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1 ine or systemic 2-deoxy-d-glucose (a glucose antimetabolite).
2 ly described cellular efflux system for this antimetabolite.
3 as comparable to that observed with specific antimetabolites.
4 il in high-risk patients, despite the use of antimetabolites.
5 oach and are being investigated as potential antimetabolites.
6  the mechanistic classes except one class of antimetabolites.
7 nct from those of calcineurin antagonists or antimetabolites.
8 fety profile compared to trabeculectomy with antimetabolites.
9  for modulating activity of chemotherapeutic antimetabolites.
10 orticosteroids, cyclosporine, and the purine antimetabolites.
11 ding of TS degradation and its regulation by antimetabolites.
12 d pantothenate analogs are growth-inhibiting antimetabolites.
13                  Treatment of cells with the antimetabolite 1-beta-D-arabinofuranosylcytosine (ara-C)
14     The present studies demonstrate that the antimetabolite 1-beta-D-arabinofuranosylcytosine (ara-C)
15 se-9, and (iv) induction of apoptosis by the antimetabolite, 1-beta-d-arabinofuranosylcytosine.
16 tion and death were decreased by the glucose antimetabolite 2-deoxyglucose and increased by high bloo
17 se deprivation or treatment with the glucose antimetabolite 2-deoxyglucose caused nontransformed cell
18 naffected by food deprivation or MA, and the antimetabolite 2-DG has no impact on GAL in any area.
19                                   The energy antimetabolites 2-deoxy-D-glucose (2-DG) and Na-2-mercap
20 C), which is phosphorylated to the activated antimetabolite, 2'3'-dideoxycytidine triphosphate by cyt
21 raperitoneal (i.p.) injection of the glucose antimetabolite, 2-deoxy-D-glucose (2DG), or saline.
22 nd the loss of functional p53 signaling, the antimetabolite 5-fluorouracil (5-FU) failed to induce ar
23                                          The antimetabolite 5-fluorouracil (5-FU) is one of the most
24 s strikingly resistant to the effects of the antimetabolite 5-fluorouracil (5-FU), the mainstay of ad
25                                          The antimetabolite 5-fluorouracil (5FU) is a widely used che
26  HMG-CoA reductase inhibitor lovastatin, the antimetabolite 5-fluorouracil, and the cyclic nucleotide
27 racerebroventricular infusion of the glucose antimetabolite 5-thioglucose selectively promoted respon
28 use of antiscarring agents, particularly the antimetabolites 5-fluorouracil and mitomycin C, have rev
29                                The cytotoxic antimetabolites, 5-flurouracil and mitomycin C both prol
30 ethyl-N'-nitro-N-nitrosoguanidine (MNNG) and antimetabolite 6-thioguanine (6-TG).
31  whether inhibition of Chk1 could potentiate antimetabolites, a mainstay of cancer therapy, which con
32 ermine more precisely the processes by which antimetabolites act as radiation sensitizers and to defi
33 protecting the tumour and allowing prolonged antimetabolite action.
34 d for at least 1 year with infliximab and an antimetabolite agent experienced a relapse within 1 year
35                                   The use of antimetabolite agents, such as mitomycin, has increased
36 s among the most efficacious and widely used antimetabolite agents.
37                                 Although the antimetabolites all target DNA replication, they differ
38                              In the subgroup antimetabolite analysis, the addition of mitomycin C to
39 east 1 year with scheduled infliximab and an antimetabolite and had been in corticosteroid-free remis
40 reatment of pancreatic cancer using combined antimetabolite and sonodynamic therapy (SDT).
41  of combination chemotherapy consisting of 2 antimetabolites and a corticosteroid.
42 d for disease modifying antirheumatic drugs, antimetabolites and biologic drugs.
43 g-term corticosteroid use include the use of antimetabolites and biological therapies.
44 acid chemistry: coenzyme forms and function; antimetabolites and cancer chemotherapy.
45        The majority of patients treated with antimetabolites and corticosteroids were able to achieve
46 < .001), and in those who received intensive antimetabolites and glucocorticoids (P < .001).
47 atients on combined maintenance therapy with antimetabolites and identified factors associated with r
48 be used in conjunction with a combination of antimetabolites and rescue agents.
49 lt and is restricted to structurally similar antimetabolites and semi-synthetic analogues of their co
50                       Some purine nucleoside antimetabolites and their monophosphate derivatives are
51 cted drug), 5-fluorouracil and methotrexate (antimetabolites), and vinblastine (a microtubule inhibit
52 en combined with Thymoglobulin induction, an antimetabolite, and corticosteroids, TAC and CsA are com
53  received Thymoglobulin, corticosteroids, an antimetabolite, and cyclosporine monitored by C2 (n=50)
54 me, Ca(2+)-independence, resistance to an AA antimetabolite, and induction by another unsaturated fat
55 h antibody induction, calcineurin inhibitor, antimetabolite, and maintenance prednisone.
56 hat consisted of Thymoglobulin induction, an antimetabolite, and prednisone.
57 h antibody induction, calcineurin inhibitor, antimetabolite, and RDP versus historical controls treat
58 phosphorylation, whereas DNA-damaging drugs, antimetabolites, and alkylating agents do not.
59  cell killing using halogenated pyrimidines, antimetabolites, and other DNA-damaging agents or sensit
60 eated with DNA-damaging agents or nucleotide antimetabolites, and p53-deficient fibroblasts and Mdm2/
61  agents: including DNA cross-linking agents, antimetabolites, and topoisomerase I and II inhibitors.
62 lasses of drugs reviewed include alkylators, antimetabolites, anthracyclines, taxanes, camptothecins,
63 treated with low-dose glucocorticoids and an antimetabolite, anti-tumour necrosis factor (TNF) monocl
64 ic utility as a modulator of the activity of antimetabolite antitumor agents by virtue of its inhibit
65 surgery using an infusion, optimal method of antimetabolites application, new adjustable sutures, and
66                           Folates and folate antimetabolites are metabolically trapped in mammalian c
67  concern when powerful immune modulators and antimetabolites are used in combination, relatively few
68 n that combines a depleting antibody with an antimetabolite, avoiding calcineurin inhibitors and ster
69 reading, scavenging of nutrients, removal of antimetabolites, balancing of metabolite pools, and esta
70 ving lower-risk leukemia and received mainly antimetabolite-based continuation therapy; the 130 cases
71 responses to therapy, should be treated with antimetabolite-based therapy designed to maintain their
72  for acute myeloid leukemia with monosomy 7; antimetabolite-based therapy for acute lymphoblastic leu
73 xtend these results to patients treated with antimetabolite-based therapy, we performed Southern blot
74 mproved survival among patients treated with antimetabolite-based therapy.
75 T-lineage ALL when treated with conventional antimetabolite-based therapy.
76 normality are best treated with conventional antimetabolite-based therapy.
77 een the substrate, allosteric regulator, and antimetabolite binding sites on pantothenate kinase and
78 ctural similarities to alkylating agents and antimetabolites, but which is non-cross-resistant with a
79 viously available immunosuppressives such as antimetabolites, calcineurin inhibitors, and alkylating
80         Bleb leaks after trabeculectomy with antimetabolites can be recalcitrant to therapy.
81                          Bevacizumab and the antimetabolites capecitabine and gemcitabine have been s
82                                   While most antimetabolites caused a cytostatic effect on cell growt
83   When challenged with both DNA damaging and antimetabolite chemotherapeutics, RB was required for pr
84                                              Antimetabolite chemotherapy exposure was associated with
85 ses remains extremely poor despite high-dose antimetabolite chemotherapy.
86                                Standard (non-antimetabolite) combination chemotherapy administered pa
87                                              Antimetabolites (cytarabine) may lead to a degeneration
88 cosatetraenoate, did not mimic AA, and an AA antimetabolite did not block responses to AA.
89  previously undergone trabeculectomy without antimetabolites, divided into two groups.
90 iazol-2-yl)-3,4-dihydroxybenzamide], a novel antimetabolite drug developed at City of Hope Cancer Cen
91                                          The antimetabolite drug, 5-fluorouracil, inhibits microbial
92                          The use and type of antimetabolite drugs had no affect on recurrence.
93  endogenous pyrimidines and pyrimidine-based antimetabolite drugs.
94  mediate bacterial resistance to sulfonamide antimetabolite drugs.
95 d the effects of 5-fluorouracil (5-FUra), an antimetabolite effective against colon tumors, on nitric
96                                              Antimetabolites, first used to treat patients in the ear
97             Therapeutic applications include antimetabolites for modulation of proliferative vitreore
98 ential growth of Huh-7 cells, the effects of antimetabolites for several nucleoside biosynthesis path
99          The mechanisms of resistance to the antimetabolite gemcitabine in non-small cell lung cancer
100                      Radiosensitization with antimetabolites has improved clinical outcome for patien
101             Although anti-inflammatories and antimetabolites have been used with success, these nonsp
102  phacoemulsification and trabeculectomy with antimetabolites have vastly improved the results of comb
103                       Azathioprine, a purine antimetabolite immunosuppressant, photosensitizes the sk
104 pathways involved in radiosensitization with antimetabolites implicate base excision repair with the
105 -Fluorouracil (5-FU) is the most widely used antimetabolite in the treatment of colorectal, breast an
106 in patients treated with corticosteroids and antimetabolites in a sex-specific manner.
107 nhibitors, but also enhances the toxicity of antimetabolites in cancer cell lines.
108 action with taxanes, anthracyclines and some antimetabolites in HER-2/neu-overexpressing breast cance
109 se (FPGS) catalyzes the activation of folate antimetabolites in mammalian tissues and tumors.
110 he major publications relating to the use of antimetabolites in ocular surface neoplasia and highligh
111 n encouraging experiences with high doses of antimetabolites in primary CNS lymphoma and with rituxim
112 they are also resistant to a number of other antimetabolites in the DNA synthesis pathway in a TNFalp
113 K ineffective in generating CoA analogues as antimetabolites in vivo.
114 est and irregular cellular morphologies, the antimetabolite-induced arrest was highly reversible and
115                                          The antimetabolite-induced p53-dependent arrest response was
116 -fluorouracil), which acts at early steps of antimetabolite-induced stress by stimulating phosphoryla
117 tations that impart resistance to pyrimidine antimetabolite inhibitors also relieve CTP inhibition an
118                               Modeling these antimetabolites into the pantothenate active site predic
119                                          The antimetabolite methotrexate (MTX) was inferred recently
120 ione (DNP-SG) and leukotriene C4 (LTC4), the antimetabolite methotrexate, and the bile acid glycochol
121 nfer greater benefits when combined with the antimetabolite methotrexate.
122 ely 1.7-fold resistance was observed for the antimetabolite methotrexate.
123 of HBL100 cells treated with 5-fluorouracil (antimetabolite), methotrexate (antimetabolite), tamoxife
124 suppression (ECI), with a TNF antagonist and antimetabolite might be a more effective strategy.
125                The intraoperative use of the antimetabolites mitomycin C and 5-fluorouracil in both t
126 andard-dose cyclosporin or tacrolimus and an antimetabolite, mostly mycophenolate mofetil (91.7%).
127 tions of cyclosporine and those treated with antimetabolites (mycophenolate and azathioprine) have a
128                         The pantothenic acid antimetabolite N-heptylpantothenamide (N7-Pan) possesses
129                         The pantothenic acid antimetabolite N-pentylpantothenamide inhibits the growt
130 ction of p53 and associated G1 arrest by the antimetabolite, N-(phosphonoacetyl)-L-aspartate (PALA),
131 n Experiment 2, rats injected with the lipid antimetabolite Na-2-mercaptoacetate (MA) responded more
132 ho have failed or who are not candidates for antimetabolite or calcineurin inhibitor immunomodulation
133 oach, when the immunosuppressive agents were antimetabolites or calcineurin inhibitors.
134 inimum of 20 mg of prednisone, cyclosporine, antimetabolites, or any combination of these agents were
135                                          The antimetabolite prodrug 3-deazauridine (3DUrd) inhibits C
136 munosuppressive armamentarium, replacing the antimetabolite prodrug azathioprine, reports have associ
137 no acids have long been recognized for their antimetabolite properties and tendency to be uncovered t
138             The combination of high doses of antimetabolites, R-HDS, and ASCT is feasible and effecti
139                                          The antimetabolite radiosensitizers may inhibit thymidylate
140                       Refinement of existing antimetabolite regimens can improve surgical results, es
141                               Treatment with antimetabolites results in chemically induced low nucleo
142 ocedure, phacoemulsification-trabeculectomy, antimetabolites, results and complications, as well as c
143    Additionally, many surgeons are employing antimetabolites routinely in combined phacoemulsificatio
144 s of riboswitches serves as a target for the antimetabolite S-(2-aminoethyl)-L-cysteine (AEC).
145 ould probably not be tested further, but its antimetabolite schedules and frequent drug administratio
146  results suggest that chlorambucil and/or an antimetabolite should be administered before cyclophosph
147                                 However, the antimetabolites still have many potential problems and s
148 l pathways has allowed the emergence of new 'antimetabolite' strategies to increase the therapeutic e
149 ent approach, we identified a novel targeted antimetabolite strategy to exploit arginine deprivation
150                            Purine nucleoside antimetabolites, such as clofarabine, are effective anti
151                                          The antimetabolites, such as methotrexate, azathioprine, lef
152                                              Antimetabolites, such as the DNA-hypomethylating agent 5
153 ence shows that second-line agents including antimetabolites, T-cell inhibitors and alkylating agents
154  Immunosuppressed patients were treated with antimetabolites, T-cell inhibitors, and/or alkylating ag
155 fluorouracil (antimetabolite), methotrexate (antimetabolite), tamoxifen (antiestrogen/antiproliferati
156 d trabeculectomy with releasable sutures and antimetabolites, techniques have improved considerably i
157       Pemetrexed (ALIMTA, Lilly) is a folate antimetabolite that has been approved by the U.S. Food a
158                            Mitomycin-C is an antimetabolite that has seen increased use in ophthalmol
159  Nucleoside analogs are structurally similar antimetabolites that have a broad range of action and ar
160 y when used in combination with conventional antimetabolites that reduce "bulk" tumor size.
161 study, we assessed the effects of an intense antimetabolite therapy alternating with APO on overall s
162 s with T-cell ALL treated with standard-dose antimetabolite therapy and implies that higher-dose meth
163 he targeted delivery of combined sonodynamic/antimetabolite therapy in pancreatic cancer.
164 s protocols, in that more intensive systemic antimetabolite therapy was given before and during radio
165 tation in DHFS prevents the formation of the antimetabolite, thereby conferring resistance to PAS.
166      The antifolates were the first class of antimetabolites to enter the clinics more than 50 years
167 eated with 2 of the most commonly prescribed antimetabolite treatments.
168                          The class of folate antimetabolites typified by (6R)-dideazatetrahydrofolate
169 reless incisions, filtration procedures, and antimetabolite use are studied.
170 ts who underwent transplantation after 2000, antimetabolite use at 1 year was associated with improve
171            5-Fluorouracil (5-FU) is a potent antimetabolite used for chemotherapy of gastrointestinal
172         Cytarabine arabinoside (ara-C) is an antimetabolite used to treat hematologic malignancies.
173  (DHFS) to generate a hydroxyl dihydrofolate antimetabolite, which in turn inhibits DHFR enzymatic ac
174  cause marked resistance to tetrahydrofolate antimetabolites, while still allowing cell survival.
175 ntensity than CAF and improved scheduling of antimetabolites with sequential methotrexate and 5-FU, a

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