Frances S. KENNY1, Julia M.W. GEE3, Robert I. NICHOLSON3, Ian O. ELLIS2, Teresa M. MORRIS4, Susan A. WATSON4,
Richard P. BRYCE5 and John F.R. ROBERTSON1*
1 Professorial Unit of Surgery, City Hospital, Nottingham, United Kingdom
2 Department of Histopathology, City Hospital, Nottingham, United Kingdom
3 Tenovus Cancer Research Centre, University of Wales College of Medicine, Cardiff, United Kingdom
4 Cancer Studies Unit, Department of Surgery, Queen’s Medical Centre, Nottingham, United Kingdom
5 Scotia Pharmaceuticals, Stirling, United Kingdom
Gamma linolenic acid (GLA) possesses a number of selective
anti-tumour properties including modulation of steroid
receptor structure and function. We have investigated the
effect of dietary GLAon the growth, oestrogen receptor (ER)
expression and fatty acid profile of ER1ve human breast
cancer xenografts. Experimental diets A, B, C, D were commenced
after subcutaneous implantation of 40 female nude
mice with the MCF-7 B1M cell line (Group A 5 control diet:
B 5 control diet 1 GLA supplement: C 5 control diet 1
tamoxifen: D 5 control diet 1 GLA 1 tamoxifen; 10 mice/
group). The mice were terminated when tumour cross-sectional
area reached 250 mm2. ER H-scores were assessed by
immunohistochemical assay and fatty acid profiles by gasliquid
chromatography of termination tumour samples.
Groups C and D displayed significantly slower tumour
growth (p5.0002, p5.0006) with trend for slower growth in
B (p 5 .065) compared to control Group A. ER was significantly
reduced in all groups compared to A (p < .0001) with
Group D (combined therapy) displaying markedly lower ER
expression than with either therapy alone (p5.0002). There
were significantly raised levels of tumour GLA and metabolites
in the two groups (B and D) receiving GLA (p < .0001).
This xenograft model of ER1ve breast cancer has demonstrated
significantly lower tumour ER expression in those
groups receiving GLA, an effect which appears to be additive
to the reduced ER expression resulting from tamoxifen
alone. The effects of GLA on ER function and the possibility
of synergistic inhibitory action of GLA with tamoxifen via
enhanced down-regulation of the ER pathway require further
investigation.
© 2001 Wiley-Liss, Inc.
Key words: gamma linolenic acid; tamoxifen; oestrogen receptor;
endocrine response; breast cancer
Gamma linolenic acid (GLA) is a Gamma linolenic acid (GLA) is a member of the n-6 family of
essential polyunsaturated fatty acids (EFAs) found in evening
primrose and borage oils. GLA is well established as an effective
treatment for benign cyclical mastalgia where the mechanism of
action is thought to involve attenuation of breast hormone receptor
sensitivity to circulating oestrogens.1 More recently GLA and
other n-6 and n-3 EFAs have raised interest as novel anti-cancer
agents as they have been shown to exert a number of selective
cytotoxic and anti-proliferative effects on human cancer cells
without affecting normal tissues.2 In vitro experiments have identified
a variety of EFA anti-tumour actions. These include direct
cytotoxicity via liberation of free radicals and lipid peroxides;
up-regulation of cell surface adhesion molecules; inhibition of
angiogenesis; induction of apoptosis; interaction with secondary
messenger and cell-signalling pathways and modulation of cellular
receptor structure and function including steroid hormone receptors.
3 A number of animal studies have demonstrated inhibitory
effects of dietary supplementation of EFAs on experimental tumours.
4–6 More recently, pilot clinical trials of GLA have
achieved useful tumour regression and improved quality of life
with negligible systemic toxicity in a variety of advanced solid
malignancies.7–10
Archive for the ‘docetaxel’ Category
EFFECT OF DIETARY GLA1/2TAMOXIFEN ON THE GROWTH, ER EXPRESSION AND FATTY ACID PROFILE OF ER POSITIVE HUMAN BREAST CANCER XENOGRAFTS
Category Breast Cancer, docetaxel, GLA omega-6 oil, Tamoxifen
A novel controlled release formulation for the anticancer drug paclitaxel (Taxol®): PLGA nanoparticles containing vitamin E TPGS
Category docetaxel, Docetaxel (deoxycytidine drug), Vitamin E (succinate)
aDivision of Bioengineering, The National University of Singapore, 9 Engineering Drive 1, Singapore 117576, Singapore
b Department of Chemical and Environmental Engineering, The National University of Singapore, 9 Engineering Drive 1, Singapore 117576, Singapore
Abstract
Paclitaxel (Taxol®) is one of the best antineoplastic drugs found from nature in the past decades. Like many other anticancer drugs, there are difficulties in its clinical administration due to its poor solubility. Therefore an adjuvant called Cremophor EL has to be employed, but this has been found to cause serious side-effects. However, nanoparticles of biodegradable polymers can provide an ideal solution to the adjuvant problem and realise a controlled and targeted delivery of the drug with better efficacy and fewer side-effects. The present research proposes a novel formulation for fabrication of nanoparticles of biodegradable polymers containing d-α-tocopheryl polyethylene glycol 1000 succinate (vitamin E TPGS or TPGS) to replace the current method of clinical administration and, with further modification, to provide an innovative solution for oral chemotherapy. In the modified solvent extraction/evaporation technique employed in this research, the emulsifier/stabiliser/additive and the matrix material can play a key role in determining the morphological, physicochemical and pharmaceutical properties of the produced nanoparticles. We found that vitamin E TPGS could be a novel surfactant as well as a matrix material when blended with other biodegradable polymers. The nanoparticles composed of various formulations and manufactured under various conditions were characterised by laser light scattering (LLS) for size and size distribution, scanning electron microscopy (SEM) and atomic force microscopy (AFM) for morphological properties, X-ray photoelectron spectroscopy (XPS) for surface chemistry and differential scanning calorimetry (DSC) for thermogram properties. The drug encapsulation efficiency (EE) and the drug release kinetics under in vitro conditions were measured by high performance liquid chromatography (HPLC). It was concluded that vitamin E TPGS has great advantages for the manufacture of polymeric nanoparticles for controlled release of paclitaxel and other anti-cancer drugs. Nanoparticles of nanometer size with narrow distribution can be obtained. A drug encapsulation efficiency as high as 100% can be achieved and the release kinetics can be controlled.
Author Keywords: Biodegradable polymer; Drug delivery; d-α-Tocopheryl polyethylene glycol 1000 succinate; Emulsifier; Surfactant stabiliser; Taxol
Abbreviations: AFM, atomic force microscopy; DCM, dichloromethane; DSC, differential scanning calorimetry; FDA, US Food and Drug Administration; HPLC, high performance liquid chromatography; LLS, laser light scattering; PBS, phosphate-buffered saline; PLGA, poly (lactic-co-glycolic acid); PVA, polyvinyl alcohol; SEM, scanning electron microscopy; Vitamin E TPGS or TPGS, d-α-tocopheryl polyethylene glycol 1000 succinate; XPS, X-ray photoelectron spectroscopy
Article Outline
- 2. Materials and methods
- 2.1. Materials
- 2.2. Nanoparticle preparation
- 2.3. Encapsulation efficiency
- 2.4. Nanoparticle characterisation
- 2.5. In vitro release study
Curcumin found safe with Docetaxol and found to enhance gemcitabine
Category CURCUMIN, docetaxel, Gemcitabine
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All-trans retinoic acid potentiates Taxotere-induced cell death mediated by Jun N-terminal kinase in breast cancer cells
Category all-trans retinoic acid (ATRA), Breast Cancer, docetaxel
Oncogene (2004) 23, 426–433. doi:10.1038/sj.onc.1207040
1Department of Medicine, Division of Oncology/Hematology, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, MSB I-596, 185 South Orange Avenue, Newark, NJ 07103, USA
Correspondence: R Wieder, E-mail: wiederro@umdnj.edu
Received 4 July 2003; Revised 21 July 2003; Accepted 22 July 2003.
Abstract
Taxotere is a cytotoxin effective in treating breast and prostate cancer. It stabilizes microtubules and causes catastrophic cell cycle arrest in G2/M. Taxanes also initiate apoptosis by activating signal pathways, such as the jun N-terminal kinase (JNK) pathway. Strategies aimed at potentiating cell death signaling may improve their efficacy while lessening the potential side effects. We reported that all-trans retinoic acid (ATRA) potentiated taxane-mediated cell death. Here we investigated whether ATRA potentiates cell death signaling through the JNK pathway. Activation of JNK by Taxotere 0.01, 0.1 and 1.0 
M was observed at 24 h in adherent cells and increased at 48 h. Taxotere 0.001 M-induced JNK activation started after 48 h and increased at 72 h. The timing and intensity of PARP cleavage was similar to that of JNK activation. JNK activation and PARP cleavage induced by 30 nM Taxotere at 48 h were reversed by curcumin, PD169316 and SP600125, JNK inhibitors in order of progressive specificity. None of these inhibitors had an effect on p38 or ERK phosphorylation. All three inhibitors reversed Taxotere-induced phosphorylation of Bcl-2. ATRA induced JNK activation at 24, 48 and 72 h. Incubating cells with ATRA 0.01 M for 3 days prior to Taxotere treatment potentiated Taxotere-induced JNK activation 24 and 48 h later, an effect sustained for 72 h. Cytotoxicities from 3-day ATRA 0.01 M incubations were synergistic with subsequent 1-h Taxotere 0.01, 0.1 and 1.0 M incubations in breast cancer cell lines MCF-7 and MDA-MB-231 and in prostate cancer cell lines LNCaP and PC-3, and additive in breast cancer cell line SK-Br-3. These data demonstrate the potentiation of Taxotere-induced cell death by ATRA pretreatment in breast and prostate cancer cells, and support a mechanism through accentuated and sustained JNK activation.
Keywords:
apoptosis, JNK, retinoic acid, Taxotere, breast cancer
Epigallocatechin-3-gallate Inhibits Activation of HER-2/neu and Downstream Signaling Pathways in Human Head and Neck and Breast Carcinoma Cells
Category Breast Cancer, docetaxel, Docetaxel (deoxycytidine drug), Green Tea (Epigallocatechin-3-gallate), Head and Neck
+ Author Affiliations
Abstract
Overexpression of the HER-2/neu receptor (HER-2) is associated with a poor prognosis in patients with breast carcinoma and also in patients with head and neck squamous cell carcinoma (HNSCC). In a previous study on HNSCC cell lines, we found that epigalocathechin-3-gallate (EGCG), a major biologically active component of green tea, inhibited activation of the epidermal growth factor receptor (EGFR) and thereby inhibited EGFR-related downstream signaling pathways in HNSCC cells. In the present study, we examined the effects of EGCG on activation of the HER-2 receptor in human HNSCC and breast carcinoma cell lines that display constitutive activation of HER-2. Treatment of these cells with 10 or 30 μg of EGCG, respectively, doses that cause 50% inhibition of growth, markedly inhibited the phosphorylation of HER-2 in both cell lines. This was associated with inhibition of Stat3 activation, inhibition of c-fos and cyclin D1 promoter activity, and decreased cellular levels of the cyclin D1 and Bcl-XL proteins. Although these concentrations of EGCG are quite high, we found that concentrations of 0.1–1.0 μg/ml, which are in the range of plasma concentrations after administering a single oral dose of EGCG or a green tea extract, markedly enhanced the sensitivity of both types of cell lines to growth inhibition by Taxol, a drug frequently used in the treatment of breast carcinoma and HNSCC. These results, taken together with previous evidence that EGCG also inhibits activation of the EGFR in carcinoma cells, suggest that EGCG may be useful in treating cases of breast carcinoma and HNSCC in which activation of the EGFR and/or HER-2 plays important roles in tumor survival and growth.
- Received December 3, 2002.
- Revision received March 3, 2003.
- Accepted March 21, 2003.
Taxol Does Not Help Prevent Recurrence of Most Common Breast Cancers – Part Two
Category Breast Cancer, docetaxel
| (Previously we began a two-part newsletter on a newly-released study concluding that the chemotherapy drug Taxol, which is commonly used in the adjuvant treatment of breast cancer, brings no benefit to the majority of women for whom it is currently prescribed. We conclude the discussion, with references.)
“The days of ‘one size fits all’ therapy for patients with breast cancer are coming to an end,” said Anne Moore, MD, of Weill Cornell Medical College, who wrote an editorial accompanying the study in the New England Journal of Medicine.
“We should have done this [analysis, ed.] a long time ago,” said study co-author, Donald Berry, MD, of the University of Texas M.D. Anderson Cancer Center, but the tools were lacking and researchers now have the advantage of longer follow-up of these women. Now, he added, “We can begin to use the biology of the cancer to decide whether the chemotherapy will work” before subjecting women to it.
“We want to make sure these data are correct before withholding it [Taxol] from some patients… the stakes are high,” said the lead researcher, Daniel Hayes, MD, of the University of Michigan. “On the other hand, we don’t want to keep a therapy that doesn’t work.”
Should women with HER2-negative and ER-positive cancers reject the use of Taxol? Probably, according to the current data. Yet, despite this study’s surprising findings, there are indications that many doctors will continue to give Taxol to most women with breast cancer, according to Julie Gralow, MD, of the University of Washington School of Medicine. Some doctors fear lawsuits if the cancer recurs and chemotherapy was withheld. “It’s just so much easier to give the chemotherapy and know you’ve been super-aggressive.”
Women who have less aggressive types of breast cancer should also realize that the absolute benefit of chemotherapy in this situation might in any case be rather small. For instance, take the case of a 50-year-old woman of average health, who has a 1.1-2.0 centimeter, grade I tumor, and 1-3 positive lymph nodes. According to adjuvantonline.com, the risk assessment and prognostic tool used by many oncologists, this woman will typically have an 86.6 percent chance of being alive 10 years later, even if she does not receive adjuvant chemotherapy treatment after surgery. Her chance of dying of cancer over this 10 year period is 8.8 percent and her chance of dying of other causes in the same period is 4.6 percent.
If she takes hormonal therapy alone (typically, tamoxifen or an aromatase inhibitor) she will improve her chances of being alive at 10 years by 2.7 percent. If she takes adjuvant chemotherapy, such as ACT, she will improve her chances of being alive by a similar 2.8 percent. But if she takes both hormonal therapy and chemotherapy then her odds improve by 4.6 percent. In other words, chemo improves the odds of survival over surgery plus hormonal treatment by just 1.7 percent.
If this woman opted for the older CMF regimen (instead of ACT or one of the other so-called second or third generation chemotherapy regimens) then her benefit would be 1.4 percent and the improvement over hormonal treatment alone would be 0.9 percent. According to adjuvantonline.com, she would thereby lose a mere 0.8 percent survival benefit. But at least she would avoid the more serious potential side effects of both Adriamycin and Taxol.
Of course, this is just one scenario out of a large number of possibilities. Tumors vary in their size, grade, genetic characteristics, degree of invasiveness, etc. And, yes, there are clearly instances in which aggressive adjuvant chemotherapy is justifiable. But most of those cases involve HER2 positive and ER negative tumors, where, as we have seen, Taxol (and also Herceptin) can improve the survival figures and make them closer to those experienced by women with the more common HER2 negative and ER positive tumors.
In addition, I would call the reader’s attention to a pending, as yet unpublished, study that is still hanging over the heads of oncologists. According to reputable press reports, scientists affiliated with the BCIRG 006 clinical trial have found that anthracyclines such as Adriamycin (doxorubicin) also provide no benefit to 92 percent of breast cancer patients (Bazell 2007). Only 8 percent of all women with breast cancer – those who over-express a specific gene called Topoll-2 (topoisomerase II alpha) – are said to benefit from anthracycline-based chemotherapy, since these drugs work by directly targeting Topoll-2. This paper was fully discussed in a previous newsletter:
http://www.cancerdecisions.com/070107.html
If that is the case, then it appears that Adriamycin – nicknamed “the red death” by some oncologists – will also need to be eliminated from the adjuvant treatment of the great majority of women with breast cancer. From the much-vaunted ACT regimen this would then leave only cyclophosphamide (Cytoxan), an old and somewhat less toxic drug that was first approved by the Food and Drug Administration (FDA) in November 1959 – 48 years ago this month! Wouldn’t this be an opportune time for oncologists to step up efforts to individualize the treatment of all patients – and to seriously examine the use of nontoxic treatments from the realm of complementary and alternative medicine?
References:Casarella WJ. A patient’s viewpoint on a current controversy. Radiology 2002;224:927
Hayes DF, Thor AD, Dressler LG, et al. HER2 and Response to Paclitaxel in Node-Positive Breast Cancer. N Engl J Med 2007;357:1496-1506.
FDA tabulation of Taxol side effects:
“Red death” attribution is taken from Jerome Groopman’s book, How Doctors Think. Available at:
Robert Bazell’s report on the problems facing the use of Adriamycin can be found at:
My book, Questioning Chemotherapy, is available in bookstores or from Amazon: |
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| Last Updated ( Friday, 20 June 2008 ) |
Resveratrol confers resistance against taxol via induction of cell cycle arrest in human cancer cell lines.
Category docetaxel, Resveratrol
Source
Department of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, PR China.
Abstract
Resveratrol, which is highly concentrated in the skin of grapes and is abundant in red wine, has been demonstrated to account for several beneficial properties, including antioxidant, anticoagulant, anti-inflammatory and anticancer effects. Taxol is a microtubule-stabilizing drug that has been extensively used as effective chemotherapeutic agents in the treatment of solid tumors. Here, we investigated whether the combination of the two compounds would yield increased antitumor efficacy in human cancer cells. Unexpectedly, resveratrol effectively prevented tumor cell death induced by taxol in 5637 bladder cancer cells. This pronounced antagonistic function of resveratrol against taxol was associated with changes in multiple signal transduction pathways, but not with tubulin polymerization. Importantly, cell cycle analysis showed that resveratrol prevented the cells from entering into mitosis, the phase in which taxol exerts its action. Furthermore, resveratrol blocked the cytotoxic effects of vinblastine but not cisplatin in 5637 cells. Interestingly, resveratrol pre-treatment followed by taxol resulted in synergistic cytotoxicity. Finally, we extended our studies to various human cancer cell lines. Taken together, our results indicate that resveratrol may have the potential to negate the therapeutic efficacy of taxol and suggest that consumption of resveratrol-related products may be contraindicated during cancer therapy with taxol.
The flavonoid quercetin transiently inhibits the activity of taxol and nocodazole through interference with the cell cycle.
Source
Pathobiology Department, Tuskegee University, College of Veterinary Medicine, Nursing and Allied Health, Tuskegee, Alabama 36088, USA. tsamuel@tuskegee.edu
Abstract
Quercetin is a flavonoid with anticancer properties. In this study, we examined the effects of quercetin on cell cycle, viability, and proliferation of cancer cells, either singly or in combination with the microtubule-targeting drugs taxol and nocodazole. Although quercetin induced cell death in a dose-dependent manner, 12.5-50 μM quercetin inhibited the activity of both taxol and nocodazole to induce G2/M arrest in various cell lines. Quercetin also partially restored drug-induced loss in viability of treated cells for up to 72 h. This antagonism of microtubule-targeting drugs was accompanied by a delay in cell cycle progression and inhibition of the buildup of cyclin-B1 at the microtubule organizing center of treated cells. However, quercetin did not inhibit the microtubule targeting of taxol or nocodazole. Despite the short-term protection of cells by quercetin, colony formation and clonogenicity of HCT116 cells were still suppressed by quercetin or quercetin-taxol combination. The status of cell adherence to growth matrix was critical in determining the sensitivity of HCT116 cells to quercetin. We conclude that although long-term exposure of cancer cells to quercetin may prevent cell proliferation and survival, the interference of quercetin with cell cycle progression diminishes the efficacy of microtubule-targeting drugs to arrest cells at G2/M.
- PMID:
- 21058190
- [PubMed - indexed for MEDLINE]
- PMCID: PMC3021775
- [Available on 2011/11/
High-throughput screen finds compounds that regulate cancer cell invasion
Category Bioinformatics, CDK5, docetaxel, genetic research, Individualized treatment, Metastases, paclitaxel, Personalized, Robotic chemical genomics, Targeted Cancer Therapy, taxol, taxotere, Tumor biomarkers, Understanding Cancer
Related images
(click to enlarge)
Metastasis—the spread of cancer from the place where it first started to another place in the body—is the most common reason that cancer treatments fail. To metastasize, some types of cancer cells rely on invadopodia, cellular membrane projections that act like feet, helping them “walk” away from the primary tumor and invade surrounding tissues. To determine how cells control invadopodia formation, scientists at Sanford-Burnham Medical Research Institute (Sanford-Burnham) screened a collection of pharmacologically active compounds to identify those that either promote or inhibit the process. The study, led by Sara Courtneidge, Ph.D. and postdoctoral researcher Manuela Quintavalle, Ph.D. in collaboration with scientists in Sanford-Burnham’s Conrad Prebys Center for Chemical Genomics (Prebys Center), revealed compounds that inhibit invadopodia formation without causing toxicity. The search also turned up several other compounds that increased the number of invadopodia. Two major findings came out of this research. First, several of the newly identified invadopodia inhibitors targeted a family of enzymes called cyclin-dependent kinases (Cdks), revealing a previously unrecognized role for Cdks in invadopodia formation. Secondly, one of the pro-invadopodia compounds was the chemotherapeutic agent paclitaxel—a finding that might have implications for the drug’s current use in treating cancer. These findings will appear online July 26 in Science Signaling.
“Previous studies by our group and others have demonstrated that we might be able to target invadopodia to prevent cancer cell invasiveness,” said Dr. Courtneidge, professor and director of the Tumor Microenvironment Program in Sanford-Burnham’s NCI-Designated Cancer Center. “In this study, we established a cell-based screening assay to help us identify regulators of invadopodia formation.”
Dr. Courtneidge’s group has been studying invadopodia for a number of years with the goal of unraveling how they regulate tumor cell invasion. Sanford-Burnham’s Prebys Center provided them with expertise in chemical genomics, the robotic technology necessary to rapidly and reproducibly screen more than 1,000 compounds with known pharmacological activity in cell-based assays, and automated microscopy capable of detecting and measuring invadopodia formation.
This screening study identified several compounds that block invadopodia, and therefore cancer cell invasion. The team was surprised to find that many of these compounds targeted Cdks, a family of enzymes that were not previously associated with invadopodia. In follow-up experiments, the researchers demonstrated that one of these enzymes, Cdk5, is required for the formation and function of invadopodia and for cellular invasion, important steps in cancer metastasis. Cdk5 is highly expressed in neurons, where it’s involved in neuronal migration and outgrowth, but this is the first time the enzyme has been implicated in invadopodia formation.
Taking the study a step further, Drs. Courtneidge and Quintavalle and the team also worked out how Cdk5 promotes invadopodia formation. Cdk5′s action leads to the degradation of another protein called caldesmon. Caldesmon was previously shown to negatively regulate invadopodia, so Cdk5 essentially removes that brake. That’s why the Cdk inhibitors identified in the screening study also inhibited invadopodia.
Another pharmacologically active compound shown by the screen to regulate invadopodia was paclitaxel, a drug currently used to treat patients with many forms of cancer. Paclitaxel’s anti-tumor activity is based on its ability to bind and stabilize microtubules, one component of the cellular cytoskeleton, thereby halting cell division and inducing cellular suicide. In this study, paclitaxel promoted invadopodia formation and cancer cell invasion. This makes sense because invadopodia formation also depends on microtubules, which are stabilized by paclitaxel. These results raise the concern that continued treatment with paclitaxel might be counterproductive in cancer patients who aren’t responding well to the drug or in cases where the tumor has not yet been removed. Moreover, paclitaxel could actually provoke cancer metastasis in these patients.
“Although our results suggest paclitaxel might increase metastasis, we also observed that the drug did not promote invasive behavior in cells treated with an invadopodia inhibitor,” said Dr. Courtneidge. “This defines a potential clinical path for testing inhibitors in the context of paclitaxel treatment. In other words, a patient could still benefit from paclitaxel’s cancer cell-killing effect if physicians also have the ability to add a therapeutic invadopodia inhibitor when resistance develops.”
This study provides the proof-of-concept that the identification of invadopodia regulators might also lead to new strategies for controlling metastatic cancer growth.
Source: Sanford-Burnham Medical Research Institute
What should breast cancer patients eat during Taxol (paclitaxel) chemotherapy?
Category Breast Cancer, docetaxel, Drug Interactions, Vitamins and Supplements
Many breast cancer patients who under chemotherapy are given Taxol (paclitaxel) as part of their regimen. Chemotherapy is designed to destroy any remaining cancer cells in the breast and the remainder of the body before or after surgery. Chemotherapy is effective in improving breast cancer survivorship: numerous studies have found that it protects against breast cancer recurrence and metastases in other organs of the body. Please discuss this article with your oncologist before starting Taxol or any other taxane therapy (e.g., docetaxel (Taxotere)).
Taxol and other taxanes can result in side effects such as hair loss, bone marrow suppression, nausea, fatigue, muscle and joint pain, and serious infections. While obtaining relief from these side effects obviously is desirable, it is very important for breast cancer patients to avoid consuming foods or taking supplements that will lessen the cytotoxic impact of chemotherapy on breast cancer cells. While various micronutrients found in fruits, vegetables and other foods have been shown to help protect against breast cancer development and metastasis, some of the same micronutrients might enable breast cancer cells to survive chemotherapy.
Therefore, the strategy we recommend during chemotherapy and for the following month is to consume the foods recommended below, as well as those listed on the bland chemotherapy diet (also below), while limiting or avoiding the foods that should not be consumed while on Taxol (as well as those on our avoid list).
Foods that enhance the effectiveness of Taxol
The following foods are very good sources of compounds that have been shown to increase the anti-cancer effects of Taxol:
In addition, sour cherries, olive oil and vitamin D might relieve joint and muscle pain, although their effectiveness has not specifically been studied in the context of taxane chemotherapy.
Foods and other products that should not be used during Taxol chemotherapy
The following foods and supplements have been found either to interfere with the effectiveness of Taxol or, in the case of raw shellfish, should not be consumed by those with impaired immunity:
- Açaí berries
- Grapefruit
- Hormone replacement therapy, including bioidentical or natural hormones
- Mint tea
- Multivitamins & antioxidant supplements
- Sage
- Shellfish, raw
Bland diet for use during Taxol chemotherapy
The foods listed below have been selected based on our research concerning their antimutagenic, antioxidant, and cancer-protective properties. The list de-emphasizes antimutagenic and high-antioxidant foods such as brightly colored fruits and vegetables, while featuring bland, as well as somewhat bitter-tasting foods that have no known carcinogenic effects. Select as wide a variety of these foods as possible and consume any one of them in moderation in addition to the foods recommended above.
Overcoming Taxol resistance
There is limited evidence that certain foods might be beneficial for those on longer-term Taxol chemotherapy. While initial responses are often very favorable, most patients eventually develop resistance to Taxol. One study has demonstrated that it is possible to overcome Taxol resistance in breast cancer cells the laboratory. Please see the related news story.
Additional comments
Regular exercise has been shown to reduce fatigue in cancer patients undergoing chemotherapy. However, one study suggested that intense or prolonged physical activity a couple of days before the start of radiation or chemotherapy has significant potential to reduce the benefits of the treatments. Based on the available evidence, light aerobic exercise appears advisable during treatment with Taxol.
We caution against taking curcumin, EGCG, GLA, I3C, DIM, luteolin, quercetin or resveratrol in supplement form because of the possibility of unintended consequences. Safe and effective dosages for these supplements during chemotherapy have not been established.
Curcumin has been shown to be an iron chelator, which could negatively impact some women undergoing chemotherapy by reducing their iron stores.
