Risk Cancer Research Results

Risk, Risk: Click to Expand ⟱
Source:
Type:
Risk: by definition reduces risk of disease or cancer.
Down Target direction of risk indicates lower cancer risk.
ChemoPreventive also mean lower cancer risk. But for Chemopreventive an up arrow indicates more preventive. 
Cancer Risk Impact Score (CRIS)
CRIS scale:
–5 = very strong risk reduction
–4 = strong risk reduction
–3 = moderate risk reduction
–2 = modest risk reduction
–1 = weak / context-dependent
0 = neutral




CRIS Exposure / Compound Evidence Cancers Notes




-5 Exercise (overall)
VStrong Hum BC, CRC, Endo, PCa, Liv






-5 Aerobic + resistance VStrong Hum Broad inc + mort






-4 Aerobic exercise (mod–vig) VStrong Hum BC, CRC, Endo






-4 Resistance training (alone) Strong Hum BC, CRC






-3 High-intensity interval training Mod–Strong Hum BC, CRC






-2 NEAT / low-intensity activity Moderate Hum CRC






-5 Cruciferous vegetable pattern Strong Hum Lung, CRC, BC, PCa






-5 Sunlight exposure (physiologic) Strong Hum CRC, BC, PCa






-4 Fasting (metabolic pattern)
Strong Mech + Hum BC, CRC, PCa 






-4 Curcumin
Hum + Pre GI, BC, PCa






-4 Sulforaphane
Hum + Pre Lung, CRC, BC






-4 PEITC
Hum + Pre Lung, CRC, PCa






-4 EGCG (tea matrix)
Strong Hum GI, PCa, BC






-4 Lycopene
Strong Hum PCa






-4 Apigenin
Pre + Diet Hum BC, PCa, CRC 






-4 Luteolin
Pre + Diet Hum Lung, CRC, BC 






-4 Kaempferol
Diet Hum Ov, Panc, Lung






-4 Fisetin
Pre + Early Hum CRC, PCa, Mel






-4 Ellagic acid → Urolithin A
Hum (microbiome) CRC, PCa, BC






-3 Omega-3 (EPA/DHA)
Strong Hum CRC, BC






-3 Vitamin D3 (supp)
Obs + RCT CRC, BC






-3 Garlic (allicin)
Mod Hum GI






-3 Mushroom beta-glucans
Hum adjunct GI, BC






-3 Melatonin
Hum + Mech BC, PCa






-3 Coffee (whole)
Strong Hum Liv, Endo






-2 Quercetin
Limited Hum Lung, CRC






-2 Resveratrol
Limited Hum CRC, BC






-2 I3C / DIM
Mod Hum BC, Cerv






-2 Thymoquinone
Early Hum BC, CRC






-2 Beta-carotene (food)
Hum Lung






-1 Vitamin K2 (MK-4/7)
Limited Hum Liv, PCa






-1 Boron
Obs PCa, Lung






0 Vitamin C (oral)
Strong Hum —






0 Genistein (soy)
Strong Hum BC, PCa






0 Selenium (diet)
Mixed Hum PCa






0 Capsaicin
Mixed Gastric






+2 Vitamin E (alpha only)
Strong RCT PCa






+2 Green tea extract (high-dose)
Case reports Liv






+4 Beta-carotene (supplement)
Strong RCT Lung (smokers)






+5 Alcohol (ethanol)
Strong Hum BC, Liv, Eso







Evidence
Hum        human data
VStrong    very strong
Strong     strong
Mod        moderate
Obs        observational
Pre        preclinical
RCT        randomized controlled trial
Mech       mechanistic
Adjunct    adjunct clinical use


Scientific Papers found: Click to Expand⟱
4132- Alum,    Relation between aluminum concentrations in drinking water and Alzheimer's disease: an 8-year follow-up study
- Study, AD, NA
*Risk↑, These findings support the hypothesis that aluminum in drinking water is a risk factor for AD. This result was confirmed for AD (adjusted relative risk=2.20, 95 percent CI 1.24–3.89)
*cognitive↓,
*BioAv↑, As suggested by Taylor,30 it is plausible that there is an increase in aluminum absorption with age, so the effect of aluminum may be larger after 75 years than before.

4135- Alum,    Aluminum Should Now Be Considered a Primary Etiological Factor in Alzheimer's Disease
- Review, AD, NA
*Risk↑, The unequivocal neurotoxicity of aluminum must mean that when brain burdens of aluminum exceed toxic thresholds that it is inevitable that aluminum contributes toward disease.
*cognitive↓, EVIDENCE NOW POINTS TO ALUMINUM AS A CONTRIBUTORY FACTOR IN ALL FORMS OF ALZHEIMER’S DISEASE
*neuroP↓, We also know that the addition of aluminum to feed or water exacerbates the many symptoms of Alzheimer’s disease in these animal models
*other↑, Postmortem analyses of their brain tissues revealed very high levels of aluminum.
*other↝, physical exercise can increase the perspiration volume many times and so improve the excretion of aluminum from the body.

5399- ASA,    Effect of Aspirin on Cancer Incidence and Mortality in Older Adults
- Trial, Nor, NA
Risk↝, aspirin was associated with an increased risk of incident cancer that had metastasized
Risk↑, These findings suggest that in older persons, aspirin may accelerate the progression of cancer and, thus, suggest caution with its use in this age group.
Risk∅, There was no association of aspirin with the overall incidence of solid tumors (HR = 1.05, 95% CI = 0.95 to 1.15) or with the incidence of cancers that were diagnosed at stages 1, 2, or 3.
Risk↑, By contrast, aspirin was associated with an increase in the incidence of cancers presenting at stage 4 (HR = 1.22, 95% CI = 1.02 to 1.45).
other↝, Prostate, colorectal, breast, melanoma, and lung were the most common incident cancers, accounting for 80% of all solid tumor cancers.

4621- Bor,    Boron
- Review, BPH, NA
*other↝, Men with higher boron intakes (about 6 mg/day) had significantly smaller prostate glands than men who consumed less boron (0.64–0.88 mg/day)
Risk↑, Several observational studies found that boron intakes are inversely associated with prostate cancer risk in men and with lung and cervical cancer risk in women
*Dose↑, Tolerable Upper Intake Levels (ULs) for Boron: 19+ years 20 mg

1265- CAP,    Capsaicin shapes gut microbiota and pre-metastatic niche to facilitate cancer metastasis to liver
- in-vivo, CRC, NA
GutMicro↓, Capsaicin not only changes the abundance of mucin-related bacteria like Akkermanisa and Muribaculaceae, but also bacteria involved in bile acids metabolism
Risk↑, hese findings reveal long term consumption of capsaicin increases the risk of cancer metastasis through modulating the gut microbiota.

6111- Chol,    The gut microbiota-derived metabolite trimethylamine N-oxide is elevated in Alzheimer’s disease
- Human, AD, NA
*Risk↑, CSF TMAO is higher in individuals with MCI and AD dementia compared to cognitively-unimpaired individuals, and elevated CSF TMAO is associated with biomarkers of AD pathology (phosphorylated tau and phosphorylated tau/Aβ42)
*TMAO↑, First, gut microbes enzymatically generate trimethylamine (TMA) from dietary constituents such as choline or l-carnitine [9]
*Dose↝, long-term dietary habits can influence TMAO accumulation via changes in gut microbiota composition, which modulates TMA production potential.
*eff↑, In this scenario, pharmacological agents designed to inhibit gut microbial TMAO production may be useful in slowing AD pathology

6102- Chol,    Higher dietary choline intake is associated with increased risk of all-cause and cause-specific mortality: A systematic review and dose-response meta-analysis of cohort studies
- Analysis, CardioV, NA
*Risk↑, The linear dose-response analysis showed that each 100 mg/day increase in choline intake was significantly associated with 6% and 11% increases in risk of all-cause (RR = 1.06, 95% CI: 1.03, 1.10, I2 =83.7%, P < .001) and cardiovascular diseases mort

6097- Chol,    Choline intake and risk of lethal prostate cancer: incidence and survival
- Study, Pca, NA
Risk↑, Of the 47,896 men in our study population, choline intake was associated with an increased risk of lethal prostate cancer.
other↝, Choline is highly concentrated in prostate cancer cells, and blood concentrations of choline have been associated with an increased risk of prostate cancer

2159- dietP,    Postdiagnostic Fruit and Vegetable Consumption and Breast Cancer Survival: Prospective Analyses in the Nurses' Health Studies
- Human, BC, NA
Risk↑, Apple juice largely accounted for these higher risks
Risk∅, and orange juice was not associated with risk
OS↑, higher vegetable consumption, particularly green leafy and cruciferous vegetables, was associated with better overall survival among patients with breast cancer.
OS↓, Higher fruit juice consumption, but not orange juice, was associated with poorer breast cancer–specific and all-cause survival.

4938- PEITC,    Clinical Trial of 2-Phenethyl Isothiocyanate as an Inhibitor of Metabolic Activation of a Tobacco-Specific Lung Carcinogen in Cigarette Smokers
- Trial, Nor, NA
*Risk↑, PEITC as an inhibitor of lung carcinogenesis by NNK in smokers
*P450↓, Multiple studies have clearly demonstrated that the major mechanism by which PEITC inhibits carcinogenesis by NNK is inhibition of its metabolic activation by cytochrome P450 enzymes
*BioAv↑, Urinary levels of both PEITC-NAC and total isothiocyanates (ITC) were significantly elevated in the PEITC treatment periods compared with the placebo periods among all subjects by a magnitude of more than 150 times
*BioAv↑, PEITC is fat soluble. Thus, delivery of PEITC in olive oil avoids concerns about bioavailability;
*BioAv↑, urinary excretion of PEITC equivalents (measured as PEITC-NAC) averaged 13.5 mg in 24 hours in the study participants, which was approximately only one-third the amount of PEITC equivalents (36.6–37.7 mg) excreted
*Dose↝, phase I study with a daily dose of 120 mg PEITC, the maximum amount of PEITC-NAC in the urine was not reached until 2 weeks of daily dosing
Dose↝, watercress consumption is an attractive way to deliver PEITC because of the relatively high concentrations of the PEITC precursor gluconasturtiin in this vegetable, which can be consumed in a more pleasing way than the dosing form used here

1700- Se,    Metabolism of Selenium, Selenocysteine, and Selenoproteins in Ferroptosis in Solid Tumor Cancers
- Review, Var, NA
Dose↝, In humans, the optimal range of Se in the serum is around 125 μg/L
Risk↑, Additionally, serum Se levels > 150 μg/L were associated with a modest increase in cancer mortality among adults in the United States.
Dose↝, same study also noticed a rise in cancer mortality with serum Se levels below 130 μg/L, which could be considered optimal
Risk↓, other side of the curve, inadequate amounts of Se or Se deficiency are also linked to an elevated risk of several diseases.

1429- SFN,    Preclinical and clinical evaluation of sulforaphane for chemoprevention in the breast
- in-vivo, Nor, NA - Human, Nor, NA
*NADPH↑,
*NQO1↑, x3
*HO-1↑, x4
*Risk↑, strong rationale for evaluating the protective effects of a broccoli sprout preparation in clinical trials of women at risk for breast cancer.

1706- SSE,    Selenium in Prostate Cancer: Prevention, Progression, and Treatment
- Review, Pca, NA
Risk∅, randomized controlled studies have shown that selenium supplementation does not prevent prostate cancer (HR: 0.95; 95% CI 0.80–1.13).
ChemoSen↑, In the context of combinatorial therapy, selenium has demonstrated promising synergistic potential in the treatment of prostate cancer.
Risk↓, Moreover, there is increasing evidence suggesting that selenium can serve as a preventive agent, and the levels of selenium in the bloodstream may be linked to the development of prostate cancer
toxicity↝, Interestingly, both low and high levels of selenium have shown potential implications.
Risk↑, Generally, lower serum selenium status has been correlated with an increased risk of cancer.
eff↑, Furthermore, foundational studies have proposed that antioxidants, such as vitamin E and lycopene [50], may enhance the effectiveness of selenium in preventing the formation of mammary tumors.
*toxicity↑, selenium supplementation after diagnosis and found that supplementation of 140 μg/day or more following a nonmetastatic prostate cancer diagnosis increased prostate cancer mortality.
RadioS↑, Sodium selenite, for instance, has demonstrated a significant enhancement of the radiosensitizing effect in both HI–LAPC-4 and PC-3 xenograft tumors
eff↓, Additionally, another study [59] provided valuable evidence indicating that prostate cancer patients with low levels of selenium and lycopene are more susceptible to DNA damage induced by ionizing radiation.
eff↑, Husbeck et al. highlighted that selenite increases sensitivity to gamma radiation in prostate cancer by reducing the ratio of GSH:GSSG
ChemoSen↑, while selenium supplementation alone did not demonstrate a positive effect on prostate cancer progression, it shows promise in enhancing the efficacy of chemotherapy and radiotherapy while mitigating their associated side effects during cancer treatm
ChemoSideEff↓,

1688- SSE,    Potential Role of Selenium in the Treatment of Cancer and Viral Infections
- Review, Var, NA
IL2↑, in mice promoted T cell receptor signaling that pushed T cell differentiation toward a Th1 phenotype by increasing interleukin -2 (IL-2) and interferon gamma (INF-γ) production
INF-γ↑,
Th1 response↑, 18 human subjects treated with 200 μg selenium-enriched broccoli daily for three days showed that selenium supplementation resulted in substantially higher levels of both Th1 and Th2 cytokines secreted by peripheral blood mononuclear cells
Th2↑,
Dose↑, Wang et al. on hens supplemented selenium (5 mg/kg, 10 mg/kg, and 15 mg/kg) orally for three time periods (15, 30, and 45 days) found that excessive selenium intake leads to a substantial reduction in the amount of IFN-γ and IL-2 cytokines
AntiCan∅, after 5.5 years, the results of this study revealed no relationship between selenium supplementation and prostate cancer risk reduction in men with low selenium levels
Risk↑, instead, they discovered that taking selenium supplements raised the high-grade prostate cancer risk in men who had high selenium levels
chemoP↑, selenium provided protection of normal tissues from drug-induced toxicity
Hif1a↓, Selenium down-regulates HIFs,
VEGF↓, leading to the subsequent down-regulation in expression of several genes including those involved in angiogenesis such as vascular endothelial growth factor (VEGF)
selectivity↑, Selenium also helps with DNA repair in response to DNA-damaging agents, which improves the effectiveness of chemotherapeutic agents by protecting normal cells from their toxicity.
*GADD45A↑, selenium protected WT-MEF from DNA damage in a p53-dependent manner by increasing the expression of p53-dependent DNA repair proteins such as XPC, XPE, and Gadd45a. Thus, cells lacking p53, such as tumor cells, did not receive the same protection
NRF2↓, a defined dose and schedule of selenium down-regulates and up-regulates Nrf2 in tumor tissue and normal tissue, respectively
*NRF2↑, a defined dose and schedule of selenium up-regulates Nrf2 in normal tissue
ChemoSen↑, These differential effects were associated with selective sensitization of tumor tissues to subsequent treatment with chemotherapy. Overactivation of Nrf2 increases the expression of MRPs, consequently decreasing the effectiveness of chemotherapy .
angioG↓, The inhibition of hypoxia-induced activation of HIF-1α and VEGF by knocking down Nrf2 suppresses angiogenesis, demonstrating a crosstalk mechanism between Nrf2 and HIF-1α in angiogenesis
PrxI↓, Selenium was shown to reduce drug detoxification and increase cytotoxic effects of anti-cancer drugs in tumor cells through suppression of the Nrf2/Prx1 pathway,
ChemoSideEff↓, showed that selenium supplementation attenuated the cardiotoxic effects of doxorubicin by decreasing oxidative stress and inflammation through Nrf2 pathway activation
eff↑, combination of niacin and selenium reduced the reactive oxygen species generated by sepsis and diminished the resultant lung injury by upregulating Nrf2 signaling

5082- SSE,    Rationale for the treatment of cancer with sodium selenite
- Review, Var, NA
Risk↑, low blood Se levels were found to be associated with an increased incidence and mortality from various types of cancers
antiOx↑, Se compounds, generally considered to be antioxidants
ROS↑, selenite is not an antioxidant, but possesses oxidizing properties in the presence of specific substrates.
Imm↑, Selenite by virtue of oxidizing cell membrane thiols, can prevent the formation of the coat and consequently makes cancer cells vulnerable to the immune surveillance and destruction.
NK cell↑, selenite may directly activate NK cells, as well as inhibit angiogenesis without undesirable decrease in the oxidative potential of cellular environment.
angioG↓,
toxicity↓, postulated that sodium selenite, in view of its relative low toxicity, might become a drug of choice for many types of cancer including leukemia.

4325- VitB5,    Localized Pantothenic Acid (Vitamin B5) Reductions Present Throughout the Dementia with Lewy Bodies Brain
- Study, AD, NA - Study, Park, NA
*Risk↑, As such, decreased dietary pantothenic acid intake may be associated with both PD incidence and severity.
*Dose↝, Due to the ease of obtaining sufficient amounts of pantothenic acid from food sources (5 mg daily for adults [19]), deficiency is rare, and usually only present in individuals with severe general malnutrition.
*Dose↓, Despite the rarity of pantothenic acid deficiency, significantly lower levels of dietary pantothenic acid intake have been observed in individuals with PD in comparison to healthy individuals
*other↝, despite a lack of outright pantothenic acid deficiency, supplementation may be a potential therapeutic option for the treatment of these neurodegenerative diseases.

4052- VitB6,    B-Vitamin Intake and Biomarker Status in Relation to Cognitive Decline in Healthy Older Adults in a 4-Year Follow-Up Study
- Study, AD, NA
*neuroP↑, Lower vitamin B6 status, as measured using pyridoxal-5-phosphate (PLP; <43 nmol/L) was associated with a 3.5 times higher risk of accelerated cognitive decline,
*other↑, More importantly, it also demonstrated that B-vitamin supplementation reduced the rate of brain atrophy by 30% as measured using MRI
*other↑, This study showed that combined B-vitamin supplementation for two years had beneficial effects on cognitive performance in participants with MCI and elevated plasma homocysteine concentrations
*cognitive↑, Lower dietary intake and biomarker status of vitamin B6 were associated with a greater rate of cognitive decline over a subsequent 4 years follow-up period. (PLP < 30 nmol/L)
*eff↝, No significant association of dietary intake or biomarker status with cognitive decline were observed for the other B-vitamins (folate, vitamin B12 and riboflavin).
*Risk↑, Consistent with the biomarker data, those with lower dietary intakes of vitamin B6 at baseline were 4 times more likely to have a greater rate of cognitive decline over the 4 years time period.
*other↑, higher vitamin B6 intakes have been associated with greater grey matter volume

4087- VitE,    Vitamin E and Alzheimer's disease: what do we know so far?
- Review, AD, NA
*Risk↑, Diminished circulating concentrations of vitamin E have been demonstrated in individuals with AD. Reduced plasma levels have furthermore been associated with an increased risk of AD
*Half-Life↑, The plasma half-life of α-tocopherol is estimated at 20 hrs, which is considerably longer than that of other isoforms, particularly the tocotrienol congeners
*antiOx↑, potent antioxidant capabilities of vitamin E are well known
*BioAv↑, α-tocopherol retains a superior in vivo role in neuroprotection due to its relatively greater bioavailability and preferential retention by tissues.
*neuroP↑, includes other neuro-protective, anti-inflammatory and cholesterol-reducing properties, in addition to influencing gene expression and potentially ensuing AD pathology.
*Inflam↑,
*LDL↓,
*cognitive↑, vitamin E supplementation was associated with decreased risk of cognitive decline in a cohort of 560 AD patients from the Canadian Study of Health and Aging


Showing Research Papers: 1 to 18 of 18

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 18

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   NRF2↓, 1,   PrxI↓, 1,   ROS↑, 1,  

Transcription & Epigenetics ⓘ

other↝, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   Hif1a↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL2↑, 1,   Imm↑, 1,   INF-γ↑, 1,   NK cell↑, 1,   Th1 response↑, 1,   Th2↑, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 3,   Dose↑, 1,   Dose↝, 3,   eff↓, 1,   eff↑, 3,   RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

GutMicro↓, 1,  

Functional Outcomes ⓘ

AntiCan∅, 1,   chemoP↑, 1,   ChemoSideEff↓, 2,   OS↓, 1,   OS↑, 1,   Risk↓, 2,   Risk↑, 10,   Risk↝, 1,   Risk∅, 3,   toxicity↓, 1,   toxicity↝, 1,  
Total Targets: 33

Pathway results for Effect on Normal Cells:


NA, unassigned ⓘ

TMAO↑, 1,  

Redox & Oxidative Stress ⓘ

antiOx↑, 1,   HO-1↑, 1,   NQO1↑, 1,   NRF2↑, 1,  

Core Metabolism/Glycolysis ⓘ

LDL↓, 1,   NADPH↑, 1,  

Transcription & Epigenetics ⓘ

other↑, 4,   other↝, 3,  

DNA Damage & Repair ⓘ

GADD45A↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 5,   Dose↓, 1,   Dose↑, 1,   Dose↝, 3,   eff↑, 1,   eff↝, 1,   Half-Life↑, 1,   P450↓, 1,  

Functional Outcomes ⓘ

cognitive↓, 2,   cognitive↑, 2,   neuroP↓, 1,   neuroP↑, 2,   Risk↑, 9,   toxicity↑, 1,  
Total Targets: 25

Scientific Paper Hit Count for: Risk, Risk
3 Choline
3 Selenite (Sodium)
2 Aluminum
1 Aspirin -acetylsalicylic acid
1 Boron
1 Capsaicin
1 diet Plant based
1 Phenethyl isothiocyanate
1 Selenium
1 Sulforaphane (mainly Broccoli)
1 Vitamin B5,Pantothenic Acid
1 Vitamin B6,pyridoxine
1 Vitamin E
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:785  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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