Re-bound growth after Avastin therapy?

I found & copied the following post on the Inspire discussion board and don't know the original source of it.

Is anyone knowledgable about this information?

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Serum (testing human serum derived from colon cancer patients who had either been treated with chemotherapy alone or with chemotherapy + Avastin) from Avastin-treated patients actually support endothelial cell growth in cell culture better than serum from control patients, without Avastin treatment.

The serum from patients treated with Avastin supports more rapid re-growth of endothelial cells than did serum from patients who weren't treated with Avastin. This implies that the body is, indeed, cranking out more endothelial cell survival/growth factors in Avastin-treated patients. When you get rid of VEGF with Avastin, the body cranks out other types of blood vessel growth (survival) factors.

So, in regards to Avastin "rebound effect," it will take combination antivascular therapy to make a big difference, but this is definitely coming and it's the most promising thing on the near term therapeutic horizon.

The consistent and specific cure or control of cancer will require developing and using a set of drugs, given in combination, targeted to patterns of normal cellular machinery related to proliferation and invasiveness.

A sufficient number of independent methods of cell killing must be employed so that it is too improbable for a cancer cell to evolve that can escape death or inactivation. It must examine every cell in the body and must do so for a prolonged period of time.

Given the current state of the art, in vitro drug sensitivity testing could be of significant clinical value.

If an in vitro drug resistance test can demonstrate the presence of cancer cells that are resistant to a drug combination, then it is rational to use alternative therapy.

If an in vitro drug sensitivity test has the ability to demonstrate which drug combinations would be synergistic to cell death in all cancer cells present, then it is rational to use the drugs indicated in the test.

One aspect of a functional tumor cell profiling assay is that microvascular viability can measure dead microvascular cells in tissue, fluid and peripheral blood specimens to identify potential responders to anti-angiogenic drugs (Avastin, Nexavar, Sutent) and to assess direct and potentiating anti-angiogenic effects of tyrosine kinase targeted therapy drugs (Tarceva, Iressa).

Endothelial cells are present in tumor microclusters and drug effect upon these cells can be assessed in the microvascular viability assay. The "target" is not the cells themselves but rather a hormone (VEGF) secreted by the tumor cells. Anti-angiogenesis drugs complexes with free VEGF and blocks its action.

VEGF-receptor tyrosine kinases are expressed preferentially by endothelial cells of the growing neovasculature of a tumor and VEGF is a key survival (anti-apoptic) factor for the endothelial cells of newly formed vessels. There are several signalling pathways and molecular mechanisms by which VEGF can inhibit apoptosis (cell death) in endothelial cells.
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