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Lani · 09-23-2006, 09:33 AM

Thanks--I looked at the original article and they tried two VDAs (vascular disrupting agents) both of which had long abreviations and numbers and were not clinically available chemotherapies.

I found the following last few sentences, paragraph which might put people thinking "counterintuitively" as they said:

"Together, these results reinforce our hypothesis that CEPs mobilized from the bone marrow are a major contributor to the growth of the viable tumor rim after treatment with VDAs.

Our results illustrate that although CEP levels in vessels of untreated tumors are typically low, these levels can suddenly rise in response to acute stress, such as that caused by treatment with a VDA and possibly with other treatments such as maximum-tolerated-dose cytotoxic chemotherapy (17). This situation may be analogous to the rapid reactive mobilization and homing of CEPs to damaged vessels or arteries that occurs after pathological cardiovascular events such as myocardial infarcts (18). Our results also provide an additional mechanistic rationale for the enhanced efficacy of VDAs when combined with an antiangiogenic drug (9). Finally, they suggest that when a VDA is to be combined with chemotherapy, consideration should be given to the counterintuitive idea of administering chemotherapy shortly after VDA treatment, rather than the opposite sequence, because of the ability of chemotherapy to target CEPs (17, 19)."

09-23-2006, 09:33 AM	#3
Lani Senior Member Join Date: Mar 2006 Posts: 4,778	Tom Thanks--I looked at the original article and they tried two VDAs (vascular disrupting agents) both of which had long abreviations and numbers and were not clinically available chemotherapies. I found the following last few sentences, paragraph which might put people thinking "counterintuitively" as they said: "Together, these results reinforce our hypothesis that CEPs mobilized from the bone marrow are a major contributor to the growth of the viable tumor rim after treatment with VDAs. Our results illustrate that although CEP levels in vessels of untreated tumors are typically low, these levels can suddenly rise in response to acute stress, such as that caused by treatment with a VDA and possibly with other treatments such as maximum-tolerated-dose cytotoxic chemotherapy (17). This situation may be analogous to the rapid reactive mobilization and homing of CEPs to damaged vessels or arteries that occurs after pathological cardiovascular events such as myocardial infarcts (18). Our results also provide an additional mechanistic rationale for the enhanced efficacy of VDAs when combined with an antiangiogenic drug (9). Finally, they suggest that when a VDA is to be combined with chemotherapy, consideration should be given to the counterintuitive idea of administering chemotherapy shortly after VDA treatment, rather than the opposite sequence, because of the ability of chemotherapy to target CEPs (17, 19)."