Efficacy and Toxicity of Addition of Bevacizumab to Chemotherapy in Patients with Metastatic Colorectal Cancer

Abstract

Background: Pre-treated patients with first-line treatment can be offered a second treatment with the aim of improving their poor clinical prognosis. The therapy of metastatic colorectal cancer (CRC) patients who did not respond to first-line therapy has limited treatment options. Recently, many studies have paid much attention to the efficacy of bevacizumab as an adjuvant treatment for metastatic colorectal cancer. Objectives: We aimed to evaluate the efficacy and toxicity of bevacizumab plus chemotherapy compared with bevacizumab-naive based chemotherapy as second-line treatment in people with metastatic CRC. Methods: Electronic databases were searched for eligible studies updated to March 2018. Randomized-controlled trials comparing addition of bevacizumab to chemotherapy without bevacizumab in MCRC patients were included, of which, the main interesting results were the efficacy and safety profiles of the addition of bevacizumab in patients with MCRC as second-line therapy. Result: Five trials were eligible in the meta-analysis. Patients who received the combined bevacizumab and chemotherapy treatment in MCRC as second-line therapy showed a longer overall survival (OS) (OR=0.80,95%CI=0.72-0.89, P<0.0001) and progression-free survival (PFS) (OR=0.69,95%CI=0.61-0.77, P<0.00001). In addition, there was no significant difference in objective response rate (ORR) (RR=1.36,95%CI=0.82-2.24, P=0.23) or severe adverse event (SAE) (RR=1.02,95%CI=0.88-1.19, P=0.78) between bevacizumab-based chemotherapy and bevacizumabnaive based chemotherapy. Conclusion: Our results suggest that the addition of bevacizumab to the chemotherapy therapy could be an efficient and safe treatment option for patients with metastatic colorectal cancer as second-line therapy and without increasing the risk of an adverse event.

<p>Predictive And Prognostic Value Of Hepatic Steatosis In Conversion Therapy For Colorectal Liver-limited Metastases: A Propensity Score Matching Analysis</p>

“…Our results also showed that patients with unresectable CLLMs would benefit from systemic therapy first mode rather than primary lesion resected mode in the overall survival, which is consistent with previous reports 36. The addition of targeted agents, like cetuximab and bevacizumab, has been reported to be associated with a favorable PFS and OS in the previous studies 3,22. And, it is also worth noting that local treatments, like TACE, are associated with poorly controlled progression of CLLMs and shorter PFS in our study, because local treatment was always used when the shrinkage of tumors was not apparent 23,29…”

“…In addition, we identify targeted therapy as another independent predictor in multivariate analysis. This was similar to previous studies, in which adding cetuximab or bevacizumab to chemotherapy was associated with facilitated radical resections of CLLMs 3,22. And TACE was also identified as another independent predictor in multivariate analysis.…”

“…The baseline characteristics were significantly unbalanced. Patients with HS tended to have smaller volume, smaller number and lower proportion of bilobar distribution in CLLMs and higher BMI, which was similar to the previous studies 3,22. A smaller volume or number of CLLMs could give rise to a higher residual volume of normal liver and implicated a higher possibility of conversion hepatectomy and a longer survival 8,9.…”

Genetic Variants of ANGPT1, CD39, FGF2 and MMP9 Linked to Clinical Outcome of Bevacizumab Plus Chemotherapy for Metastatic Colorectal Cancer

“…At the molecular level, VEGF and its receptor (VEGFR) play major roles in the angiogenesis that characterizes advanced cancer. Several authors have reported significant improvements in progression-free survival (PFS), overall survival (OS) and response rate (RR) in mCRC patients treated with CT + BVZ compared to CT alone [7][8][9][10][11][12]. However, not all patients respond in the same way to treatment probably through the development of treatment resistance mechanisms involving activation of proangiogenic pathways or tumour recruitment of cells that produce proangiogenic factors, recruitment of hematopoietic cells and inflammatory cells into the tumour, and heterogeneity of genetically unstable tumour cells [13,14].…”