Therapeutic potential of purine analogue combinations in the treatment of lymphoid malignancies

Johnson, Stephen A.; Thomas, W.

doi:10.1002/1099-1069(200012)18:4<141::aid-hon666>3.0.co;2-#

Cited by 23 publications

(9 citation statements)

References 42 publications

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“…91,92 Recent clinical observations have demonstrated that the combinations of FAMP or 2-CdA with mitoxantrone, doxorubicin or epirubicin are effective in CLL. 56,[93][94][95][96] Combined treatment with NA, mitoxantrone and CY has been undertaken both in previously treated and untreated patients with B-CLL. 93,97,98 However, the efficacy of these regimens seem to be similar to that observed after treatment with FAMP or 2-CdA alone.…”

Section: Nucleoside Analogues In Combination With Other Agentsmentioning

confidence: 99%

“…56,[93][94][95][96] Combined treatment with NA, mitoxantrone and CY has been undertaken both in previously treated and untreated patients with B-CLL. 93,97,98 However, the efficacy of these regimens seem to be similar to that observed after treatment with FAMP or 2-CdA alone. In addition, the toxicity, especially myelosuppression and infections of such combined therapy is high and reduction of NA doses is essential.…”

Section: Nucleoside Analogues In Combination With Other Agentsmentioning

confidence: 99%

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Alkylating agents and nucleoside analogues in the treatment of B cell chronic lymphocytic leukemia

Robak

Kasznicki

2002

Leukemia

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Section: Nucleoside Analogues In Combination With Other Agentsmentioning

confidence: 99%

Section: Nucleoside Analogues In Combination With Other Agentsmentioning

confidence: 99%

Alkylating agents and nucleoside analogues in the treatment of B cell chronic lymphocytic leukemia

Robak

Kasznicki

2002

Leukemia

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“…27,28 In addition, many purine nucleoside analogs (fludarabine, cladribine, pentostatin, nelarabine, and clofarabine) are clinically administered in the treatment of solid and hematological malignancies. [29][30][31][32] A large number of investigations indicate that purine nucleobases and purine nucleosides target a series of pathways in chemotherapy-induced cell death mechanisms, such as apoptosis, necrosis, senescence, autophagy, and mitotic catastrophe. 25,[33][34][35] Also, various purine scaffolds and their analogs have been studied as potential anticancer agents that contain cyclin-dependent kinase and heat shock protein inhibition.…”

Section: Introductionmentioning

confidence: 99%

Design, Synthesis and In Vitro Cytotoxic Activity of New 6,9-Disubstituted Purine Analogues

Küçükdumlu

Tunçbìlek

Güven

et al. 2020

ACSi

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A series of new 6,9-disubstituted purine analogs with 4-substituted piperazine at C-6 and 4-substituted benzyl at N-9 were designed and synthesized in four steps. All synthesized compounds (7-26) were screened initially for their in vitro anticancer activity on Huh7 liver, HCT116 colon and MCF7 breast carcinoma cell lines. Cytotoxic bioactivity studies revealed that all compounds screened, with compound 19 being the exception, were found to have promising cytotoxic activities at IC 50 range of 0.05-21.8 μM against cancer cells Huh7, HCT116 and MCF7. Among the prepared purine analogs, two of them (12 and 22) exhibited excellent cytotoxic activities, with IC 50 0.08-0.13 μM, on Huh7 cells comparable to camptothecin (CPT) and better than cladribine, fludarabine and 5-FU. Afterwards, the evaluation of cytotoxicity of the most potent purine analogs was screened against further hepatocellular cancer (HCC) cell lines. The 6-(4-(4-trifluoromethylphenyl)piperazine (12) and 6-(4-(3,4-dichlorophenyl)piperazine analogs (25) displayed a significant IC 50 values (IC 50 < 0.1-0.13 μM) comparable to CPT and better cytotoxic bioactivity when compared with 5-FU, cladribine and fludarabine on HCC cells (Huh7 and HepG2).

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“…Fludarabine, 9-β-D-arabinofuranosyl-2-fluoroadenine, is an analog to adenosine cytotoxic against dividing and resting cells. 6–7 In vivo , the combination of a DNA damaging agent, e.g. adriamycine or cyclophosphamide combined with fludarabine is clinically active against B cells in CLL and low-grade follicular lymphomas.…”

Section: Introductionmentioning

confidence: 99%

Up-front fludarabine impairs stem cell harvest in multiple myeloma: report from an interim analysis of the NMSG 13/03 randomized placebo controlled phase II trial

et al. 2009

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The impact of chemotherapy resistant B cells in multiple myeloma (MM) needs to be evaluated by in vivo targeted therapy. Here we report the conclusions from a phase II randomized, placebo controlled trial adding fludarabine to the induction with cyclophosphamide-dexamethasone. Based on an interim toxicity and safety analysis, the trial was stopped following inclusion of 34 of a planned 80 patients due to a reduced number of patients (4/17) actually harvested in the experimental arm compared to the control arm (11/17; p<0.05). In conclusion, the scheduled fludarabine dosage in 2 cycles combined with alkylating therapy impairs stem cell mobilization and standard therapy in young MM patients and should not be administrated up-front.

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Therapeutic potential of purine analogue combinations in the treatment of lymphoid malignancies

Cited by 23 publications

References 42 publications

Alkylating agents and nucleoside analogues in the treatment of B cell chronic lymphocytic leukemia

Alkylating agents and nucleoside analogues in the treatment of B cell chronic lymphocytic leukemia

Design, Synthesis and In Vitro Cytotoxic Activity of New 6,9-Disubstituted Purine Analogues

Up-front fludarabine impairs stem cell harvest in multiple myeloma: report from an interim analysis of the NMSG 13/03 randomized placebo controlled phase II trial

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