RBC Cancer Research Results
RBC, Red Blood Cells: Click to Expand ⟱
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Scientific Papers found: Click to Expand⟱
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*RBC↑, RBC production is increased to compensate for the amount of degradation, and RBC metabolism is increased.
*antiOx↑, Ingestion of Ge-132 increases fecal antioxidant capacity.
RBC↑, Patients receiving chemotherapy, along with IP6 + Inositol did not have cytopenia, drop in leukocyte and platelet counts.
QoL↑, patients who took IP6 + Inositol had significantly better quality of life
eff↑, combination of IP6 and inositol was significantly better in different cancers (colon, breast and metastatic lung cancer model) than was either one alone
Imm↑, Due to its strong antioxidant activity, and health beneficial effects, such as immune stimulation, prevention of kidney stone formation and hypocholesterolemic effect, IP6 + Inositol is available as dietary supplement.
ChemoSen↑, It has been shown in vitro that IP6 acts synergistically with doxorubicin and tamoxifen
chemoP↑, several case studies have shown that when IP6 and inositol were given in combination with chemotherapy, side effects of chemotherapy were diminished and patients were able to perform their daily activities
Dose↝, recommended prophylactic dosage of IP6 + Inositol is 1-2 g/day and a cancer therapeutic dosage is 8-12 g/day
*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
Dose↝, Test group (15 patients) received oral bLF 250 mg/day beside chemotherapy for three months. Control group (15 patients) received chemotherapy only.
toxicity↓, 3 months after treatment indicates that no significant difference in mean values of serum creatinine, AST, ALT, serum LF, serum GST enzyme, INF-γ, WBCs count, platelet count, CEA, RBCs count, neutrophil count, and Hb level of patients
INF-γ↝, Mean percent of change of main parameters (serum LF, serum GST enzyme, and INF-γ) after than before treatment among the studied patients indicate significant improvement in patients who received oral bLF 3 months
other↑, The results of this trial indicate that oral bLF made a significant increase in serum LF levels of patients in the test group 3 months after treatment compared to patients in the control group (P ≤ 0.05).
*ROS↓, Iron is essential as a catalyst for the production of reactive oxygen species. Therefore, lactoferrin can diminish the harmful influence of reactive oxygen species produced by leukocytes at the sites of inflammation
Imm↑, This result indicates that oral bLF enhances the immune system of colorectal cancer patients.
WBC↑, As a result of this increase in WBCs and neutrophil count patients disease state may be improved, because the body immune system can fight the disease more efficiently compatible with some previous studies
Neut↑,
T-Cell↑, These results support the proposal that oral supplements of bovine lactoferrin may be a useful adjunct toward modulation of immune activity, in particular T-cell activation and antioxidant status
*antiOx↑, The effect of antioxidants such as LF increase intracellular glutathione (GSH) levels in vascular endothelial cells by modulation of the GSH redox
*GSH↑,
*chemoP↑, On the other hand, oral bLF administration decreased chemotherapy related side effects as it enhances both renal and hepatic function tests.
*RenoP↑, Also, LF decreased chemotherapy related side effects by protecting liver and kidney from toxicity and improving their function test values
*hepatoP↑, Oral lactoferrin may increase liver functions and protect it from damage by reactive oxygen species since LF can function as an antioxidant, reducing intracellular levels of ROS
BUN↓, mean serum BUN decreased from 16.23 mg/dL before treatment to 11.43 mg/dL after 3 months of treatment in patients in the test group
creat↓, This decrease in BUN and serum creatinine may be due to the antioxidant effect of LF as mentioned in a former preclinical study on rat model of ferric nitrilotriacetate- (Fe-NTA-) induced renal tubular oxidative injury.
ALAT↓, Also, there was a significant decrease in serum ALT and AST in patients in test group 3 months after treatment compared to patients in the control group
AST↓,
RBC↑, Oral bLF administration enhanced anemia which is a very common chemotherapy related side effect; as results have shown, there were significant increases in RBCs count and serum Hb in patients in test group 3 months after treatment compared to patient
PC↑, There was a significant increase in platelets count in patients in test group after 3 months compared to control group
Mucositis↓, Patients in test group had less severed mucositis than patients in control group after every chemotherapy cycle;
*AntiBio↑, As mentioned before, lactoferrin has protective effects that range from direct antimicrobial activities against a large panel of microorganisms, including bacteria, viruses, fungi, and parasites, to anti-inflammatory and anticancer activities [
*AntiViral↑,
*AntiFungal↑,
*Inflam↓,
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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 5 of 5
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
Mucositis↓, 1, PC↑, 1, RBC↑, 3, WBC↑, 2,
Redox & Oxidative Stress(tgid=1) ⓘ
Ferroptosis↑, 1, Iron↝, 1, ROS↓, 1,
Metal & Cofactor Biology(tgid=2) ⓘ
IronCh↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 1, BUN↓, 1,
Cell Death(tgid=5) ⓘ
Ferroptosis↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
Imm↑, 3, INF-γ↝, 1, Inflam↓, 1, Neut↑, 1, T-Cell↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 1, Dose↝, 3, eff↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, AST↓, 1, creat↓, 1, HemoG↑, 1,
Functional Outcomes(tgid=23) ⓘ
chemoP↑, 2, QoL↑, 2, toxicity↓, 1,
Total Targets: 27
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
anemia↓, 1, AntiBio↑, 1, Aβ42↓, 1, FPN↑, 1, RBC↑, 2,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 3, Fenton↓, 1, GPx↑, 1, GSH↑, 2, ROS↓, 2, 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,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
PTEN↓, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
IL6↓, 1, Inflam↓, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
tau↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, BioAv↑, 2, BioAv↝, 1, ChemoSen↑, 1, eff↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
Ferritin↓, 1, GutMicro↑, 1, HemoG↑, 1, IL6↓, 1,
Functional Outcomes(tgid=23) ⓘ
chemoP↑, 1, hepatoP↑, 1, RenoP↑, 1,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 1, AntiViral↑, 1, Sepsis↓, 1,
Total Targets: 39
Scientific Paper Hit Count for: RBC, Red Blood Cells
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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