Targeted Therapies

Formerly BioOncology Watch

www.tgt-therapies.com

APRIL 2005

BEVACIZUMAB THERAPY FOR BREAST CANCER

Bevacizumab plus capecitabine vs capecitabine alone. A recently completed study demonstrated that the addition of bevacizumab (Avastin; Genentech Inc), a monoclonal antibody directed against vascular endothelial growth factor (VEGF), to first-line chemotherapy for metastatic colorectal cancer prolonged overall and progression-free survival (Hurwitz H, et al. N Engl J Med. 2004; 350:2335–2342).  Now, Kathy Miller and associates report the results of a randomized phase III study that compared the efficacy and safety of oral capecitabine (2500 mg/m2 daily for 14 days every 21 days) with or without bevacizumab (15 mg/kg intravenously on
day 1 of each 3-week cycle) in 462 patients with metastatic breast cancer previously treated with an anthracycline and a taxane.  Patients receiving combination therapy had a greater response rate than did patients treated with capecitabine alone (19.8% vs 9.1%). However, length of overall survival (15.1 vs 14.5 months) and progression-free survival (4.86 vs 4.17 months) was comparable in both treatment groups. Hypertension requiring treatment developed in 17.9% of patients given combination therapy and in 0.5% of patients treated with capecitabine alone.  No significant differences were observed in the incidence of diarrhea, hand-foot syndrome, thromboembolic events, or serious bleeding events between the treatment groups. These results showed that the addition of bevacizumab to capecitabine treatment was well tolerated but did not prolong overall or progression-free survival in patients with previously treated metastatic breast cancer.  (Miller KD et al. J Clin Oncol. 2005;23:792–799)

 

LENALIDOMIDE

Efficacy in myelodysplastic syndromes (MDS).  Alan List and coworkers treated 43 MDS patients with transfusion-dependent or symptomatic anemia with lenalidomide, a novel analogue of the immunomodulatory drug thalidomide. All patients were either refractory to recombinant erythropoietin therapy or had high endogenous serum erythropoietin levels.  Three oral lenalidomide dosing schedules were sequentially evaluated: 25 mg daily, 10 mg daily, and 10 mg daily for 21 days every 28 days.  Twenty-four (56%) patients achieved an erythroid response, and 20 patients had sustained independence from red blood cell (RBC) transfusions.  The median blood hemoglobin level achieved was 13.2 g/dL (range, 11.5 to 15.8 g/dL); after a median follow-up of 81 weeks, the median duration of RBC transfusion independence had not been reached. The erythroid response rate was highest (83%) in patients in which the MDS clone had an interstitial deletion involving chromosome 5q31.1 and in patients with lower-prognostic-risk MDS.  Among 20 patients with karyotypic abnormalities at baseline, 10 patients achieved complete cytogenetic remissions and 1 patient achieved a partial cytogenetic remission.  Neutropenia and thrombocytopenia necessitated a dose reduction in 25 (58%) patients.  Other adverse events were mild and infrequent. These data suggest that lenalidomide has hematologic activity in patients with low-risk MDS. Further studies are warranted.  (List A, et al. N Engl J Med. 2005;352:549–557)

 

TYROSINE KINASE INHIBITORS

Mechanisms of resistance.  Acquired resistance to kinase-targeted anticancer therapy has been most extensively studied in cancers treated with imatinib. Secondary resistance in CML has been associated with newly developed mutations in the ABL kinase domain that interfere with imatinib binding to ABL. Crystallographic studies predict that new BCR-ABL kinase inhibitors with less stringent structural requirements than imatinib will retain activity against most imatinib-resistant BCR-ABL mutants.  Maria Debiec-Rychter and coworkers screened 26 imatinib-resistant gastrointestinal stromal tumors and detected secondary mutations in KIT that were sensitive to PKC412, a novel small molecule that interacts with the ATP sites of KIT, VEGFR, PDGFR, PKC, FLT3, and the CDK1/cyclin B complex.  Similarly, lung adenocarcinomas that respond to the tyrosine kinase inhibitors gefitinib or erlotinib eventually develop acquired resistance. William Pao and Susumu Kobayashi and their associates report cases of non–small cell lung cancers that relapsed after responding to gefitinib or erlotinib and were found to have second mutations in the EGFR kinase domain.  These findings may help guide the development of more effective anticancer therapies. (Debiec-Rychter M, et al. Gastroenterology. 2005;128:270–279; Pao W, et al. PLoS Med. 2005;2:e73; and Kobayashi S, et al. N Engl J Med. 2005;352:786–792)

 

RITUXIMAB

Optimizing therapy for patients with low-grade non–Hodgkin's lymphoma (NHL). Recent studies have attempted to define improvements in the administration of rituximab to NHL patients. John Hainsworth and colleagues evaluated the feasibility of following standard rituximab therapy (375 mg/m2 weekly ´ 4) with 3 instead of 6 cycles of R-CHOP or R-CVP in 86 patients with previously untreated follicular NHL.  Overall and complete response rates (93% and 55%, respectively) were similar to those reported with chemotherapy and rituximab combinations of longer durations of treatment. Thomas Witzig and associates found that the administration of rituximab 375 mg/m2 weekly ´ 4 to 37 patients with advanced-stage, follicular grade 1 NHL showed a 72% response rate and was an acceptable alternative to observation.  However, rituximab monotherapy was not recommended for patients with high serum LDH levels, because they had low response rates (33%) and short times to progression (only 6 months). In a randomized study of 114 patients with previously treated indolent NHL, John Hainsworth and coworkers found that the duration of rituximab benefit was similar in patients who received maintenance rituximab therapy or rituximab re-treatment at the time of progression.  Finally, Lucio Gordan et al utilized pharmacokinetic data to demonstrate that a rational maintenance schedule is a single dose of rituximab 375 mg/m2 every 3 to 4 months. These studies may be used to individualize rituximab therapy so that efficacy is maintained or increased and toxicity is minimized. (Hainsworth JD, et al. J Clin Oncol. 2005;23:1500–150; Witzig TE, et al. J Clin Oncol. 2005; 23:1103–1108; Hainsworth JD, et al. J Clin Oncol. 2005;23:1088–1095; and Gordan LN, et al. J Clin Oncol. 2005;23:1096–1102)

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