HemoG Cancer Research Results

HemoG, Hemoglobin: Click to Expand ⟱
Source:
Type:
Hemoglobin (often abbreviated as "HemoG") is a protein in red blood cells responsible for transporting oxygen throughout the body. While hemoglobin itself is not directly linked to cancer, there are several important aspects of its relationship with cancer that are worth noting:
Many cancer patients experience anemia, which is a condition characterized by low levels of hemoglobin. This can be due to various factors, including the cancer itself, chemotherapy, or nutritional deficiencies.
Tumors often have regions of low oxygen (hypoxia) due to inadequate blood supply. Hypoxia can promote tumor progression, metastasis, and resistance to therapy. Hemoglobin's role in oxygen transport makes it a critical factor in the tumor microenvironment, as oxygen levels can influence cancer cell behavior.
Changes in hemoglobin levels or the presence of specific hemoglobin variants may serve as potential biomarkers for certain cancers.
Scientific Papers found: Click to Expand⟱
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

7640- IP6,  Ins,    Effects of Inositol Hexaphosphate and Myo-Inositol Administration in Breast Cancer Patients during Adjuvant Chemotherapy
- Trial, BC, NA
*antiOx↑, Inositol hexaphosphate (IP6) is known as a strong antioxidant agent, able to improve local (i.e., breast region) side effects, functional status and quality-of-life.
QoL↑,
RBC↑, The Inositol Group showed a lower decrease in red blood cells, hemoglobin levels and white blood cells with respect to controls
HemoG↑,
WBC↑,
chemoP↑, , as well as amelioration in scores related to breast and arm local symptoms (p ≤ 0.02), body image (p = 0.04) and quality-of-life related symptoms
Dose↝, BC patients enrolled in the Inositol Group received topical gel containing 5 g of 4% IP6 and capsules containing 390 mg of myo-inositol

8135- LF,    Lactoferrin-A Regulator of Iron Homeostasis and Its Implications in Cancer
- Review, Var, NA - Review, AD, NA
IronCh↑, Lactoferrin (LF), a glycoprotein with strong iron chelating properties, can regulate its availability to cancer cells, thereby limiting their growth and progression.
ROS↓, By chelating free Fe ions, LF reduces oxidative stress and inhibits the mechanisms that promote carcinogenesis.
Imm↑, Additionally, it exhibits immunomodulatory and anti-inflammatory effects and may enhance the body’s anti-tumor response.
Inflam↓,
*BBB↑, LF crosses from the blood into the cerebrospinal fluid through the blood–brain barrier [25], where its beneficial effects have been documented in the context of neurodegenerative diseases such as Parkinson’s disease, Alzheimer’s disease, and de
Iron↝, Among the many biological properties of lactoferrin, its ability to strongly bind and transport iron ions over a wide range of pH values is a key function, determining its effectiveness in regulating iron homeostasis
*Fenton↓, LF, due to its ability to chelate iron, reduces its availability for the Fenton reaction, which reduces oxidative stress
*ROS↓,
*TAC↑, antioxidant properties of LF supplementation resulted in an increase in hydrophilic antioxidant capacity [151], a decrease in oxidative stress markers [152,153], and an increase in total antioxidant status (TAS)
*SOD↑, It also improved the levels of antioxidant markers, such as SOD, GPx, and glutathione, compared with the placebo group
*GPx↑,
*GSH↑,
*TBARS↓, Supplementation with LF-containing colostrum led to lower levels of thiobarbituric acid reactive substances (TBARS).
*PTEN↓, In addition, in patients with Alzheimer’s disease, LF supplementation led to the decreased expression of phosphatase and tensin homolog (PTEN), tau, and mitogen-activated protein kinase (MAPK1), as well as decreased serum levels of Aβ42, which ma
*tau↓,
*MAPK↓,
*Aβ42↓,
*Apoptosis↓, Reducing hydrogen peroxide-induced apoptosis through the inhibition of caspase-3 and Akt activation
*Casp3↓,
*Akt↑,
*GutMicro↑, LF shows a beneficial effect on the composition of the microbiota, promoting the growth of beneficial bacteria such as Bifidobacterium and Lactobacillus, while inhibiting the growth of pathogens such as Escherichia coli, Salmonella, and Shigella.
*Sepsis↓, A meta-analysis suggests that it may reduce the risk of fungal sepsis and shorten the hospitalization of preterm infants
*anemia↓, LF administration is a promising therapy for iron deficiency (ID) conditions, including iron deficiency anemia (IDA), both as a primary treatment and as an adjunctive therapy.
*IL6↓, ability to inhibit interleukin-6 (IL-6) expression, LF decreases hepcidin synthesis, which in turn increases ferroportin levels, restoring iron export from cells to the blood i
*FPN↑,
*TfR1/CD71↑, In addition, LF induces an increase in transferrin receptor 1 (TfR1) levels and a decrease in ferritin (Ftn) levels
*Ferritin↓,
*HemoG↑, Numerous intervention studies have confirmed the efficacy of LF supplementation, showing an increase in hemoglobin (Hb), total iron, erythrocyte count (RBC), and serum ferritin levels.
*RBC↑,
*eff↑, Most studies have shown similar or superior efficacy of bLF to traditionally used therapy (ferrous sulfate and ferric hydroxide) in restoring iron deficiency, with significantly fewer gastrointestinal side effects
*BioAv↓, Orally administered LF has low bioavailability due to degradation at unfavorable gastric pH and by proteolytic enzymes in the intestinal lumen and poor permeability through the intestinal epithelium, which limits its effective delivery to target site
*BioAv↑, LF is much better absorbed when administered directly into the duodenum. Therefore, ... coating enteral capsules containing LF, encapsulating it in nanocarriers, which allows it to be released at a site with less gastric pepsin activity
*BioAv↝, Other routes of administration, including transdermal or inhalation, are also being considered, which could avoid degradation in the gastrointestinal tract.
*ChemoSen↑, studies suggest that LF may act synergistically with other therapies such as chemotherapy, immunotherapy, and targeted therapy
*BioAv↑, Additionally, the use of probiotic bacteria as internal producers of LF in the body may open new perspectives for its therapeutic use.
Ferroptosis↑, LF also induces ferroptosis—iron-dependent cell death, which leads to excessive lipid oxidation in cell membranes and the destruction of cancer cells.


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

RBC↑, 1,   WBC↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Ferroptosis↑, 1,   Iron↝, 1,   ROS↓, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 1,  

Cell Death(tgid=5) ⓘ

Ferroptosis↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Imm↑, 1,   Inflam↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

HemoG↑, 1,  

Functional Outcomes(tgid=23) ⓘ

chemoP↑, 1,   QoL↑, 1,  
Total Targets: 13

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

anemia↓, 1,   Aβ42↓, 1,   FPN↑, 1,   RBC↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Fenton↓, 1,   GPx↑, 1,   GSH↑, 1,   ROS↓, 1,   SOD↑, 1,   TAC↑, 1,   TBARS↓, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

Ferritin↓, 1,   TfR1/CD71↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↑, 1,   Apoptosis↓, 1,   Casp3↓, 1,   MAPK↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

PTEN↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

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

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 1,   GABA↑, 1,   tau↓, 2,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 2,   BioAv↝, 1,   ChemoSen↑, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

Albumin↑, 1,   Ferritin↓, 1,   GutMicro↑, 1,   Hcy/homoC↓, 1,   HemoG↑, 2,   IL6↓, 2,  

Functional Outcomes(tgid=23) ⓘ

neuroP↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

Sepsis↓, 1,  
Total Targets: 42

Scientific Paper Hit Count for: HemoG, Hemoglobin
1 Folic Acid, Vit B9
1 IP6 (Inositol 1,2,3,4,5,6-hexakisphosphate)
1 Inositol
1 Lactoferrin/Talactoferrin
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

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