Table 1.
Summary of Studies Reviewed to Improve Outcomes in Specific Cancer Patients.
| Study | Design | Primary endpoint | Results | Dietary Recommendations | |
|---|---|---|---|---|---|
| Colon cancer | O’Keefe et al. [4] | Clinical; 40 patients | Effect of high-fiber diet on microbiota | High-fiber diet promoted diversification of gut flora, decreased Ki67 expression, and decreased macrophage and lymphocyte presence in colonic tissue | 1. Plant-based diet with fiber intake approaching 50g/d |
| Segain et al. [5] | Clinical; 17 patients | Effect of butyrate enemas on colonic inflammation | SCFAs decreased TNF production and pro-inflammatory cytokine mRNA expression | ||
| Borges-Canha et al. [6] | Clinical; systematic review of 31 studies | Link between microbiota and colon cancer | Microbiota dysbiosis was suggestive of colorectal carcinogenesis | ||
| Van Blarigan et al. [7] | Clinical; prospective cohort; 992 patients | Effect of fruit and vegetable diet, healthy body weight, and increased physical activity on survival in stage 3 colon cancer | Plant-based diet, physical activity, and healthy body weight was associated with longer survival | ||
| Soret et al. [8] | Preclinical; rat model | Effect of SCFAs on enteric nervous system | SCFAs increased cholinergic-mediated muscle contractile response | ||
| Yue et al. [9] | Preclinical; mouse model | Effect of Lactobacillus plantarum on colon cancer progression and locoregional inflammation | L. plantarum inhibited tumor development and locoregional inflammation | ||
| Escamilla et al. [10] | Preclinical; in vitro | Effect of Lactobacillus spp. on colon cancer invasion | Lactobacillus supernatants inhibited metastatic ability | ||
| Prostate cancer | Cipolla et al. [11] | Clinical; double-blind randomized controlled trial; 78 patients | Effect of sulforaphane intake on PSA doubling time | Intake of sulforaphane was associated with 86% longer doubling time | 1. Plant-based diet with high cruciferous vegetable intake, particularly vegetables containing sulforaphanes 2. Low-carbohydrate, ketogenic diet with high omega-3 intake |
| Alumkal et al. [12] | Clinical; phase 2; 20 patients | Effect of sulforaphane intake on PSA doubling time | Intake of sulforaphane was associated with approximately 50% longer doubling time | ||
| Aronson et al. [13] | Preclinical; mouse model | Effect of fat intake on prostate cancer tumor progression | Fat-restricted diet slowed tumor progression | ||
| Ngo et al. [14] | Preclinical; mouse model | Effect of fat intake on prostate cancer tumor progression | Fat-restricted diet slowed tumor progression | ||
| Wang et al. [15] | Preclinical; mouse model | Effect of fat intake on prostate cancer tumor progression | Fat-restricted diet slowed tumor progression | ||
| Caso et al. [16] | Preclinical; mouse model | Effect of carbohydrate restriction on prostate cancer tumor progression and insulin axis | Carhobhydrate restriction slowed tumor progression and decreased insulin levels; ratio of IGF to IGFBP lowered however not statistically significant | ||
| Freedland et al. [17] | Preclinical; mouse model | Effect of NCKD on prostate cancer tumor progression and insulin axis | NCKD decreased tumor progression compared to western diet, lowered insulin and IGF levels, and increased expression of IGFBP | ||
| Masko et al. [18] | Preclinical; mouse model | Effect of carbohydrate restriction on prostate tumor progression and insulin axis | Carhobhydrate restriction slowed tumor progression and decreased insulin levels; ratio of IGF to IGFBP lowered however not statistically significant | ||
| Bagga et al. [19] | Preclinical; in vitro | Effect of omega-6 on production of inflammatory cytokines | Excess omega-6 promoted increased IL-6 production and mitogenic activity of fibroblasts; omega-3 attenuated this response | ||
| Malignant gliomas | Nebeling et al. [20] | Clinical; case report; 2 patients | -- | A ketosis diet resulted in 21% decrease in PET-avidity; 1 patient maintained on ketosis diet for 12 months and did not experience disease progression | 1. Ketogenic diet |
| Zuccoli et al. [21] | Clinical; case report; 1 patient | -- | Ketogenic diet with fat to carbohydrate ratio of 4:1 (as percentage of calories) resulted in PET-negative disease | ||
| Abdelwahab et al. [22] | Preclinical; mouse model | Effect of ketogenic diet on radiation therapy for malignant glioma | Ketogenic diet enhanced anti-tumor effects of radiation | ||
| Stafford et al. [23] | Preclinical; mouse model | Effect of ketogenic diet on malignant glioma progression | Ketogenic diet slowed tumor progression and decreased reactive oxygen species production | ||
| Breast cancer | WHEL study | Clinical; randomized controlled trial; 2,448 patients | Role of dietary pattern in prognosis | No statistical difference in breast cancer recurrence, improvement in prognosis, or all-cause mortality with adherence to plant-based diet | 1. Plant-based diet with high cruciferous vegetable intake, particularly vegetables containing sulforaphanes |
| Thomson et al. [24] | Clinical; sub-group analysis of WHEL study | -- | Women with hormone receptor-positive breast cancer on tamoxifen who adhere to plant-based diet with high cruciferous vegetable intake may have benefit in breast cancer recurrence | ||
| WINS study | Clinical; randomized controlled trial; 2,437 patients | Effect of low-fat diet on early stage breast cancer | Adhering to a low-fat diet post-treatment resulted in lower recurrence rates | ||
| After Breast Cancer Pooling Project | Clinical; prospective cohorts; 18,314 patients (84% stage 1-2 breast cancer) | Effect of physical activity, dietary factors, and quality of life in breast cancer prognosis | Vegetable intake was not associated with breast cancer outcomes | ||
| Ghoncheh et al. [25] | Clinical; retrospective case-control | Risk factors for breast cancer | Diet rich in processed meats and refined carbohydrates was a risk factor for breast cancer | ||
| Thomson et al. [26] | Preclinical; review article; animal model and in vitro | Effect of DIM, a major bioactive compound in cruciferous vegetables, on breast cancer growth | DIM inhibited breast cancer tumor growth by downregulating UPA, which controls VEGF and MMP-9 production; DIM reduced cytokine receptor CXCR4 and CXCL12, which are signaling receptors associated with metastatic growth | ||
| Saati et al. [27] | Preclinical; in vitro | Effect of DIM on breast cancer cell growth | DIM inhibited breast cancer line growth likely by inhibiting expression of transcription factor Sp1 | ||
| Immunotherapy | Spencer et al. [28] | Clinical; prospective cohort; 113 patients | Relationship between lifestyle factors and response in melanoma patients undergoing immunotherapy | Patients with high-fiber diet noted to have highest odds of response to immunotherapy | 1. High-fiber diet |
| Gopalakrishnan et al. [29] | Clinical; prospective cohort; 112 patients | Relationship between gut microbiome and response to immunotherapy in metastatic melanoma patients | Patients with abundance of Clostridiales were noted to have higher response to immunotherapy, while non-responders were predominantly rich in Bacteroidales | ||
| Iida et al. [30] | Preclinical; mouse model | Effect of modulating tumor micro-environment on IL-10 immunotherapy response | Antibiotic treatment induced gut microbiome changes, attenuated IL-10 response |
Abbreviations: CXCL12: C-X-C motif chemokine 12, CXCR4: C-X-C motif chemokine receptor 4, DIM: 3,3′-diindolylmethane, IGF: insulin growth factor, IGFBP: insulin growth factor binding protein, IL-6: interleukin-6, IL-10: interleukin 10, MMP-9: matrix metalloproteinase-9, NCKD: no-carbohydrate ketogenic diet, PET: positron emission tomography, PSA: prostate specific antigen, SCFAs: short chain fatty acids, Sp1: specificity protein 1, TNF: tumor necrosis factor, UPA: urokinase plasminogen activator, VEGF: vascular endothelial growth factor.