- Cooking and Eating to Fight Leukemia
- Leukemia pill ‘can melt away’ cancer cells
- ‘Remarkable’ results for idelalsib
- ‘These drugs will change patients’ lives’
- Avocado compound holds promise for treating leukemia
- Avocatin B targets and destroys leukemia stem cells
- New treatment of acute myeloid leukemia achieves remarkable results in a disease formerly with little hope
- DIET GUIDELINES FOR IMMUNOSUPPRESSED PATIENTS
- Basic Guidelines to Follow
- Neutropenic Diet
Cooking and Eating to Fight Leukemia
Diet can be a powerful weapon in the fight against leukemia. It’s important for patients to eat foods full of antioxidants that help fight cancer and keep the body strong, so it can keep on fighting.
Here’s how to arm yourself with the right foods when you have leukemia.
Cooking To Battle Leukemia
A healthy diet for someone with leukemia is pretty similar to a healthy diet for the general population, says registered dietitian Dee Sandquist, a spokeswoman for the American Dietetic Association in Fairfield, Iowa. But with leukemia, it’s even more important to follow healthy eating guidelines, because leukemia treatment can make patients nauseated and reduce their appetites, interfering with their best intentions to eat well.
Here’s what Sandquist recommends to bolster your body’s healing power:
Aim for 10 fruits and vegetables a day. The vitamins, minerals, antioxidants, and phytochemicals in fruits and vegetables are known to fight cancer cells, and most Americans, especially those with leukemia, need to eat more of them, Sandquist says. Sprinkle berries on top of cereal or whole-grain pancakes, top ice cream or frozen yogurt with peaches and blackberries, bake apples and sprinkle them with cinnamon, make fruit smoothies with strawberries and yogurt, and have an apple or banana as a snack during the day.
Steam your vegetables. This way, you get the most nutrients from them. And look for ways to add more to your plate. Try a stir-fry made from a variety of peppers, mushrooms, broccoli, and carrots; add steamed sweet peas, cauliflower, and zucchini to a salad; top a baked potato with broccoli or tomatoes; make vegetable soup with spinach, kale, mustard greens, collard greens, or chard; and drink low-sodium vegetable juice.
Go for whole grain. Every bite you take should have as much nutrition as possible, Sandquist says. That means choosing 100-percent whole-wheat bread (check the ingredients list), brown rice instead of white rice, whole-grain cereal, and ancient grains such as quinoa.
Make protein a priority. The side effects of chemotherapy can include nausea and vomiting, which takes away some people’s appetite for meat, Sandquist says. But it’s very important for patients with leukemia to get protein because it will keep them strong. If a hamburger doesn’t appeal to you, try cooking something a little more bland, such as a piece of fish or chicken without much seasoning. It may also be easier to eat chicken or fish in soup, she says. If you are vegetarian, good protein foods include nuts and seeds, soy products such as tofu or soy milk, wheat or oat cereals, and eggs.
Soothe your stomach. When chemotherapy side effects such as nausea wreak havoc on your diet, Sandquist suggests eating foods like crackers and sipping ginger ale and other liquids, or even eating popsicles if it’s too difficult to eat solid foods. In general, it’s a good idea to pass up spicy foods and caffeine to avoid an upset stomach.
Fill up on healthy bacteria. Your stomach has healthy bacteria that help your body better handle food, Sandquist says. You can feed those healthy bacteria — called probiotics — by eating yogurt with live active cultures and drinking kefir, a liquid yogurt that contains healthy bacteria. Some cereals and bars even contain probiotics, Sandquist says.
Eat every two to four hours. People with leukemia tend to lose weight because of a loss of appetite and nausea, but it’s very important to maintain the weight to stay strong, Sandquist says. If it’s hard to eat a big meal, eating small snacks or meals every two to four hours may help.
When you’re eating a healthful diet — and you’re getting exercise, managing stress, and getting enough sleep — you’ll know you’re doing everything you can to fight the disease.
Sept. 9, 2004 — Helping prevent childhood leukemia might be as simple as consuming oranges, bananas, orange juice, and an exotic spice called turmeric, according to researchers in Chicago and California.
First, here’s the scoop on the fruits.
“Regular consumption of oranges/bananas and orange juice during the first two years of life was associated with a reduction in risk of childhood leukemia diagnosed between the ages of 2 and 14,” say researcher Marilyn Kwan of the University of California at Berkeley, and colleagues.
Kwan’s team based its findings on the Northern California Childhood Leukemia Study, which ran from 1995 to 2002.
For every child with leukemia, a healthy child was included in the study for comparison. The researchers looked at 240 such pairs.
The kids’ biological mothers were asked how often their children ate nine foods or food groups in their first two years. The researchers focused on hot dogs/lunchmeats, beef/hamburger, vegetables, oranges/bananas, apples/grapes, orange juice, fruit juice, milk, and soda.
Oranges/bananas and orange juice had a “protective association” against childhood leukemia, say the researchers, who presented their findings at the Childhood Leukemia: Incidence, Causal Mechanisms, and Prevention conference in London this week.
The reason might be the high levels of potassium and vitamin C in the fruits, says Kwan’s team, which also found no link between childhood leukemia and hot dogs/lunchmeats.
Leukemia pill ‘can melt away’ cancer cells
According to the National Cancer Institute, there were an estimated 48,610 new cases of leukemia last year, with 23,720 deaths from the condition. Now, new research suggests that a pill taken twice daily could turn the blood cancer into a treatable disease and allow patients to avoid chemotherapy.
The team, led by researchers from Weill Cornell Medical College in New York, focused their research on chronic lymphocytic leukemia (CLL) – the second most common form of the disease among adults.
CLL is a blood and bone marrow disease that can occur when the bone marrow makes an excessive amount of lymphocytes – a type of white blood cell.
These lymphocytes become abnormal and are unable to effectively stave off infection. The increased number of these blood cells also leaves limited room for healthy white blood cells, red blood cells and platelets. This can cause anemia, infection and easy bleeding.
CLL is usually treated with chemotherapy drugs. Although the majority of patients respond to these drugs, the researchers say most patients relapse and need repeated cycles of the treatments.
With each cycle, the remission periods tend to decrease. The researchers say that as a result, patients often stop responding to treatment or are forced to stop because of severe side effects.
According to the investigators, these side effects are a result of the chemotherapy medication being unable to distinguish between healthy cells and cancer cells.
With this in mind, the research team set out to find an alternative treatment.
‘Remarkable’ results for idelalsib
For their study, published in The New England Journal of Medicine, the researchers tested a combination of two targeted medications – drugs that can attack cancer cells without damaging healthy cells – on 220 patients with CLL who were not able to undergo chemotherapy.
The combination treatments were:
- Rituximab and idelalsib, or
- Rituximab and a placebo pill.
The researchers found that compared with the group who received rituximab and a placebo pill, patients who received rituximab and idelalsib avoided disease progression for a longer period of time.
When monitoring the patients 6 months after treatment, 93% of patients who received treatment with rituximab and idelalsib did not suffer disease progression, compared with 46% of patients who were treated with rituximab and a placebo.
Furthermore, the investigators found that 81% of patients responded to treatment with rituximab and idelalsib, while only 13% responded to treatment with rituximab and a placebo.
And 1 year after the baseline of the study, 92% of patients treated with rituximab and idelalsib were still alive, compared with 80% of rituximab and placebo patients.
The research team says that the combination of rituximab and idelalsib proved so successful in patients that the study was stopped early in order to prescribe all patients the treatment.
Commenting on the findings, Dr. Richard Furman, of Weill Cornell Medical College and lead researcher of the study, says:
“We saw incredible responses in patients who used idelalisib. Their cancer quickly melted away. These types of responses were even seen in patients who didn’t respond to chemotherapy.”
Dr. Furman notes that chemotherapy-resistant patients tend to be the most difficult patients to treat. But he says that even these patients responded to the treatment within 1 week.
‘These drugs will change patients’ lives’
These new findings follow on from a phase II clinical trial that the team conducted last year, which found that ibrutinib – also a targeted cancer drug – was effective against mantle cell lymphoma. This is a rare form of leukemia.
Dr. Furman has already been using ibrutinib as the first treatment option for patients, allowing them to avoid chemotherapy completely.
He says that these most recent findings, combined with his past research, suggest that ibrutinib and idelalisib may overtake chemotherapy as the preferred treatment option for leukemia.
“These drugs will change the lives of many patients. Given the long-term toxicities of chemotherapy, leading to bone marrow failure, infections and death, moving this therapy up front in the treatment algorithm and providing it to all patients is the next step.”
Medical News Today recently reported on a study detailing how an infection-fighting cellular process may be a cause of childhood leukemia.
Avocado compound holds promise for treating leukemia
They are responsible for one of our favorite Mexican dips and can brighten up any salad, but a new study finds there may be much more to avocados; a compound found in the fruit could help tackle acute myeloid leukemia.
Share on PinterestAvocatin B – a compound in avocados – targets and destroys leukemia stem cells, according to the researchers.
Prof. Paul Spagnuolo, of the University of Waterloo in Ontario, Canada, and colleagues publish their findings in the journal Cancer Research.
Acute myeloid leukemia (AML) is a cancer that begins in the bone marrow, where blood stem cells (immature cells) turn into mature blood cells. In AML, the blood stem cells in the bone marrow become abnormal myeloblasts – a form of white blood cell – red blood cells or platelets.
It is estimated that more than 20,000 people in the US will be diagnosed with AML this year, and more than 10,000 people will die from the cancer.
Most common among people aged 65 and older, AML has a poor survival rate, with around 90% of seniors with the cancer dying within 5 years of diagnosis.
But according to Prof. Spagnuolo and colleagues, there is a compound in avocados – called avocatin B – that holds promise for a new treatment for AML.
Avocatin B targets and destroys leukemia stem cells
Using a high-throughput cell-based screen to assess the effects of avocatin B on human leukemia stem cells, the researchers found the compound selectively targets and destroys them while leaving healthy blood cells unscathed.
“Not only does avocatin B eliminate the source of AML, but its targeted, selective effects make it less toxic to the body, too,” explains Prof. Spagnuolo.
While the researchers say it is many years before avocatin B can be used in clinical settings to treat AML, they have teamed up with Canada’s Centre for Commercialization of Regenerative Medicine (CCRM) to file a patent for the compound for this use.
“It’s an exciting time for our lab,” says Prof. Spagnuolo. “With the help of CCRM we are now pursuing commercial partnership that would take avocatin B into clinical trials.”
Avocatin B falls into a category of compounds known as nutraceuticals, defined as food-derived products that have potential clinical benefits.
Prof. Spagnuolo and colleagues say they are one of very few research teams globally who are applying the vigorous drug-investigation processes incorporated within the pharmaceutical industry to nutraceuticals.
While most researchers investigate food or plant extracts for their potential clinical use, Prof. Spagnuolo says using nutraceuticals offers a more clear-cut insight.
“Extracts are less refined,” he says. “The contents of an extract can vary from plant to plant and year to year, depending on lots of factors – on the soil, the location, the amount of sunlight, the rain.”
“Evaluating a nutraceutical as a potential clinical drug requires in-depth evaluation at the molecular level,” he adds. “This approach provides a clearer understanding of how the nutraceutical works, and it means we can reproduce the effects more accurately and consistently. This is critical to safely translating our lab work into a reliable drug that could be used in oncology clinics.”
This is not the first study to hail avocados for their potential health benefits. In January, Medical News Today reported on a study claiming that eating one avocado daily as a part of a moderate-fat diet could reduce levels of “bad” cholesterol among people who are overweight or obese.
Our Knowledge Center article on the health benefits of avocado reveals some of the other health benefits the fruit may have.
New treatment of acute myeloid leukemia achieves remarkable results in a disease formerly with little hope
Every year almost 1000 Australians die of the disease and clinical trials into new therapies for older patients have largely failed.
A new Australian drug trial has achieved a remarkable result, clearing the bone marrow of leukaemia in almost 60% of patients.
The trial was considered so effective that the US Food and Drug Administration approved its use last November for the treatment of AML.
Kaye Oliver, 74, was the first patient in the world enrolled on this trial at the Alfred Hospital in 2015 — the results of which are published today in the Journal of Clinical Oncology.
Given little hope of survival beyond a few months at diagnosis, Kaye remains well and without evidence of the cancer four years later.
Associate Professor Andrew Wei, from the Alfred Hospital and Monash University Clinical School, commenced research in this area almost two decades ago at the Walter and Eliza Hall Institute of Medical Research. He is now the lead clinician/researcher on the international trial of the cancer drug, currently combined with cytarabine to treat older adults with AML.
Taken separately these drugs achieve little, according to Associate Professor Wei. Venetoclax alone led to a 19% response rate in a US trial and cytarabine had a similar result, he said.
“But combining LDAC with venetoclax in older patients led to a 54% response rate, with half the study population surviving longer than 10 months,” he added.
The trial tested 82 patients with a median age of 74 years and was conducted in Australia, Europe and the USA.
The current research is supported by another trial in older AML patients, which combined venetoclax with another drug, azacytidine and led to a 71% remission rate with an average life expectancy of almost 17 months.
Based on the early results of these two studies, the Food and Drug Administration in the US approved the use of these combination drug therapies in older people with AML on November 21 last year.
The drug combination acts on a protein prevalent in leukaemia cells called BCL-2 which controls the survival of the cells. Venetoclax acts by effectively switching off the protein and activating a self-destruct program in the cell.
Associate Professor Wei said that a randomised trial of the therapy, where patients on the therapy are compared to those who are not, has recently been completed and the results are awaited to support a submission to the Therapeutic Goods Association in Australia.
The findings are important not just because of the success of the treatment in a disease that, previously, was fatal, but because with an aging population AML is likely to become more prevalent in the future.
“AML arises due to mutations accumulating in the bone marrow over time. It also arises in patients who have previously had chemotherapy. With an expected doubling in the number of over people over 65 in the next 30 years, the need to find more effective treatments for this disease is paramount,” Associate Professor Wei said.
“AML research used to be likened to a ‘clinical trial graveyard’ because trials of new drugs into AML were rarely successful,” Associate Professor Wei said.
“It was widely seen as an untreatable and inevitably fatal condition for older patients by most doctors. These two new trials have given real hope to patients who previously had little.”
Current treatments for B-chronic lymphocytic leukemia (B-CLL) include purine analogues (fludarabine) and monoclonal antibodies (rituximab) (1). While people can live for years with B-CLL, there is no effective cure. Hence, new targeted therapies are vital to improving clinical outcomes for patients with B-CLL. In this issue of Clinical Cancer Research, Ghosh et al. (2) investigate, in the preclinical setting, a novel approach to treating B-CLL that combines two naturally-occurring compounds: curcumin and epigallocatechin-3-gallate (EGCG). Using natural compounds for the treatment of cancer is not new. Sixty-two percent of cancer drugs approved by the U.S. FDA between 1981 and 2002 were of natural origin (3). For example, all-trans retinoic acid, which is a vitamin A derivative, is a very effective treatment for acute promyelocytic leukemia. A wealth of data supports a role for curcumin, the active ingredient in the spice turmeric, as an anti-neoplastic agent (4,5). This work extends previous observations by examining the molecular pathways involved in curcumin-induced apoptosis of B-CLL cells. In particular, in primary CLL cultures, curcumin inhibited expression of pro-urvival molecules, including STAT3, Akt, and NF-κB, as well as the anti-apoptotic proteins Mcl-1 and XIAP. Curcumin also up-regulated the pro-apoptotic protein, BIM. Sequential administration of EGCG followed by curcumin resulted in increased CLL cell death and neutralized stromal protection.
Curcumin has impressive antioxidant, chemo-preventive, chemotherapeutic, and chemo-sensitizing activities (4,5). The apoptosis of B-CLL cells induced by curcumin is dose-dependent, and normal B lymphocytes are less sensitive to its cytotoxic effects than B-CLL cells (2,6). Curcumin induces PARP cleavage in primary B-CLL cells (2), reflecting the activation of programmed cell death. PARP cleavage is induced by curcumin in other tumor types, including pancreatic and colorectal cancer (7–9). Interestingly, the authors did not observe activation of upstream caspases following curcumin treatment. This differs from several other studies that demonstrate specific caspase-3 activation by curcumin in HL-60 and other tumor cell lines (4,5,10). In primary B-CLL, the mechanism of PARP cleavage remains unclear. Other cellular events that contribute to curcumin-induced apoptosis include the release of cytochrome c from the mitochondrial membrane. This occurs in several different cell lines following treatment with curcumin, as do changes in mitochondrial membrane potential (4,5). The role of mitochondrial events in curcumin-induced apoptosis in B-CLL cells was not examined in this study.
Curcumin also inhibits the constitutive activation of pro-survival pathways, some of which are preferentially active in primary B-CLL cells, including STAT3, Akt, and NF-κB. Constitutive activation of STAT3 has been reported in several cancers, including breast, prostate, head and neck squamous cell carcinoma, multiple myeloma, and pancreatic cancer (4,8,11). STAT3 plays an important role in the induction of anti-apoptotic genes and angiogenic factors, and is vital to various cytokine signaling pathways (4,5,11). Curcumin effectively inhibits constitutive STAT3 phosphorylation in B-CLL (2), agreeing with other studies which demonstrate that curcumin is an effective inhibitor of STAT3 function (4,5,11). Mcl-1, a pro-survival gene downstream of STAT3, is also down-regulated by curcumin in primary B-CLL (2). Constitutive phosphorylation of Akt is down-regulated by curcumin in primary B-CLL cells (2) and other tumors including non-Hodgkin’s B cell lymphoma, prostate cancer, and renal cell carcinoma (4). However, curcumin can also induce its pro-apoptotic and anti-proliferative effects without perturbing Akt phosphorylation status (5,7,12).
A pro-survival molecule that seems to be universally inhibited by curcumin is the NF-κB transcription factor. NF-κB is down-regulated by curcumin in many different cancers (4–8,11). Constitutive phosphorylation of IκBα in primary B-CLL cells is inhibited by curcumin, indicating that genes downstream of NF-κB should be inhibited in these cells. Indeed, XIAP, a downstream target of NF-kB, is down-regulated in primary B-CLL following curcumin treatment (2). The lack of down-regulation of Bcl-2 by curcumin is an interesting finding considering previous work demonstrating that Bcl-2 is a direct transcriptional target of NF-κB and is down-regulated by curcumin (4,5). BIM, a pro-apoptotic protein, is up-regulated by curcumin in primary B-CLL. Hence, curcumin can down-regulate survival pathways and up-regulate apoptotic pathways in B-CLL.
What happens to the effectiveness of curcumin treatment when B-CLL cells are co-cultured in the context of the stromal environment? Stromal cells typically maintain an anti-apoptotic environment through direct contact and through soluble mediators. Co-culture of B-CLL cells with stromal cells provided substantial protection from curcumin-induced apoptosis at lower curcumin doses, but not at higher doses (20μM) (2). These results lend insight into the effect of the host environment on curcumin-induced apoptosis, and also indicate that higher doses of curcumin may be required to achieve the level of apoptosis seen in vitro.
It is unlikely that curcumin alone will be an effective treatment for B-CLL due to incomplete apoptotic responses. Curcumin itself enhances the effectiveness of a variety of compounds, including vincristine in B-CLL in vitro (6). Natural agents, like curcumin, are desirable candidates for adjuncts to chemotherapy because of their negligible toxicities. EGCG, the principal polyphenol in green tea, induces apoptosis in B-CLL cells in vitro through partial inhibition of VEGFR1 and VEGFR2 phosphorylation, and also by caspase-3 activation and PARP cleavage. Bcl-2 is down-regulated by EGCG, as is Mcl-1 and XIAP (2). Treatment of primary B-CLL cells with the combination of EGCG and curcumin was investigated. The sequential administration of EGCG followed by curcumin was the most effective treatment combination; whereas simultaneous administration resulted in antagonistic effects.
EGCG and curcumin target many of the same molecular pathways, including induction of PARP cleavage and the inhibition of telomerase activity (2,4,5,10). While EGCG and curcumin down-regulate many common survival pathways, including STAT3, Akt, NF-κB, and the anti-apoptotic genes Mcl-1 and XIAP, not all of their targets overlap (Figure 1.). For example, while both compounds induce PARP cleavage and apoptosis in B-CLL, EGCG accomplishes this through activation of caspase-3, while curcumin does not induce caspase-3 activation in these cells (2). Thus, these two natural agents have many pathways in common, but can diverge from each other as well, and can potentially exhibit opposing effects. Hence, further study of the molecular mechanisms involved in the anti-proliferative and pro-apoptotic effects of these agents is warranted.
Bone marrow stromal cells provide pro-survival and anti-apoptotic signals to B-CLL cells. Curcumin and EGCG inhibit pro-survival pathways (red) and induce pro-apoptotic pathways (green). GF=growth factor, GFR=growth factor receptor, 67LR=67kDa laminin receptor, BIM=Bcl-2-interacting mediator of apoptosis, XIAP=X linked inhibitor of apoptosis, PARP= poly (ADP ribose) polymerase, P.C.D.=programmed cell death, VEGFR=vascular endothelial cell growth factor receptor, b.m=bone marrow, STAT3=signal transducer and activator of transcription 3, Mcl-1=myeloid cell leukemia–1, IKK=inhibitory κB kinase.
Clinical trials with curcumin and EGCG as individual agents, or in combination with standard chemotherapy, are already underway in several cancers (4,5,11, and clinical trials.gov). A phase II clinical trial of curcumin in advanced pancreatic cancer was recently published by our group and demonstrated a patient with a 73% tumor regression, and another patient who was stable on curcumin for more than 2.5 years (11, and Kurzrock personal communication). No side effects were observed. However, overall response rates were low, perhaps because curcumin absorption after oral administration is poor (11).
Oral green tea extracts have been taken voluntarily by patients with B-CLL, and EGCG has already begun phase I clinical trials in Rai stage 0-II patients with B-CLL (2). The current study provides rationale for the combination of curcumin plus EGCG in the clinical setting, and provides information concerning the dose and administration of these two compounds. A constant ratio of 10:1 (EGCG:curcumin) was established as effective at inducing apoptosis in B-CLL. Sufficiently high doses of EGCG and of circulating curcumin will be necessary to overcome stromal protection in vivo. The data also indicate that sequential treatment of B-CLL with EGCG followed by curcumin is preferable to simultaneous treatment, and is crucial to the efficacy of the combination of these two compounds. Simultaneous treatment of B-CLL cells with EGCG and curcumin resulted in antagonistic effects. Ultimately, however, the optimal studies will probably require the use of a curcumin compound modified to enhance its bioavailability. Encapsulating curcumin in liposomes allows it to be administered systemically, and several groups are working on altering curcumin to increase its absorption when taken orally (4,5,9,13). Based on the biologic properties of curcumin alone or in combination with EGCG or other compounds, these second generation curcumin moieties should be explored for the treatment of CLL and other cancers.
DIET GUIDELINES FOR IMMUNOSUPPRESSED PATIENTS
Food safety is important during and after cancer treatments. The immune system is often weakened by cancer treatments, making the body more susceptible to foodborne illnesses.
Neutropenia is a condition where you have lower-than-normal levels of neutrophils (a type of white cell). If you have neutropenia, your doctor may suggest for you to follow special guidelines, which can help protect you from bacteria and other harmful organisms found in some food and drinks.
If you had a stem cell transplant, your diet may be stricter than that of a patient who had chemotherapy or radiation therapy and no transplant.
Diet guidelines published by institutions or doctors about handling food safely may also recommend avoiding foods that are more often associated with illness.
Basic Guidelines to Follow
Avoid raw or rare meat and fish and uncooked or undercooked eggs. Cook meat until it’s well-done.
Thoroughly cook eggs (no runny yolks) and avoid foods containing raw eggs such as raw cookie dough or homemade mayonnaise.
Avoid unpasteurized beverages, such as fruit juice, milk and raw milk yogurt.
Avoid salad bars and buffets.
Refrigerate pate, cold hot dog or deli meat (including dry-cured salami and deli prepared salads containing these items), eggs or seafood.
Consume only pasteurized milk, yogurt, cheese and other dairy products.
Avoid soft mold-ripened and blue-veined cheeses such as Brie, Camembert, Roquefort, Stilton, Gorgonzola and Bleu or other soft, unpasteurized cheeses.
Avoid raw sprouts, such as alfalfa sprouts.
Wash fresh fruits and vegetables before peeling.
Avoid well water unless it has been tested, filtered, or boiled for one minute before drinking. At home, it’s okay to drink tap water or bottled water.
Your healthcare team may refer to these guidelines as a “neutropenic diet” or you may have encountered the term on your own. This diet was supposed to help individuals with neutropenia learn how to decrease exposure to bacteria and other harmful organisms found in some foods. However, a universally-accepted definition of what foods should be included was never developed.
In a review of studies, the neutropenic diet was never proven to decrease exposure to bacteria in foods. This diet does not seem to benefit patients in any way. Safe preparation and handling of foods is more important than restricting intake of specific food groups, as balanced diet and nutrition is important for coping with chemotherapy and other treatments.
Food guidelines for immunosuppressed patients vary among cancer centers. Ask your doctor for any special instructions.
- Download or order The Leukemia & Lymphoma Society’s free fact sheet, Food and Nutrition Facts.