In this section, hear what experts have to say about drugs that disrupt the function of receptors on a cell's surface.
In this section, hear what experts have to say about drugs that disrupt the function of receptors on a cell's surface. Breast cancer – the most prevalent cancer affecting women – is being successfully treated using these "receptor blockers."
Click forward to find out more about two breast cancer drugs and their receptor targets.
Larry Norton, M.D., Memorial Sloan-Kettering Cancer Center:
“Well many cancers actually require hormones to grow. Breast cancer is a very good example. Breast cancer arises in the breast, and the breast is an organ that is responsive to the female hormone, estrogen.”
“Cancers derived in the breast, therefore, especially in older women, tend to require estrogen to grow. If we can starve that cell of estrogen, we can actually make that cancer cell die.”
“And that’s what we do right now with a couple of different approaches. One of the drugs is called tamoxifen, which actually attaches to the estrogen receptor.”
“The estrogen receptor is a protein that is found in many breast cancer cells that finds estrogen in surrounding blood, takes it into the cell, and signals the cell to grow.”
“Well, tamoxifen attaches to the estrogen receptor so the estrogen can’t attach to the receptor. And when tamoxifen and the receptor for estrogen go into the nucleus of the cell, it attaches to the DNA and actually signals the cell not only to grow but to die. So that’s a very important molecule.”
“One of the really important things to know about cancer is that no two cancers are the same. They're all different. There is tremendous variations in the molecules that are involved in making a cell cancerous. By identifying those molecules in the individual case, we can individualize therapy – give people the medicines they need, and not give medicines to people if they are not going to benefit.”
The estrogen receptor is not the only target in the treatment of breast cancer. Another important target is the human epidermal growth factor receptor (Her-2), which is overexpressed in 25% of breast cancers, leading to cellular growth and proliferation.
“If a cell has too much her2, the cell will be dividing too often because the cell will be interpreting many stimuli in the environment as stimuli cause it to divide whereas a normal cell wouldn’t. It makes that cell have too much of a tendency for cell division and to go on to form a lump and to go on and spread into the surrounding tissue like an invasion or to grow on other parts of the body.”
“We've developed an antibody that attaches to her2. Antibodies are the proteins that your body makes naturally in response to infections. And your body normally makes lots of antibodies, and should be that's how come you fight lots of infections. However, we can now make her2 antibodies – we call it Trastuzumab or Herceptin – outside the human body and give it to the patient intravenously if that patient has a cancer, particularly a breast cancer, with too much her2 in it.”
“Antibody flows in the blood, finds the cancer cell, attaches to the her2, and inactivates it so now it can’t act as a molecule, the cell is not getting the stimulus that is giving it information to make it divide so it stops dividing and stops dividing it often goes on to kill itself, called programmed cell death.”
Herceptin is one example of a treatment that targets a specific molecule in a particular type of cancer. As more of these precisely targeted therapies are developed, it will become increasingly important to understand which molecules play important roles in a particular individual’s cancer. See the Pharmacogenetics section for more information on patient-specific treatment.
female hormone estrogen, breast cancer cells, sloan kettering cancer center, larry norton, breast cancer, cancer cell, receptor blockers, estrogen receptor, target, tamoxifen, receptors, cancers
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