Many conventional chemotherapy drugs, in addition to killing tumor cells, also fight angiogenesis. The anti-angiogenic effects of therapy may be masked and marginalized by the way it is usually administered. There are generally long breaks between drug administration that are necessary to allow the patient to recover from the harmful side effects of treatment.
When administering these drugs, the endothelial cells (involved in angiogenesis) are the first in the tumor to undergo cell death (apoptosis). However, this anti-angiogenic effect does not translate into a significant therapeutic benefit because the damage to the vasculature of the tumor can be largely repaired during the long rest and recovery periods between successive cycles of therapy.
The more frequent, lower-dose therapy can have an impressive anti-angiogenic and anti-tumor effects. Blood vessel cells are less likely than tumor cells to become resistant to chemotherapy, so if cancer cells become drug resistant, these medicines should still be able to shrink tumors by destroying their blood supply.
The main targets of dose-dense chemotherapy are presumed to be proliferating tumor cells. The main targets of low-dose chemotherapy are the endothelial cells of the growing vasculature of a tumor. In other words, chemotherapeutics can be used as anti-angiogenic agents.
Higher-dose standard chemotherapy treatment has been found to reduce the activity of the immune system's natural killer cells (white blood cells) by 96% (NCI). So if there are tumors growing elsewhere in the body and if the immune system helps to control tumor growth, then this method of chemotherapy could make things worse by allowing more rapid growth of the other tumors.
Whether chemotherapy is to be given and as well, what form it will take, are determined more by the idiosyncrasises and outpatient arrangements of the particular treatment center than by objective evidence of long-term efficacy. Long-term survival Platinum + Taxol combinations remain disappointing at higher-dose levels.
Conventional chemotherapy is given at high concentrations to force a drug or drug combination into poorly perfused areas of the tumor. The entire tumor is regarded as the target. This is not an ideal drug delivery.
The goal is to maximize drug delivery to the drug-accessible target receptors and minimize drug deposition elsewhere in the body. The target is not the entire tumor, it is just that part of the tumor that drug(s) can easily and freely reach after escaping from the tumor blood vessels. Just enough drug (s) is given to bind to the drug-accessible target receptors and kill the drug-accessible tumor. Over a long enough period of time, the drug (s) will eventually get to all the malignant cells.
Bottom line: more is not always better. How the role the drug delivery schedule plays in the disease control.
Sources:
Cell Function Analysis
Annals of Oncology (2002) Volume 13, Issue 1: pp. 12-15
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