Hcy/homoC Cancer Research Results

Hcy/homoC, homocysteine: Click to Expand ⟱
Source:
Type: Biomarker
Homocysteine is a sulfur-containing amino acid produced during the metabolism of methionine. Elevated homocysteine levels and alterations in its metabolic enzymes have been associated with various pathological processes, including oxidative stress, DNA damage, and inflammation.
-Elevated plasma homocysteine levels (hyperhomocysteinemia) are a well‐established risk factor for cardiovascular diseases.
-Some studies have suggested that high levels of homocysteine might be associated with an increased risk of certain cancers.
-Vitamins like folate, B6, and B12 are key regulators of homocysteine metabolism, some research has examined whether supplementation might modulate cancer risk. However, clinical outcomes have been mixed and further research is needed.

-Various clinical trials have shown that the oral supplementation of folic acid, B6, and B12 vitamins significantly lowers circulating homocysteine levels.
Scientific Papers found: Click to Expand⟱
4061- betaCar,  VitB12,  VitB6,  FA,  VitB3  Revisiting the Role of Vitamins and Minerals in Alzheimer’s Disease
- Review, AD, NA
*cognitive↑, vitamin A supplementation has been to be effective in lowering cognitive decline and AD pathology
*cognitive↑, Studies that involved B12 supplementation have shown beneficial effects on cognition and inflammatory status.
*Inflam↓,
*Hcy/homoC↓, decreased serum homocysteine and TNF-α
*TNF-α↓,
*other↝, treatment with a high dose of B vitamins consisting of folic acid, B12, and B6 for 24 months was able to slow down the shrinkage of the whole brain volum
*memory↑, In line with the improved cognitive function, NAD+ treatment significantly alleviated neuroinflammation, impaired synaptic plasticity, DNA damage, and hippocampal neuronal loss in these mice.

2175- Chemo,  VitB12,  FA,    Systemic Chemotherapy Interferes in Homocysteine Metabolism in Breast Cancer Patients
- Study, BC, NA
other↓, During chemotherapy, homocysteine (P = 0.032) and vitamin B12 (P < 0.001) concentrations increased, while folate and platelets decreased (decreases with supplements)
other↝, we also verified a correlation between Hcy levels and cofactors (B12 vitamin and folate).
Hcy/homoC↓, The anti‐DNA action of alkylating agents would lead to a reduction of folic acid and vitamin B12 concentrations, which in turn would lead to an increase of homocysteine concentration (supplements would lower homoC)
eff↝, As seen in this study, vitamin B12 and folic acid concentrations decreased with the progression of treatment, and they are inversely related to homocysteine levels.
other↝, increase homocysteine concentration 6 months after chemotherapy, as well as a significant decrease in vitamin B12, folic acid, and platelets at the third and sixth month after beginning of chemotherapy treatment in women with BC.

4261- Chol,  VitB12,  FA,  VitB2,    B-Vitamin and Choline Supplementation Changes the Ischemic Brain
- Study, Stroke, NA
*BDNF↑, this study suggests that supplementation with folic acid, vitamin B12, riboflavin, and choline may promote post-stroke neuroplasticity through increasing levels of BDNF.
*Hcy/homoC↓, Choline reduces levels of homocysteine by converting it to methionine (Niculescu and Zeisel, 2002).

4068- FA,    Hyperhomocysteinemia in Alzheimer's disease: the hen and the egg?
- in-vivo, AD, NA
*Hcy/homoC↓, The folate derivate 5-MTHF serves as cofactor in homocysteine metabolism.
*Aβ↓, we also observed that dietary-induced folate reduction and homocysteine increase was associated with an increase of plasma (young animals) and brain (older animals) amyloid-β concentrations.

4064- FA,  VitB6,  VitB12,    High-dose B vitamin supplementation and cognitive decline in Alzheimer disease: a randomized controlled trial
- Trial, AD, NA
*Hcy/homoC↓, Although the vitamin supplement regimen was effective in reducing homocysteine levels (active −2.42±3.35; placebo -0.86±2.59; p<0.001), it had no beneficial effect on the primary cognitive measure, rate of change in ADAS-Cog over 18 months
*cognitive∅,

4074- FA,  VitB12,    Associations between Alzheimer's disease and blood homocysteine, vitamin B12, and folate: a case-control study
- Trial, AD, NA
*cognitive↑, low vitamin B12 in subjects with normal Hcy and folate was associated with AD (adjusted odds ratio [OR], 4.6; 95% confidence interval [CI]
*Hcy/homoC↓, combination of high Hcy and low folate levels in patients with normal vitamin B12 was associated with AD (adjusted OR, 17.0; 95% CI
*other↝, combination of high Hcy, low vitamin B12, and any folate level was associated with AD (adjusted OR, 30.5; 95% CI:
*other↝, Vitamin B12 was directly associated with AD. The combination of high Hcy, low vitamin B12, and any folate level represented the poorest association with AD.

4044- FA,    Effect of 3-year folic acid supplementation on cognitive function in older adults in the FACIT trial: a randomised, double blind, controlled trial
- Trial, AD, NA
*Hcy/homoC↓, Serum folate concentrations increased by 576% (95% CI 539 to 614) and plasma total homocysteine concentrations decreased by 26% (24 to 28) in participants taking folic acid compared with those taking placebo.
*memory↑, The 3-year change in memory (difference in Z scores 0.132, 95% CI 0.032 to 0.233), information processing speed (0.087, 0.016 to 0.158) and sensorimotor speed (0.064, -0.001 to 0.129) were significantly better in the folic acid group than in the plac
*cognitive↑, Folic acid supplementation for 3 years significantly improved domains of cognitive function that tend to decline with age.

6870- FA,    Folic acid supplementation improves cognitive function in participants with cerebral small vascular disease-related cognitive impairment: a randomized controlled trial
- Trial, AD, NA
*Dose↝, FA tablets (0.4 mg/tablet) administered orally at a dose of two tablets daily for six months, while the placebo tablets were identical in appearance and administration but lacked FA.
*cognitive↑, FA improved cognitive outcomes in CSVD-CI, accompanied by a reduction in serum Hcy levels and MMP-9 expression.
*Hcy/homoC↓,
*MMP9↓,
*Risk↓, Early FA supplementation could help prevent vascular-related cognitive decline in CSVD-CI patients.

6951- FA,    Folic acid supplementation improves cognitive function by reducing the levels of peripheral inflammatory cytokines in elderly Chinese subjects with MCI
- Trial, AD, NA
*Dose↝, folic acid (400 μg/day)
*cognitive↑, daily oral administration of a 400-μg folic acid supplement to MCI subjects for 12 months can significantly improve cognitive performance and reduce peripheral inflammatory cytokine levels.
*Hcy/homoC↓, Serum homocysteine (Hcy) levels showed a greater decrease in the intervention group (−39.85%) compared to the conventional-treatment group
*IL6↓, IL-6 percentages showed substantial decreases in both groups (P = 0.025, ηp2 = 0.477), but these decreases were greater in the folic acid intervention group
*TNF-α↓, we observed a significant reduction in the levels of peripheral inflammatory cytokines including IL-6, TNF-α, circulating Aβ-42, and plasma Hcy concentrations,

6949- FA,  VitB12,    A controlled trial of homocysteine lowering and cognitive performance
- Trial, AD, NA
*Hcy/homoC↓, Homocysteine-lowering treatment was a daily supplement containing folate (1000 microg) and vitamins B12 (500 microg) and B6 (10 mg)
*cognitive∅, The results of this trial do not support the hypothesis that homocysteine lowering with B vitamins improves cognitive performance.

6948- FA,  VitB12,    A randomized placebo controlled trial of homocysteine lowering to reduce cognitive decline in older demented people
- Trial, AD, NA
*Dose↝, 1 mg of methylcobalamin and 5 mg of folic acid
*Hcy/homoC↓, The supplement group had average plasma tHCY reduced to 9.3 ± 2.7 μmol/L.
*cognitive∅, Homocysteine lowering in dementia patients did not significantly reduce global cognitive decline.

6947- FA,    Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment: a randomized controlled trial
- Trial, AD, NA
*Hcy/homoC↓, The accelerated rate of brain atrophy in elderly with mild cognitive impairment can be slowed by treatment with homocysteine-lowering B vitamins.
*cognitive↑,

6946- FA,    Effects of lowering homocysteine levels with B vitamins on cardiovascular disease, cancer, and cause-specific mortality: Meta-analysis of 8 randomized trials involving 37 485 individuals
- Review, Var, NA
Hcy/homoC↓, Folic acid allocation yielded an average 25% reduction in homocysteine levels.
Risk∅, There was no significant effect on the rate ratios (95% confidence intervals) for overall cancer incidence
toxicity↓, no significant effects within 5 years on cardiovascular events or on overall cancer or mortality in the populations studied

6954- FA,    Folic acid as a potential therapeutic agent for Alzheimer's disease: Effects on inflammatory cytokines, amyloid deposition, and neurotransmitter metabolism
- Trial, AD, NA
*Inflam↓, FA supplementation can effectively delay AD progression by inhibiting neuroinflammation, reducing amyloid deposition, regulating neurotransmitter metabolism and improving nutritional status.
*Aβ↓,
*IL1β↓, levels of inflammatory factors (IL-1b, IL-6, and TNF-a), Ab1-42, and Tau were significantly lower (P<0.05), and neurotransmitters (GABA, 5-HT, and Ach) and nutritional indexes (albumin and hemoglobin) were substantially higher.
*IL6↓,
*TNF-α↓,
*tau↓,
*GABA↑,
*5HT↑,
*Ach↑,
*Albumin↑,
*HemoG↑,
*neuroP↑, GABA, 5-HT, and Ach in both groups increased after treatment, with more significant increases in the experimental group (P<0.001), indicating better neurological function
*Hcy/homoC↓, FA supplementation has been shown to effectively promote plasma conversion of Hcy to reduce plasma Hcy concentrations in patients with metabolic syndrome

6956- FA,  VitB12,    A randomized placebo-controlled trial of using B vitamins to prevent cognitive decline in older mild cognitive impairment patients
- Trial, AD, NA
*Dose↝, methylcobalamin 500 μg and folic acid 400 μg
*Hcy/homoC↓, The supplement effectively lowered serum homocysteine (mean 13.9 ± sd 3.5 μmol at baseline to 9.3 ± 2.4 μmol/L at month 24).
*cognitive↑, At month 12, the supplement group significantly improved in executive function and had lower HDRS score (P = 0.004 and 0.012 respectively).
*eff↓, Aspirin use had a negative interaction effect on cognitive functioning with B supplements.

6961- FA,  VitB12,  VitB6,  Silicon,  Alum  B Vitamins Prevent Iron-Associated Brain Atrophy and Domain-Specific Effects of Iron, Copper, Aluminum, and Silicon on Cognition in Mild Cognitive Impairment
- Trial, AD, NA
*BrainVol↝, Baseline iron, cysteine, and homocysteine were significantly associated with brain atrophy rate.
*cognitive↝, At baseline, iron, copper, aluminum, and silicon were significantly associated with one or more domains of cognition: semantic memory, verbal episodic memory, attention/processing speed, and executive function.
*cognitive↑, These factors showed domain-specific associations with cognition, which were abrogated by B vitamin therapy.
*Dose↝, daily folic acid (0.8 mg)/vitamin B12 (0.5 mg)/vitamin B6 (20 mg)
*other↝, Reducing the rate of brain atrophy is likely to slow the conversion of individuals with MCI to AD
*Hcy/homoC↓, Elevated plasma total Hcy (tHcy) is associated with brain atrophy in healthy elderly [6] and in AD patients [7].
*Risk↓, Silicon (Si) has been shown to prevent gastrointestinal absorption of Al [17]
*BrainVol∅, In contrast, we found no correlations between brain atrophy rate and baseline serum Cu, As, or Al
*BrainVol↑, B vitamin treatment abrogates associations of brain atrophy rate with Fe and Cys
*other↝, Baseline Fe, Cu, Al, and Si predict cognition in the placebo group at the end of study: multiple regression analysis
*cognitive↑, B vitamin treatment abrogates effects of Fe, Si, Al, and Cu on cognition
*cognitive↑, multiple regression analyses that baseline Fe and Si were associated with better performance in several domains of cognition at the end of study
*other↝, serum Fe levels were reduced [12] and serum Cu levels were elevated [11] in AD patients compared to healthy controls.
*Risk↝, In addition to Fe and Cu, Al is also known to accumulate in senile plaques [15] and a high daily intake of Al is associated with increased risk of dementia

2173- FA,  VitB12,    Elevated serum homocysteine levels associated with poor recurrence-free and overall survival in patients with colorectal cancer
- Study, CRC, NA
Risk↓, risk of mortality increased with increasing HCY levels in CRC patients. (meaning lower using FA and B12)
eff↝, Patients with high HCY levels were older, male, had large tumours, high carcinoembryonic antigen (CEA) levels, and long hospital stays, and incurred high hospitalisation costs
eff↝, Patients with high HCY levels were older, male, had large tumours, high carcinoembryonic antigen (CEA) levels, and long hospital stays, and incurred high hospitalisation costs
Hcy/homoC↓, Multivariate analysis showed that when HCY levels exceeded 15.2 μmol/L, the risk of adverse RFS and OS increased by 55.7% and 61.4%, respectively (supplementation using FA and B12 lowers HCY)

2174- FA,  VitB12,   
- Analysis, Var, NA
Hcy/homoC↓, Vitamin B12 and folic acid are required for the remethylation reaction of homocysteine
eff↑, Homocysteine has been reported to be increased in a number of cancers includinghead and neck cancers,breast cancers,prostate cancers and colon cancers.
eff↑, Vitamin B12 and folate levels are significantly decreased in cancer patients.
eff↑, homocysteine levels are positively associated with proliferation rates of cells in a variety of tumors including head and neck and breast cancers [2] as well as with oxidative damage to cells
eff↝, cysteine may act as prooxidant agent that causes DNA oxidative damage as a result of the over production of free radicals and hydrogen peroxide ,leading to gene mutation and subsequent cancer development
Hcy/homoC↝, It was observed that mean homocysteine levels were significantly increased almost double in cancer patients when compared to control subjects
other?, In the high homocysteine group Vitamin B12 was found to be significantly decreased

2176- FA,  VitB12,    Hyperhomocysteinemia and Cancer: The Role of Natural Products and Nutritional Interventions
- Review, Var, NA
Hcy/homoC↓, natural products and dietary interventions were evaluated for their anticancer effects through lowering plasma homocysteine.
eff↝, link between hyperhomocysteinemia and cancer and the possible role of diet and natural product in lowering plasma homocysteine.

4063- Flav,  VitB12,  VitB6,    Homocysteine and Dementia: An International Consensus Statement
- Review, AD, NA
*Hcy/homoC↓, plasma total homocysteine, which reflects the functional status of three B vitamins (folate, vitamins B12, B6).
*cognitive↑, Intervention trials in elderly with cognitive impairment show that homocysteine-lowering treatment with B vitamins markedly slows the rate of whole and regional brain atrophy and also slows cognitive decline.

4058- VitB12,  VitB6,  FA,    The preventive efficacy of vitamin B supplements on the cognitive decline of elderly adults: a systematic review and meta-analysis
- Review, AD, NA
*Hcy/homoC↓, Vitamin B supplements can lower the serum homocysteine (Hcy) level, but whether it can prevent cognitive decline or not remains unclear.
*cognitive↑, Vitamin B supplements might delay or maintain the cognitive decline of elderly adults. We can recommend that the vitamin B supplements should be considered as a preventive medication to MCI patients or elderly adults without cognitive impairment.

4054- VitB12,  VitB6,  FA,    Role of B vitamins in modulating homocysteine and metabolic pathways linked to brain atrophy: Metabolomics insights from the VITACOG trial
- Study, AD, NA
*Hcy/homoC↓, B vitamins influence metabolic pathways beyond tHcy reduction, particularly the tricarboxylic acid cycle and glutamine–glutamate cycling, critical for brain energy homeostasis and neurotransmission.
*neuroP↑,
*cognitive↑, This metabolic signature supports B vitamin supplementation as a strategy for slowing MCI progression.

4053- VitB12,  VitB6,  FA,    Vitamins in Alzheimer’s Disease—Review of the Latest Reports
- Review, AD, NA
*cognitive↑, A diet rich in antioxidant vitamins can improve the cognitive functions of patients
*Hcy/homoC↓, Vitamin B12 is involved in the transformation of homocysteine to methionine, and vitamin B6 and folic acid are cofactors for this reaction.
*SAM-e↓, This reduces the concentration of S-adenosylmethionine, which is a methyl donor.

4048- VitB12,    Plasma Homocysteine and Serum Folate and Vitamin B12 Levels in Mild Cognitive Impairment and Alzheimer’s Disease: A Case-Control Study
- Study, AD, NA
*Hcy/homoC↓, Homocysteine (Hcy) is a risk factor for brain atrophy, cognitive impairment, and dementia. Vitamin B12 and folate are cofactors necessary for the methylation of Hcy.
*other↝, The highest Hcy tertile was significantly associated with MCI (adjusted OR: 2.81; 95% CI: 1.15, 4.73) and AD (adjusted OR: 3.64; 95% CI: 1.13, 9.04) compared to the lowest tertile.
*other↝, Low levels of these B vitamins have been associated with increased homocysteine (Hcy)

4045- VitB12,  FA,    Cognitive and clinical outcomes of homocysteine-lowering B-vitamin treatment in mild cognitive impairment: a randomized controlled trial
- Trial, AD, NA
*Hcy/homoC↓, The mean plasma total homocysteine was 30% lower in those treated with B vitamins relative to placebo
*cognitive↑, There was significant benefit of B-vitamin treatment among participants with baseline homocysteine above the median (11.3 µmol/L) in global cognition (Mini Mental State Examination, P < 0.001), episodic memory
*memory↑,
*other↑, In this small intervention trial, B vitamins appear to slow cognitive and clinical decline in people with MCI, in particular in those with elevated homocysteine.

4043- VitB12,  FA,    Preventing Alzheimer's disease-related gray matter atrophy by B-vitamin treatment
- Trial, AD, NA
*other↑, we showed that high-dose B-vitamin treatment (folic acid 0.8 mg, vitamin B6 20 mg, vitamin B12 0.5 mg) slowed shrinkage of the whole brain volume over 2 y.
*other↑, Here, we go further by demonstrating that B-vitamin treatment reduces, by as much as seven fold, the cerebral atrophy in those gray matter (GM) regions specifically vulnerable to the AD process, including the medial temporal lobe
*eff↝, We additionally show that the beneficial effect of B vitamins is confined to participants with high homocysteine (above the median, 11 µmol/L)
*Hcy/homoC↓, B vitamins lower homocysteine, which directly leads to a decrease in GM atrophy, thereby slowing cognitive decline.
*cognitive↑,

4318- VitB12,    Unraveling the molecular mechanisms of vitamin deficiency in Alzheimer's disease pathophysiology
- Review, AD, NA
*Hcy/homoC↓, it regulates homocysteine levels, preventing cognitive processes
*cognitive↑,

4315- VitB2,    Unraveling the molecular mechanisms of vitamin deficiency in Alzheimer's disease pathophysiology
*GlucoseCon↑, Riboflavin (vitamin B2) is essential for the metabolism of carbohydrates, fats, and proteins into glucose for energy
*ATP↑, It acts as a precursor to flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), essential for ATP production.
*Hcy/homoC↓, Studies show that riboflavin regulates homocysteine metabolism, and its deficiency may elevate homocysteine levels, which increase the AD
*ROS↓, Riboflavin deficiency disrupts this pathway, reducing FMN and FAD levels, impairing mitochondrial function, and increasing ROS and oxidative stress. ROS buildup can harm neurons and contributes to Aβ plaques and neurofibrillary tangles, key features
*Aβ↓, Riboflavin regulates homocysteine metabolism, preventing excess Aβ formation.
*Aβ↓,
*Inflam↓, The ensuing neuroinflammation makes amyloid pathology worse, starting a vicious cycle that quickens the onset of AD

4077- VitB6,  FA,  VitB12,  VitD3,  VitE  Vitamin Supplementation as an Adjuvant Treatment for Alzheimer’s Disease
- Review, AD, NA
*antiOx↑, Vitamins are potent antioxidants and therefore can be used as an adjuvant therapy for the treatment of AD.
*cognitive↑, Among B vitamins, pyridoxine (B6), folic acid (B9), and cobalamin (B12) have shown to have potential in managing symptoms of AD.
*Hcy/homoC↓, vitamin B6, B9 and B12 have shown to decrease the level of homocysteine, thereby helping in the control of this modifiable risk-factor for AD
*Risk↓, Low levels of vitamin B6 have been implicated in the pathogenesis of AD.
*Risk↓, Low level of serum folate is another predictor for AD
*Risk↓, The plasma levels of vitamin B12 were also found to be deficient in cases of AD
*other↝, Elevated plasma level of homocysteine is an important risk factor for gray matter atrophy
*Dose↝, 0.8mg B9, 20mg B6 and 0.5mg B12, over a period of 2 years has been demonstrated to decrease homocysteine induced gray matter atrophy
*Risk↓, The analysis of current literature on the relationship between vitamin D deficiency and AD revealed a direct relation between decreased serum level of vitamin D and AD
*Risk↓, decreased levels of plasma vitamin E is associated with increased risk of neurodegenerative disorders like AD and Mild Cognitive Impairment (MCI)


Showing Research Papers: 1 to 29 of 29

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 29

Pathway results for Effect on Cancer / Diseased Cells:


Transcription & Epigenetics(tgid=7) ⓘ

other?, 1,   other↓, 1,   other↝, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↑, 3,   eff↝, 5,  

Clinical Biomarkers(tgid=22) ⓘ

Hcy/homoC↓, 5,   Hcy/homoC↝, 1,  

Functional Outcomes(tgid=23) ⓘ

Risk↓, 1,   Risk∅, 1,   toxicity↓, 1,  
Total Targets: 10

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   ROS↓, 1,   SAM-e↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

GlucoseCon↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 1,   other↑, 3,   other↝, 9,  

Migration(tgid=13) ⓘ

MMP9↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1β↓, 1,   IL6↓, 2,   Inflam↓, 3,   TNF-α↓, 3,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 1,   BDNF↑, 1,   BrainVol↑, 1,   BrainVol↝, 1,   BrainVol∅, 1,   GABA↑, 1,   tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 4,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 6,   eff↓, 1,   eff↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

Albumin↑, 1,   Hcy/homoC↓, 24,   HemoG↑, 1,   IL6↓, 2,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 19,   cognitive↝, 1,   cognitive∅, 3,   memory↑, 3,   neuroP↑, 2,   Risk↓, 7,   Risk↝, 1,  
Total Targets: 35

Scientific Paper Hit Count for: Hcy/homoC, homocysteine
25 Folic Acid, Vit B9
21 Vitamin B12
8 Vitamin B6,pyridoxine
2 Vitamin B2,Riboflavin
1 beta-carotene(VitA)
1 Vitamin B3,Niacin
1 Chemotherapy
1 Choline
1 Silicic Acid
1 Aluminum
1 flavonoids
1 Vitamin D3
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#:1257  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

Home Page