
16  article reviews mechanisms of NSAID-induced gastrointestinal toxicity.
17 rescription dose) is associated with serious gastrointestinal toxicity.
18 ANSAIDs) increases the risk of serious upper gastrointestinal toxicity.
19 associated with an increased risk of serious gastrointestinal toxicity.
20 s without the same concerns over significant gastrointestinal toxicity.
21 cted hematologic toxic effects, fatigue, and gastrointestinal toxicities.
22 associated with both late grade 2 or greater gastrointestinal toxicity (2.53 [2.07-3.08], p<0.0001) a
23 phrotoxicity (25%), neurotoxicity (23%), and gastrointestinal toxicity (21%).
24 nts had grade 3 or greater treatment-related gastrointestinal toxicity (22.0% during chemoradiotherap
25 ted to substantially increased incidences of gastrointestinal toxicity (58% of sucralfate patients v
26 urotoxicity (16%), nephrotoxicity (13%), and gastrointestinal toxicity (9%).
27 ations of c.1679T>G and c.1236G>A/HapB3 with gastrointestinal toxicity (adjusted RR 5.72, 95% CI 1.40
28 a side effect, they have been known to cause gastrointestinal toxicity, although the molecular mechan
29 hip between acute and late genitourinary and gastrointestinal toxicity among patients receiving conve
30  are antiinflammatory and analgesic but lack gastrointestinal toxicity, an undesirable side effect at
31 percent of patients experienced grade 3 to 4 gastrointestinal toxicity and 62% experienced grade 2 to
32  association between acute genitourinary and gastrointestinal toxicity and decrements at least twice
33 liosides by 69 to 75% but caused substantial gastrointestinal toxicity and failed to prevent viral in
34 I, 1.11-19.2]) polymorphisms were related to gastrointestinal toxicity and infection, respectively.
35 on was mainly a result of nonrelapse causes (gastrointestinal toxicity and infections).
36  distinct advantages with regard to both low gastrointestinal toxicity and restored therapeutic activ
37    The effects of combination therapy on the gastrointestinal toxicity and therapeutic activity of fr
38 d with foretinib were fatigue, hypertension, gastrointestinal toxicities, and nonfatal pulmonary embo
39 cities occurred in 7.6% and 0% (p = 0.4) and gastrointestinal toxicities, and, in 15.2% and 5% (p = 0
40 ive ACs was 240 mg/m2, and myelosuppression, gastrointestinal toxicity, and fatigue were the DLTs.
41 itis, mesenteric ischemia, radiation-induced gastrointestinal toxicity, and Graft vs Host Disease) we
42 e major side effects observed with CPT-11 is gastrointestinal toxicity, and we supposed that this mig
43 od (thrombocytopenia) as well as symptoms of gastrointestinal toxicity are dose-limiting adverse even
44                      Acute genitourinary and gastrointestinal toxicity as defined by the Radiation Th
45 equency of late radiation grades 3, 4, and 5 gastrointestinal toxicity ascribed to the LTAD-RT arm (2
46        The agents lacked the bone marrow and gastrointestinal toxicities associated with antiprolifer
47 etes without the concern for hypoglycemia or gastrointestinal toxicities associated with some other m
48 aling drugs) in preventing the serious upper gastrointestinal toxicity associated with another exposu
49 eces may serve as a noninvasive biomarker of gastrointestinal toxicity associated with perturbed Notc
50 tive for Cox-2 over Cox-1) seem to have less gastrointestinal toxicity associated with their use; how
51 ring pelvic radiotherapy resulted in reduced gastrointestinal toxicity both acutely and at 1 y compar
52 rtezomib-related toxicities: hematologic and gastrointestinal toxicities by Common Terminology Criter
53 subset of tumors, but may avoid the limiting gastrointestinal toxicity caused by pharmacological inhi
54          Described herein is a FGSI-mediated gastrointestinal toxicity characterized by cell populati
55                                              Gastrointestinal toxicity correlated significantly with
56 administration costs, and cardiovascular and gastrointestinal toxicities), creating a clinical need f
57                                 Unlike upper gastrointestinal toxicity, cyclooxygenase-mediated mecha
58 ding the development of malignancies, severe gastrointestinal toxicities, diabetes, cardiac arrhythmi
59 ted, and common adverse events included mild gastrointestinal toxicities (diarrhea [46%], constipatio
60 ontoured) correlated with grade 3 or greater gastrointestinal toxicity during chemoradiotherapy (45%
61  most common methods to reduce NSAID-induced gastrointestinal toxicity has been to co-prescribe proph
62 limited antileukemic cytotoxicity and severe gastrointestinal toxicity have restricted the clinical a
63 n of therapy due to AEs; common AEs included gastrointestinal toxicity, hypothyroidism, fatigue and p
64  nonsteroidal anti-inflammatory drug-induced gastrointestinal toxicity, identification of groups at h
65 ted preoperative chemotherapy with grade 3-4 gastrointestinal toxicity in 7% (seven of 94) of patient
66 ted in modest efficacy and mild but frequent gastrointestinal toxicity in MF patients.
67 , and high-fiber diets for the prevention of gastrointestinal toxicity in patients undergoing pelvic
68 treatment activity at the price of increased gastrointestinal toxicity in patients with RAS and BRAF
69 ay (ED50 = 38.7 mg/kg) with no indication of gastrointestinal toxicity in rats at doses as high as 20
70                                              Gastrointestinal toxicity includes the death and damage
71  adverse events included infection (n=7) and gastrointestinal toxicities including abdominal pain (n=
72                         Chemotherapy-induced gastrointestinal toxicity is a significant dose-limiting
73                                  The lack of gastrointestinal toxicity is likely due to the low absor
74 ed with palbociclib and ribociclib, but more gastrointestinal toxicity is observed with abemaciclib.
75                                              Gastrointestinal toxicity is the primary limiting factor
76 lencing of Brd4 in mice(6), the platelet and gastrointestinal toxicities may represent on-target acti
77 linical thrombocytopenia model than 3, while gastrointestinal toxicity may be a BRD4-driven effect.
78                                              Gastrointestinal toxicity (nausea, vomiting, and diarrhe
79           Except for the instance of grade 3 gastrointestinal toxicity, nonhematologic toxicity was r
80 ity of 23.2%, grade 3 or 4 treatment-related gastrointestinal toxicity of 26.4% (including diarrhea,
81 entiate the primary determinants of skin and gastrointestinal toxicity of erlotinib.
82 heory that inhibition of COX-1 underlies the gastrointestinal toxicity of NSAIDs in man.
83 tients, five were taken off study because of gastrointestinal toxicity or intolerance to SC.
84                However, these mAbs displayed gastrointestinal toxicity or poor plasma exposure in viv
85 educed folate carrier polymorphism predicted gastrointestinal toxicity (OR, 10.4 [95% CI, 1.35-80.4])
86 one hemorrhage, anemia, febrile neutropenia, gastrointestinal toxicity, pain, fatigue, neuropathy (on
87 ade 3 to 4 adverse events of hepatotoxicity, gastrointestinal toxicity, pneumonitis, endocrine dysfun
88                          A decreased risk of gastrointestinal toxicity remains the primary justificat
89                           Hepatotoxicity and gastrointestinal toxicity represented the major adverse
90  has been stalled by the induction of severe gastrointestinal toxicity resulting from the inhibition
91  a dramatic decrease in chemotherapy-induced gastrointestinal toxicities, significant potentiation of
92 er xenografts, and showed fewer platelet and gastrointestinal toxicities than the DbBi ABBV-075(14).
93                                     Multiple gastrointestinal toxicities that often occurred together
94 patients at this dose level experienced late gastrointestinal toxicity that required surgical managem
95               Bortezomib-related toxicities (gastrointestinal toxicity, thrombocytopenia, and paresth
96 d assessed the severity of radiation-induced gastrointestinal toxicity triggered by the two dose rate
97 nduced bone destruction without inducing the gastrointestinal toxicity typically associated with inhi
98                                              Gastrointestinal toxicity was also significantly lower f
99                     Acute grade 2 or greater gastrointestinal toxicity was associated with both late
100 imiting toxicity was observed, but low-grade gastrointestinal toxicity was common.
101                            Radiation-induced gastrointestinal toxicity was more pronounced and mouse
102                                              Gastrointestinal toxicity was most common, with 21 patie
103 co-primary endpoint of RTOG grade 2 or worse gastrointestinal toxicity was observed in 69 (11%) of 60
104                                Grade 3 CTCAE gastrointestinal toxicity was observed in three (<1%) pa
105          Consequently, a marked reduction in gastrointestinal toxicity was observed relative to irino
106 -1.3 to 4.0]; p=0.39); RTOG grade 2 or worse gastrointestinal toxicity was seen in 11 (3%) of 382 par
107 insufficiency, secondary to dehydration from gastrointestinal toxicity, was also seen.
108 herapy) grade 2 or greater genitourinary and gastrointestinal toxicities were assessed using adjusted
109                            Acute urinary and gastrointestinal toxicities were similar to those expect
110                                              Gastrointestinal toxicities were the most common treatme
111               Grades 3 and 4 hematologic and gastrointestinal toxicity were more frequent in the RT +
112 ytopenia, neurotoxicity, nephrotoxicity, and gastrointestinal toxicity were more severe with cisplati
113 ficant differences in acute genitourinary or gastrointestinal toxicity were observed.
114 etastasis, blood perfusion, oxygenation, and gastrointestinal toxicity were studied.
115 omium (Cr(VI)) exposure has been linked with gastrointestinal toxicity, whereas the molecular pathway
116 ith AML were grade 1 or 2 constitutional and gastrointestinal toxicities, which were generally manage
117  protected WT mice from DNA damage and acute gastrointestinal toxicity, which resulted in improved ov
118  efficacy, with less hematologic and greater gastrointestinal toxicity with IP.
119               There is evidence of increased gastrointestinal toxicity with the three-drug combinatio
120                                              Gastrointestinal toxicity with this regimen is most prom

 
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