Avastin provides benefit in several tumour(An abnormal growth of cells, forming a mass of tissue) types
Following the initial approval of Avastin in the USA for advanced CRC in 2004, clinical trials in different tumour types have demonstrated that VEGF(A protein that promotes angiogenesis and is known to be a prognostic factor in several types of tumour) inhibition produces clinical benefit for the patient.1–5
Avastin became the first anti-angiogenic therapy made widely available for the treatment of a range of cancer types and continues to transform cancer care through its proven clinical benefit in terms of both PFS(The time from trial entry to disease progression or death from any cause) and OS(The time from trial entry to death from any cause).1–5
Clinical data suggest that the addition of Avastin to first-line standard anticancer therapy provides superior efficacy(The capacity for beneficial change (or therapeutic effect) of a given intervention) outcomes in patients with mCRC,1 NSCLC,2 mBC3 and mRCC.4
Avastin is approved for use
- In Europe and the USA for use in the treatment of mCRC, mBC, unresectable advanced, metastatic(Pertaining to the spread of a disease, usually cancer, from one organ or part to another non-adjacent organ or part) or recurrent NSCLC and advanced and/or metastatic RCC.5,6
- In the USA for the treatment of GBM.6
All patient subgroups can benefit from Avastin
Many different factors can affect the outcome of therapy in cancer patients, but as VEGF is essential for tumour angiogenesis(The growth of new blood vessels from pre-existing vessels), it is predicted that all patient subgroups should benefit from Avastin.
In the pivotal phase III trial in mCRC, OS benefit was observed in all patient subgroups, independent of baseline risk factors such as performance status, number of metastatic sites and adjuvant chemotherapy.7
Avastin also benefited all patient subgroups in two phase III studies in non-squamous(Pertaining to cells not from squamous epithelium; relatively common, locally invasive and occasionally metastatic) NSCLC.2,8,9 One study found particular OS benefit in patients with adenocarcinoma(Cancer of the epithelium that originates in glandular tissue) (HR(An estimate of relative risk of an event occurring)=0.69); sample sizes for other histologies were small, making data for these inconclusive.10
Subgroup analysis of data from the pivotal phase III study of Avastin plus paclitaxel in first-line mBC demonstrated PFS benefit due to Avastin in all prespecified patient subgroups, including those based on age, disease-free interval, number of metastatic sites and prior therapy.3
In mRCC, benefit from Avastin plus IFN-α was independent of baseline characteristics, including MSKCC risk(A validated and widely used prognostic score in patients with metastatic renal cell carcinoma (mRCC). Also known as Motzer score) score, which groups patients according to prognostic factors.4
Summary: efficacy of Avastin
The key role of angiogenesis in tumour growth and development suggests that the angiogenesis inhibitor Avastin is likely to have potential benefits in the treatment of multiple tumour types
- Numerous controlled clinical trials have demonstrated the efficacy of Avastin in mCRC, mBC, advanced NSCLC and advanced/metastatic RCC.
- Within these tumour types, patients experienced benefit through the addition of Avastin regardless of baseline characteristics.
References
- Hurwitz H, Fehrenbacher L, Novotny W, et al. N Engl J Med 2004;350:2335–42.
- Sandler A, Gray R, Perry MC, et al. N Engl J Med 2006;355:2542–50.
- Gray R, Bhattacharya S, Bowden C, Miller K, Comis RL. J Clin Oncol 2009;27:4966–72.
- Escudier B, Pluzanska A, Koralewski P, et al. Lancet 2007;370:2103–11.
- Avastin Summary of Product Characteristics. Available at: http://www.emea.europa.eu/humandocs/Humans/EPAR/avastin/avastin.htm.
- US Prescribing Information for Avastin 2009. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2009/125085s0168lbl.pdf.
- Fyfe GA, Hurwitz H, Fehrenbacher L, et al. J Clin Oncol 2004;22(July 15 Suppl.):274s (Abstract 3617).
- Reck M, von Pawel J, Zatloukal P, et al. J Clin Oncol 2009;27:1227–34.
- Soria J, Mauguen A, Reck M, et al. Ann Oncol 2010;21(Suppl. 8):viii147 (Abstract 437P).
- Sandler A, Kong G, Strickland DK, et al. J Thorac Oncol 2008;3:11(Suppl 4.):S283.