In 1971, Dr Judah Folkman published the "angiogenic hypothesis" suggesting that a tumor cannot grow beyond 1–2 millimeters without the development (angiogenesis) of new blood vessels that provide access to oxygen and nutrients
During the 1990s, it was discovered that vascular endothelial growth factor (VEGF) stimulates the proliferation and migration of the cells that form blood vessels, leading to the formation of new blood vessels. VEGF binds to receptor tyrosine kinases (RTKs) on the cell surface and causes the RTKs to dimerize and become active, thereby initiating an intracellular signaling cascade that stimulates cell division and inhibits apoptosis. Many cancer cells secrete high levels of VEGF. Increased VEGF expression in a tumor is correlated with a poor medical outcome for the patient. Some evidence suggests that blocking VEGF-dependent signaling may prevent the formation of new blood vessels and lead to the death of immature blood vessels without disturbing mature blood vessels. You work for a biotechnology company that seeks to create anticancer drugs that prevent the growth of tumors and/or cause tumors to shrink, while leaving normal cells relatively untouched. After learning about VEGF, you have a bright idea for a new mechanism of action for a potential anticancer drug. What is your idea?
The findings on VEGF suggest several strategies for blocking angiogenesis in and around tumors, which might be a powerful weapon in the anticancer arsenal. Several mechanisms of drug action may prevent angiogenesis, including the four possibilities below.
1. The drug may prevent the production or secretion of VEGF by tumor cells.
2. The drug may bind free VEGF in the extracellular space, thus lowering the effective concentration of VEGF and preventing it from binding to the RTKs on epithelial cells in blood vessels (indeed, the antiangiogenesis drug Avastin® functions in this way).
3. The drug may bind to RTKs and prevent binding to VEGF or dimerization.
4. The drug may block the intracellular signaling cascade triggered when VEGF binds and activates RTKs.
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Which of the following describes the Skene's gland?
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How are negative stains different from other types of stains?
a. They stain the desired structure or specimen black. b. They stain more than one type of specimen. c. They stain the background, leaving the cells colorless.