Unlike local treatments, which focus on the area (or areas) where the invasive ductal carcinoma was found, systemic treatments involve the entire body. Treatments such as chemotherapy, hormonal therapy, and targeted therapies are used to destroy any cancer cells that may have left the original tumor, as well as to reduce the risk of the invasive ductal carcinoma coming back.
Chemotherapy involves taking anti-cancer medicines by injection directly into a vein or by mouth in the form of a pill. Two or more chemotherapy medications are often given in combination. The medicines travel through the bloodstream to all parts of the body. As chemotherapy damages the cancer cells, it also can damage some of the body’s healthy cells, which is why you may experience side effects.
If an invasive ductal carcinoma is larger than 1 centimeter in diameter and/or has spread to the lymph nodes, chemotherapy is usually recommended or, at the very least, seriously considered. When chemotherapy is given after surgery, it is called adjuvant therapy. In cases where the tumor is large, or breast cancer cells have traveled to many lymph nodes or other parts of the body, chemotherapy may be given before surgery to shrink the cancer. This approach is called neoadjuvant therapy. In either case, chemotherapy will be given in cycles, usually with a day (or days) of treatment followed by a period of “off” days. The exact schedule can vary depending on the medication or medications used. An entire course of chemotherapy usually takes about 3 to 6 months.
Just some examples of the many chemotherapies that may be used to treat invasive ductal carcinoma include:
- Adriamycin (chemical name: doxorubicin)
- Ellence (chemical name: epirubicin)
- Cytoxan (chemical name: cyclophosphamide)
- Taxotere (chemical name: docetaxel)
- Taxol (chemical name: paclitaxel)
- Xeloda (chemical name: capecitabine)
- Ixempra (chemical name: ixabepilone)
- fluorouracil (also called 5-fluorouracil or 5-FU)
You and your doctor will work together to determine which chemotherapy treatments are best for your situation. This can depend on the features of the cancer and any other health conditions you may have. For example, if you have a history of heart disease or heart-related risk factors, you and your doctor will want to avoid medications that can affect the heart. Your decision will also be influenced by whether or not the tumor tested positive for HER2 receptors. Some chemotherapies, such as Taxol and Cytoxan, are more commonly used with Herceptin in treating HER2-positive breast cancers.
Tests to determine the need for chemotherapy
If you have a small, early-stage invasive ductal carcinoma that did not spread to the lymph nodes and you will be taking hormonal therapy (see below), you may wonder whether chemotherapy is truly necessary as well. You and your doctor can discuss whether or not chemotherapy is right for your situation. You also may be eligible for one of three tests, called Oncotype DX, MammaPrint, or Mammostrat, which are being used to predict how likely the cancer is to recur (come back). The tests, called genomic assays, look at certain genes in the tumor to assess the risk of recurrence. A “high-risk” result is typically seen as a good reason to go ahead and proceed with chemotherapy.
- Oncotype DX, which is more common than MammaPrint and Mammostrat in the United States, tests a sample of the tumor to analyze patterns of activity in 21 genes. The test scores the likelihood of recurrence within 10 years on a scale of 0 to 100. A score of 17 or below is considered low risk for recurrence, while 31 or more indicates higher risk. This can help some people decide whether or not they want to go ahead with chemotherapy. A score of 18-30 is considered intermediate risk, so people in this group need to work with their doctors to make decisions about chemotherapy. The Oncotype DX test can be done on a sample of preserved tissue that was removed from the breast during the original biopsy or surgery.
- MammaPrint, a test developed and more frequently used in Europe, analyzes the activity of 70 genes in a sample of genetic material called RNA, which is extracted from tumor tissue. The test generates a profile that describes the risk of recurrence as low or high at 5 and 10 years into the future. The MammaPrint test can be done on a fresh tissue sample removed during surgery or biopsy, which requires special processing, or on a sample of preserved tissue that was removed from the breast during the original biopsy or surgery.
- Mammostrat measures the levels of five genes in breast cancer cells. These measurements are used to calculate a risk index score. The higher the risk index, the more likely the cancer is to come back. Women are assigned to a risk category (high, moderate, or low) based on their risk index score. The Mammostrat test can be done on a sample of preserved tissue that was removed from the breast during the original biopsy or surgery.
Doctors do not automatically order one of these tests for every person with breast cancer. Instead, they typically reserve these tests for patients who (1) have early-stage breast cancer that has not traveled to the lymph nodes, or to just a few; or (2) in the case of Oncotype DX have DCIS. If you fit these criteria, you and your doctor can determine whether genomic testing is right for you.
For more information on these tests, visit the Breast Cancer Tests: Screening, Diagnosis, and Monitoring section.
If the cancer tested positive for hormone receptors, your doctor likely will recommend some form of hormonal therapy. In some cases of advanced invasive ductal carcinoma, hormonal therapy can be given before surgery to help shrink the tumors. Usually, though, hormonal therapy starts after other treatments such as chemotherapy or radiation therapy, unless these treatments aren’t needed.
Hormone receptors are special proteins found on the surface of certain cells throughout the body, including breast cells. These receptor proteins are the “eyes” and “ears” of the cells, receiving messages from the hormones in the bloodstream and then telling the cells what to do. In other words, the receptors act like an on-off switch for a particular activity in the cell. If the right substance comes along that fits into the receptor — like a key fitting into a lock — the switch is turned on and a particular activity in the cell begins.
When breast cells have hormone receptors, estrogen and/or progesterone can attach to those receptors and tell the cell to grow and divide. Many breast cancer cells have high numbers of receptors for estrogen, progesterone, or both. This means that when these hormones are present, the cells receive a strong message to keep on growing and dividing — and this creates more cancer. If you take the hormone away or block it, the cancer cells lose their “growth fuel” and are less likely to survive.
Hormonal therapy, also called anti-estrogen therapy, works by lowering the amount of estrogen in the body or blocking the estrogen from signaling breast cancer cells to grow. You and your doctor will work together to decide which form of hormonal therapy is best in your situation. There are two types of hormonal therapy that are most frequently used:
- Selective estrogen-receptor response modulators (SERMs): The best-known SERM is tamoxifen. Tamoxifen “pretends” to be estrogen and attaches to the receptors on the breast cancer cells, taking the place of real estrogen. As a result, the cells don’t receive the signal to grow. Other examples of SERMs are Evista (chemical name: raloxifene) and Fareston (chemical name: toremifene). Tamoxifen is usually recommended for women who have not yet gone through menopause, although it can be used after menopause as well.
- Aromatase inhibitors: These medications — which include Arimidex (chemical name: anastrozole), Aromasin (chemical name: exemestane), and Femara (chemical name: letrozole) — reduce the amount of estrogen produced in a woman’s body after she goes through menopause. The main sources of estrogen for post-menopausal women are the adrenal glands and fat tissue, not the ovaries.
Other types of hormonal therapy include:
- Estrogen-receptor downregulators (ERDs): ERDs destroy the estrogen receptors in the cells, which prevents the estrogen from getting its message through. Faslodex (chemical name: fulvestrant) is an ERD approved for use in postmenopausal women with advanced breast cancer.
Ovarian shutdown or removal: The ovaries are the main source of estrogen in women before menopause. Shutting the ovaries down temporarily (for a set period of time) or even permanently can reduce the amount of estrogen in the body. Treatments include:
- Medicines such as Zoladex (chemical name: goserelin) and Lupron (chemical name: leuprolide), given by injection once a month for several months to stop the ovaries from producing estrogen.
- Surgery to remove the ovaries, called oophorectomy.
If an invasive ductal carcinoma is HER2-positive, then its cells make too much of a protein called HER2, and they also have too many HER2 receptors at the cell surface. With too many receptors, breast cancer cells pick up too many growth signals and start growing too much and too fast. One way to slow down or stop the growth of the cancer cells is to block the receptors at the cell surface so they don't pick up as many growth signals.
Herceptin (chemical name: trastuzumab) works at the cancer cell’s surface to block the chemical signals that stimulate uncontrolled cell growth. Herceptin can be used to treat the 1 in every 4 breast cancers that are HER2-positive. Treatment is usually given intravenously (through a needle that is inserted into a vein) every week for 52 weeks after surgery. In some cases of advanced invasive ductal carcinoma, Herceptin may be given before surgery to help shrink the tumors. Herceptin can cause damage to the heart, so it may not be recommended for people with certain heart conditions or heart-related risk. Herceptin also generally cannot be given with other chemotherapy medications that can affect the heart.
Tykerb (chemical name: lapatinib) is a type of anti-HER2 therapy that works inside the cell, rather than at the cell surface as Herceptin does. Inside HER2-positive breast cancer cells, HER2 receptors use protein signals, called kinases, to cause the cell to grow and divide abnormally. Kinases control how much energy the cells have to grow and multiply. Breast cancer cells that overexpress HER2 can have too much kinase activity, so the cancer cells grow too much, too fast. Tykerb works by interfering with HER2-related kinases inside the cell, limiting the amount of energy breast cancer cells have to grow and multiply.
Tykerb is a pill taken by mouth. Tykerb has been approved by the U.S. Food and Drug Administration (FDA) to:
- to be given in combination with the chemotherapy medicine Xeloda (chemical name: capecitabine) to treat advanced-stage, HER2-positive breast cancer that has stopped responding to anthracyclines, taxanes, and Herceptin
- to be given in combination with the hormonal therapy medicine Femara (chemical name: letrozole) to treat postmenopausal women diagnosed with hormone-receptor-positive, HER2-positive metastatic breast cancer
Perjeta (chemical name: pertuzumab) works like Herceptin by attaching itself to the HER2 receptors on the surface of breast cancer cells and blocking them from receiving growth signals. Perjeta targets a different area on the HER2 receptor than Herceptin does, so it’s believed to work in a way that’s complementary to Herceptin.
Perjeta is given intravenously, through a needle inserted into a vein.
Perjeta is approved by the FDA to be used in combination with Herceptin and the chemotherapy medicine Taxotere (chemical name: docetaxel) to treat HER2-positive, metastatic breast cancer that hasn’t been treated with either Herceptin or chemotherapy yet.
Perjeta also is approved to be used before surgery to treat HER2-positive, early-stage (the cancer must be larger than 2 cm or cancer must be in the lymph nodes), inflammatory, or locally advanced-stage breast cancer with a high risk of metastasizing or becoming fatal.
Other targeted therapies
Like hormonal therapy and HER2-targeted therapies, other targeted therapies are designed to interfere with specific processes that breast cancer cells use to grow and thrive.
Just one example is Avastin (chemical name: bevacizumab), a medication that targets a protein called VEGF, or vascular endothelial growth factor. VEGF plays a key role in stimulating the process cancer cells use to create new blood vessels, which is known as angiogenesis. Cancer cells have to create new blood vessels so they can get the oxygen and nutrients they need to grow and thrive. Avastin works by attaching itself to VEGF, which can prevent it from stimulating the formation and growth of new blood vessels.
Avastin can be used in combination with a chemotherapy medication called Taxol (chemical name: paclitaxel) to treat advanced breast cancer.
New targeted therapy medicines are still being studied in clinical trials. For more information about them, visit the Targeted Therapies section. You also may wish to visit our Clinical Trials section.