Why Receiving Chemotherapy Full Dose and On Schedule Is Important
Your chemotherapy schedule is designed to be as effective as possible in destroying cancer cells, while keeping damage to healthy tissues down to levels that can be managed by your body (with the help of treatment).
The effectiveness of chemotherapy drugs in killing cancer cells depends on receiving full doses as frequently as needed. However, the doses can't be so high—or given so often—as to cause physically unmanageable side effects.
This means that recommended chemotherapy schedules all "walk a fine line" between delivering as much toxicity to cancer cells as possible, while staying short of the level that would be too unsparing of normal body tissues. The need for effectiveness must be balanced by the need for safety.
When there are unintended delays in chemotherapy, that carefully calculated balance no longer applies. The effectiveness of chemotherapy drops even with small changes in dose or schedule. As a result, you may no longer be receiving the level of cancer cell destruction that would be ideal for your type and stage of cancer. For maximum effectiveness, your doctor would like to provide you with full-dose, on-schedule (FDOS) chemotherapy when possible.
Remember that the amount of chemotherapy any patient can tolerate varies and can't always be predicted in advance. For all patients, safety and comfort considerations may make delays in chemotherapy unavoidable. Your doctor has your well-being foremost in mind and in addition to monitoring you with tests, wants to know exactly how you are feeling. For your safety, be upfront and tell your doctor everything he or she needs to know. See Questions to Ask Your Doctor about Cancer Treatment.
Use the Chemotherapy Planner to stay on schedule with your chemotherapy treatments.
What makes chemotherapy effective?
Chemotherapy kills cells in your body that are rapidly dividing. The drugs travel throughout your body and can kill these cells in areas distant from the original location of the tumor.
One characteristic of cancer cells is that they are often rapidly dividing. Smaller tumors in particular may have actively dividing cancer cells (which are more vulnerable to chemotherapy drugs), as opposed to cells at rest.
Because chemotherapy drugs kill rapidly dividing cells, they interfere with the development and spread of tumors. If enough cancer cells are killed, your natural immune reactions will usually be better able to attack and eliminate any that remain, and prevent them from organizing into tumors.
The type of chemotherapy that works best in killing cancer cells is different for each type and stage of cancer. When possible, chemotherapy with combinations of drugs are recommended. This is because there is always variation in cancer cells, even within a single tumor. Cancer cells that are resistant to one type of chemotherapy drug may be vulnerable to another. For this reason, a combination of drugs is more likely to be effective in killing as many of these cells as possible.
Full-dose, on-schedule chemotherapy is intended to deliver killing doses of drug to individual cancer cells and to the groups of cancer cells that are organized as tumors. If enough cancer cells within a tumor die as a result of chemotherapy drugs, and if the time interval between drug doses is short enough, the surviving cancer cells within the tumor will not have time to grow back effectively. The tumor is then likely to fall apart and be destroyed by natural immune processes. Depending on the type and stage of cancer, this can be effective in eliminating even distant tumors, and is one of the goals of chemotherapy.
Researchers are even now trying to find ways to safely shorten the time interval between effective doses of chemotherapy (sometimes described as increasing the dose density of chemotherapy). Chemotherapy doses and schedules are continually under study. New developments in chemotherapy drugs, or in drugs that help keep side effects under control, can lead to better and more effective chemotherapy regimens. Over time, this type of advancement has led to better chances of survival and recovery after a diagnosis of cancer.
Why does chemotherapy cause side effects?
Chemotherapy drugs do not "know" which of the cells in your body are cancer cells that need to be destroyed. Instead, they act against all rapidly dividing cells.
Even in an adult body, there are a number of healthy cell types that divide rapidly as part of their normal function. Unfortunately, chemotherapy damages these cells too. This cell damage is seen and felt as part of the side effects of chemotherapy, and is the major factor limiting the amount of chemotherapy that can be given at any one time.
Because more effective treatments are now available for managing side effects, they are often not as severe or as difficult to cope with as they were in past years. However, side effects resulting from damage to the bone marrow can still limit the amount of chemotherapy administered.
Cells in the bone marrow naturally divide rapidly. Certain bone marrow cells are responsible for forming red and white blood cells and supplying them to your circulation on an ongoing basis. You need your red blood cells to keep your body tissues supplied with oxygen. You need white blood cells to defend your body against infection.
Bone marrow cells may be temporarily affected by chemotherapy and fail to produce enough red blood cells (a condition called anemia, or white blood cells (a condition called neutropenia). Because the body's need for more blood cells is too urgent to ignore, your chemotherapy is cycled to allow for "rest" periods, during which your bone marrow cells recover.
Unfortunately, tumor cells may recover during these "rest" periods as well. Today, drug treatments to stimulate bone marrow cells and increase their production of red or white blood cells are available. These treatments have made it possible for more aggressive chemotherapy regimens for certain cancers to be explored and put into practice.
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This content was last reviewed
August 15, 2010 by Dr. Reshma L. Mahtani.