Lactoferrin/Talactoferrin / ROS Cancer Research Results

LF, Lactoferrin/Talactoferrin: Click to Expand ⟱
Features:
Lactoferrin is a protein in human and animal milk that helps regulate iron absorption and fight infections.Found in milk, saliva, tears and nasal secretions.
***"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"

Lactoferrin — Lactoferrin (LF, Lf) is an approximately 80-kDa iron-binding glycoprotein of the transferrin family that is abundant in human and bovine milk and is also present in saliva, tears, mucosal secretions and neutrophil granules. It functions as an innate-defense, iron-homeostasis and immunoregulatory protein rather than as a conventional small-molecule drug. Commercial supplements predominantly use bovine lactoferrin (bLF), whereas talactoferrin alfa is a recombinant human lactoferrin that has undergone oncology clinical trials. Lactoferricin is a bioactive peptide generated by proteolysis of lactoferrin and can have stronger direct membrane-disruptive anticancer effects than intact LF. Lactoferrin is available in licensed natural-health products in Canada, but it is not an approved anticancer treatment. Anticancer effects are strongly context-, formulation- and tumor-dependent.

-Talactoferrin alfa is recombinant human lactoferrin (rhLF) developed specifically as an oral pharmaceutical/immunotherapy. Its amino-acid sequence corresponds to human lactoferrin, whereas most commercial lactoferrin supplements are bovine lactoferrin (bLF). Human and bovine LF are homologous and share the same broad iron-binding protein architecture

Primary mechanisms (ranked):

  1. Modulation of iron availability and iron-redox homeostasis, potentially limiting iron-dependent tumor growth and altering oxidative signaling.
  2. Antitumor immune modulation, including activation or recruitment of NK cells, T cells, dendritic cells and other innate/adaptive immune components, particularly through gut-associated lymphoid tissue after oral administration.
  3. Induction of tumor-cell apoptosis and cell-cycle arrest through pathways including p53, caspases, mitochondrial apoptosis, AKT/mTOR and JAK/STAT3, with substantial tumor- and model-dependence.
  4. Suppression of invasion, migration, EMT and metastasis through effects on TGF-β and other motility-associated signaling pathways.
  5. Suppression of angiogenesis and tumor-supportive inflammatory signaling in several experimental models.
  6. Inhibition of plasmalemmal V-H+-ATPase in some highly metastatic cancer cells, reducing extracellular acidification and disrupting tumor-cell pH homeostasis.
  7. Direct membrane-disruptive cytotoxicity, particularly for the lactoferricin peptide rather than intact lactoferrin.
  8. Context-dependent regulation of ferroptosis. Although iron restriction may be anticancer in many settings, recent prostate-cancer evidence indicates endogenous lactoferrin can increase ferritin and suppress p53-ALOX12-mediated ferroptosis, potentially promoting tumor progression in that specific biological context.

Bioavailability / PK relevance: Oral intact lactoferrin has limited and variable systemic bioavailability because the protein is susceptible to gastric and intestinal proteolysis. Biological activity after oral administration does not necessarily require high circulating intact LF because local intestinal receptors and gut-associated immune tissues can mediate systemic immunologic effects. Enteric protection, liposomes, nanoparticles and other encapsulation approaches can improve stability and delivery. Recombinant talactoferrin used gram-level oral doses in oncology trials. Bovine LF doses in the principal colorectal-polyp RCT were 1.5 or 3 g/day.

In-vitro vs systemic exposure relevance: Many direct tumor-cell experiments expose cells to approximately tens to hundreds of micrograms per mL, and some studies use substantially higher concentrations. These direct extracellular concentrations should generally not be assumed to be achievable as circulating intact LF after ordinary oral supplementation. Gastrointestinal tumors and mucosal immune tissues can experience much greater local exposure after oral administration, making colorectal and gut-mediated immunologic findings more pharmacologically plausible than extrapolation of high-concentration cell-culture effects to distant tumors.

Clinical evidence status: Predominantly preclinical with limited human evidence. A randomized placebo-controlled trial in patients with small colorectal adenomas found that 3 g/day bovine LF for one year reduced polyp growth in a prespecified younger subgroup, but this is prevention-oriented evidence rather than treatment of established colorectal cancer. A small randomized adjunct study in colorectal-cancer patients receiving chemotherapy did not demonstrate a significant between-group clinical benefit. Recombinant human talactoferrin produced encouraging phase I/II signals in NSCLC and renal-cell carcinoma, but the large phase III FORTIS-M NSCLC trial was negative for overall survival, progression-free survival and disease control. Lactoferrin therefore has no established or approved role as systemic anticancer therapy. Oral bovine LF is generally well tolerated; important practical precautions include cow's-milk protein allergy/hypersensitivity and product-specific contraindications.

Lactoferrin Mechanistic Profile

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Iron availability and iron homeostasis ↓ labile iron availability ↔ / regulated iron handling R-G Restricts iron-dependent proliferation and modifies redox signaling Central biochemical property of LF; effects depend on iron saturation, tumor iron demand and cellular handling of LF.
2 Antitumor immune response ↑ immune-mediated tumor killing ↑ NK, T-cell and dendritic-cell activity (context-dependent) G Enhances tumor immune surveillance Especially important for orally administered LF and talactoferrin because gut-associated lymphoid tissue can mediate effects without requiring high systemic intact-protein exposure.
3 Apoptosis ↑ caspase activation, ↑ Bax, ↓ BCL-2 ↔ / substantially less cytotoxicity in several models G Promotes programmed tumor-cell death Mitochondrial and receptor-associated mechanisms have been reported; selectivity varies among tumor types.
4 AKT mTOR survival signaling ↓ AKT, ↓ mTOR signaling ↔ (model-dependent) R-G Reduces survival and proliferative signaling Demonstrated in gastric and oral squamous carcinoma models; not established as a universal LF response.
5 p53 and cell-cycle control ↑ p53, ↑ G0/G1 or G1/S arrest ↔ (model-dependent) G Suppresses proliferation Reported in OSCC and hepatocellular carcinoma models and linked to apoptosis in responsive cells.
6 JAK STAT3 signaling ↓ STAT3 signaling ↔ (context-dependent) R-G Reduces prosurvival and proliferative signaling SOCS3 activation and reduced JAK/STAT3 signaling have been demonstrated in oral squamous carcinoma cells.
7 EMT and TGF-β signaling ↓ EMT, ↓ TGF-β-associated signaling ↓ pathological EMT (context-dependent) G Reduces invasive phenotype and supports epithelial integrity The existing Nestronics entry emphasizes this axis, but its current evidence set contains only one associated paper and should not be treated as the dominant overall anticancer mechanism.
8 Migration invasion and metastasis ↓ migration, ↓ invasion, ↓ metastasis ↔ G Suppresses metastatic behavior Supported by multiple experimental models; mechanisms include EMT regulation, immune effects and modification of tumor acidity.
9 V-H+-ATPase and tumor acidity ↓ plasmalemmal V-H+-ATPase, ↓ extracellular acidification ↔ in tested non-tumorigenic cells R Disrupts pH regulation in highly metastatic cells Mechanistically compelling but demonstrated particularly in V-H+-ATPase-rich metastatic breast-cancer models rather than across cancers generally.
10 Angiogenesis ↓ tumor vascularization ↔ / context-dependent G Restricts tumor blood supply Most evidence remains preclinical; effects may partly reflect immune and inflammatory modulation.
11 ROS and oxidative stress ↔ / ↓ oxidative stress (context-dependent) ↓ excessive oxidative stress R-G Modifies iron-driven redox biology LF usually acts as an iron-buffering antioxidant, but redox consequences vary with iron saturation, cell type and treatment conditions. ROS elevation is not a universal primary LF anticancer mechanism.
12 Lactoferricin membrane disruption ↑ membrane permeabilization and cytotoxicity Lower susceptibility in many models P-R Direct tumor-cell killing Primarily attributable to lactoferricin and related cationic LF-derived peptides; should not automatically be assigned to intact oral LF.
13 Ferroptosis ↓ ferroptosis in prostate cancer (context-dependent) Iron-redox homeostasis G Potentially protects selected cancer cells from ferroptotic death A 2026 prostate-cancer study found an AR-LF-ferritin axis that suppressed p53-ALOX12-mediated ferroptosis and accelerated tumorigenesis. This is an important exception to treating LF as universally anticancer.
14 Chemosensitization ↑ chemotherapy response (model-dependent) Potential protection from chemotherapy toxicity (preclinical) G Potential adjunct effect Strong responses have been demonstrated in animal models, especially with iron-saturated LF, but convincing human therapeutic benefit has not been established.
15 Clinical Translation Constraint Variable Generally well tolerated G Limits translation of experimental anticancer findings Intact oral LF undergoes gastrointestinal degradation; systemic exposure is low and variable. Many direct cell-culture concentrations exceed plausible circulating exposure. Human oncology evidence is limited, and phase III talactoferrin treatment of refractory NSCLC was negative.

P: 0–30 min    R: 30 min–3 hr    G: >3 hr



Alzheimer's disease relevance: Lactoferrin has preliminary neuroprotective evidence in Alzheimer's disease (AD), including cellular and animal models and one small randomized human pilot study. Proposed effects include reduced amyloidogenic processing and Aβ burden, reduced tau phosphorylation, suppression of neuroinflammation and oxidative stress, and enhancement of neuronal survival signaling through PI3K/Akt, ERK/CREB and ADAM10-associated pathways. A 50-patient pilot study reported improvements in cognitive scores and several circulating AD-associated biomarkers after 3 months of lactoferrin supplementation. Evidence remains preliminary and has not been confirmed in large replicated clinical trials; published reviews also identify inconsistent experimental findings.

AD clinical evidence status: Small human pilot study plus preclinical evidence; not an established AD treatment.

Lactoferrin in Alzheimer's Disease

Rank Pathway / Axis Modulation Primary Effect Notes / Interpretation
1 Amyloidogenic processing and Aβ ↓ Aβ production / accumulation Potential reduction of amyloid pathology Linked to altered amyloid-processing pathways including ADAM10 and, in experimental studies, reduced amyloidogenic enzyme activity. Evidence is primarily preclinical.
2 PI3K Akt PTEN signaling ↑ PI3K, ↑ Akt, ↑ p-Akt, ↓ PTEN Promotes neuronal survival and suppresses pathological stress signaling A central pathway identified in the small human AD pilot study.
3 Tau phosphorylation ↓ p-tau Potential reduction of tau-associated pathology Reduced circulating p-tau and tau were reported in the human pilot study; CNS disease-modifying significance remains uncertain.
4 Neuroinflammation ↓ IL-6 and inflammatory signaling Reduces inflammatory stress Consistent with the broader immunomodulatory properties of lactoferrin.
5 Oxidative stress ↓ oxidative stress Protects neurons from oxidative injury Likely involves iron sequestration and modulation of cellular antioxidant pathways.
6 ERK CREB signaling ↑ ERK CREB signaling Supports neuronal survival, plasticity and memory-associated signaling Mainly supported by mechanistic and preclinical literature.
7 ADAM10 and non-amyloidogenic APP processing ↑ ADAM10 Favors non-amyloidogenic APP processing Potential mechanism for reducing Aβ generation; predominantly preclinical evidence.
8 Cognitive function ↑ cognitive performance Potential symptomatic or disease-modifying benefit Improved MMSE and ADAS-Cog measures were reported in one small human study; replication is required.
9 Clinical Translation Constraint Uncertain Limits confidence in therapeutic relevance Human evidence is based largely on one small study. CNS exposure of orally administered intact lactoferrin and the optimal formulation, dose and treatment duration remain uncertain.


ROS, Reactive Oxygen Species: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy 
ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination




Item ROS↑ NRF2 Condition Mechanism Class Remarks 



ROS">Piperlongumine
+++ ↓ [D][T] ROS-dominant






ROS">Shikonin
+++↓/±[D][T]ROS-dominant






ROS">Vitamin K3 (menadione)
+++↓[D]ROS-dominant






ROS">Copper (ionic / nano)
+++↓[Fe][F]ROS-dominant






ROS">Sodium Selenite
+++↓[D]ROS-dominant






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






ROS">Photodynamic Therapy (PDT)
+++0[L][O₂]ROS-dominant






ROS">Radiotherapy / Radiation
+++0[O₂]ROS-dominant






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






ROS">Salinomycin
++↓[D][T]ROS-dominant






ROS">Artemisinin / DHA
++↓[Fe][T]ROS-dominant






ROS">Sulfasalazine
++↓[C][T]ROS-dominant






ROS">FMD / fasting
++↓[M][C][O₂]ROS-dominant






ROS">Vitamin C (pharmacologic)
++↓[Fe][D]ROS-dominant






ROS">Silver nanoparticles
++±[F][D]ROS-dominant






ROS">Gambogic acid
++↓[D][T]ROS-dominant






ROS">Parthenolide
++↓[D][T]ROS-dominant






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






ROS">Ashwagandha (Withaferin A)
++↓[D][T]ROS-dominant






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






ROS">Methionine restriction
+↓[M][C][T]ROS-secondary






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






ROS">Galloflavin
+0[D]ROS-secondary






ROS">Piperine
+±[D][F]ROS-secondary






ROS">Propyl gallate
+↓[D]ROS-secondary






ROS">Scoulerine
+?[D][T]ROS-secondary






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






ROS">Alpha-lipoic acid (ALA)
±↑[D][M]NRF2-dominant






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






ROS">Quercetin
±↑/↓[D][Fe]NRF2-dominant






ROS">Resveratrol
±↑[D][M]NRF2-dominant






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
8145- LF,    Neuroprotective Effects of Lactoferrin in Alzheimer's and Parkinson's Diseases: A Narrative Review
- Review, AD, NA - Review, Park, NA
*AntiBio↑, *Imm↑, *AntiCan↑, *neuroP↑, *BBB↑, *APOE4↓, *ROS↓, *Inflam↓, *Apoptosis↓, *Learn↑, *memory↑, *ADAM10↑, *PSEN1/PS1↑, *cl‑APP↑, *BACE/β-secretase↓, *cognitive↑, *MDA↓, *IL6↓, *TNF-α↓, *neuroP↑, *Dose↝, *IronCh↑, *SOD↑, *BioAv↝,
8144- LF,    A pilot study on the effect of lactoferrin on Alzheimer's disease pathological sequelae: Impact of the p-Akt/PTEN pathway
- Human, AD, NA
*Ach↑, *5HT↑, *TAC↑, *Inflam↓, *Akt↑, *PI3K↑, *Aβ42↓, *LDL↓, *ROS↓, *IL6↓, *HSP90↓, *Casp3↓, *tau↓, *MAPK↓, *PTEN↓, *cognitive↑, *Dose↝,
8135- LF,    Lactoferrin-A Regulator of Iron Homeostasis and Its Implications in Cancer
- Review, Var, NA - Review, AD, NA
IronCh↑, ROS↓, Imm↑, Inflam↓, *BBB↑, Iron↝, *Fenton↓, *ROS↓, *TAC↑, *SOD↑, *GPx↑, *GSH↑, *TBARS↓, *PTEN↓, *tau↓, *MAPK↓, *Aβ42↓, *Apoptosis↓, *Casp3↓, *Akt↑, *GutMicro↑, *Sepsis↓, *anemia↓, *IL6↓, *FPN↑, *TfR1/CD71↑, *Ferritin↓, *HemoG↑, *RBC↑, *eff↑, *BioAv↓, *BioAv↑, *BioAv↝, *ChemoSen↑, *BioAv↑, Ferroptosis↑,
8129- LF,    Study on the Therapeutic Benefit on Lactoferrin in Patients with Colorectal Cancer Receiving Chemotherapy
- Trial, CRC, NA
Dose↝, toxicity↓, INF-γ↝, other↑, *ROS↓, Imm↑, WBC↑, Neut↑, T-Cell↑, *antiOx↑, *GSH↑, *chemoP↑, *RenoP↑, *hepatoP↑, BUN↓, creat↓, ALAT↓, AST↓, RBC↑, PC↑, Mucositis↓, *AntiBio↑, *AntiViral↑, *AntiFungal↑, *Inflam↓,

Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

Mucositis↓, 1,   PC↑, 1,   RBC↑, 1,   WBC↑, 1,  

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↑, 2,   INF-γ↝, 1,   Inflam↓, 1,   Neut↑, 1,   T-Cell↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   creat↓, 1,  

Functional Outcomes(tgid=23) ⓘ

toxicity↓, 1,  
Total Targets: 22

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

anemia↓, 1,   AntiBio↑, 2,   APOE4↓, 1,   Aβ42↓, 2,   FPN↑, 1,   Learn↑, 1,   PSEN1/PS1↑, 1,   RBC↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Fenton↓, 1,   GPx↑, 1,   GSH↑, 2,   MDA↓, 1,   ROS↓, 4,   SOD↑, 2,   TAC↑, 2,   TBARS↓, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

Ferritin↓, 1,   IronCh↑, 1,   TfR1/CD71↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

LDL↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↑, 2,   Apoptosis↓, 2,   Casp3↓, 2,   MAPK↓, 2,  

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

HSP90↓, 1,  

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

PI3K↑, 1,   PTEN↓, 2,  

Migration(tgid=13) ⓘ

cl‑APP↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL6↓, 3,   Imm↑, 1,   Inflam↓, 3,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 1,   ADAM10↑, 1,   tau↓, 2,  

Protein Aggregation(tgid=19) ⓘ

BACE/β-secretase↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

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

Clinical Biomarkers(tgid=22) ⓘ

Ferritin↓, 1,   GutMicro↑, 1,   HemoG↑, 1,   IL6↓, 3,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   chemoP↑, 1,   cognitive↑, 2,   hepatoP↑, 1,   memory↑, 1,   neuroP↑, 2,   RenoP↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,   AntiViral↑, 1,   Sepsis↓, 1,  
Total Targets: 59

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
4 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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:111  Target#:275  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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