Figure 1. Evidence of rapid tumor regrowth following bevacizumab cessation, within 1 month, with accelerated kinetics in patient 2 (A) before first BV treatment, (B) during first BV treatment, before surgery, (C) 1 month after colon and liver surgery and (D) during second BV treatment, after surgery.
Ré sumé : La chimiothé rapie des cancers colorectaux a é té profondé -ment modifié e ces derniè res anné es. Alors mê me que la place respective de l'irinoté can et de l'oxaliplatine n'é tait pas complè tement dé finie, les thé rapies ciblé es sont arrivé es. De nombreuses questions de straté gie thé rapeutique restent non ré solues, mais des informations scientifiques ré centes permettent d'y voir un peu plus clair au quotidien pour traiter les malades. Le but de cet article est de faire le point sur ces donné es ré centes dans un domaine en permanente é volution.Mots clé s : Cancer colorectal -Chimiothé rapie -Thé rapies ciblé esOxaliplatine -Irinoté can -Bé vacizumab -Cé tuximab -Panitumumab Developments in chemotherapy treatment of metastatic colorectal cancer Abstract: Chemotherapy of colorectal cancer has been dramatically modified during the last 10 years. Before the roles of oxaliplatin and irinotecan had been satisfactorily evaluated, targeted therapies appeared in the field of treatment for these patients. Numerous questions remain unanswered. However, recent data is helping to clarify matters concerning the day to day treatment of such patients. Clearly it is time to evaluate these recent studies and that is the aim of this article.
14119 Background: The addition of bevacizumab (BV), an anti-VEGF monoclonal antibody with antiangiogenic activity, to cytotoxic chemotherapy (CH) improves survival in metastatic colorectal cancer patients (pts). Reversal of VEGF inhibition is associated with rapid vascular regrowth in tumors in vivo (M.R. Mancuso et al, J Clin Invest; 116(10): 2610–2621, 2006). In the clinical setting, the consequences of BV interruption are poorly documented, especially in interactions with the surgical resection of liver metastases. Methods: We describe the kinetics of tumor growth prior to, during, and after interruption of BV and under BV reintroduction, in consecutive colorectal cancer pts experiencing objective response under CH+BV, followed by surgical resection of metastases. We measured either clinically, of using CT-scan, the diameter of target lesions according to RECIST criteria, and the doubling time. Results: 7 pts (3 F, 4M), with median age of 54 years (41–70), were treated with 5-FU based CH (+oxaliplatin: 5; + irinotecan: 1 pt) and BV for metastatic colo- (6 pts) rectal (1 pt) cancer received a median number of 6 (4–18) cycles. Median time between BV interruption and surgery: 8 weeks (3–12). Under BV, all pts experienced objective response, with a median tumor reduction of 13%/month (extr: 6–15%). After BV interruption, under CH alone, 2/7 pts experienced disease progression, with a tumor growth of the residual disease of +7% and +200%/month, respectively. In pts who underwent surgery, during the off therapy period, tumor growth occurred in all 7 pts with a kinetics of +17 to +400%/month. Tumor growth doubling time after BV interruption ranged between 2 and 5 weeks. Reintroduction of BV re-induced a tumor response in 5/7 pts with a median time to response of 8 weeks (6–12) and a reduction of 10%/month. Conclusions: We show reproducible evidence of tumor growth acceleration following BV interruption. Surgery might transiently modify the balance between angiogenic and anti-angiogenic factors. We suggest to reduce the duration of BV interruption and to restart BV as soon as possible after surgery. These observations justify a large prospective analysis of the variations of tumor growth in this setting. No significant financial relationships to disclose.
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