Iron Cancer Research Results

Iron, Iron: Click to Expand ⟱
Source:
Type:
Iron is an essential nutrient that is crucial for various cellular processes, including DNA synthesis, cell proliferation, and oxygen transport.
Cancer cells often have increased iron requirements due to their rapid growth and proliferation. Some tumors can acquire iron through various mechanisms, including upregulating iron transport proteins. This can support their growth and survival.
Excess iron can lead to the production of reactive oxygen species (ROS) through Fenton reactions, which can cause oxidative damage to DNA, proteins, and lipids. This oxidative stress can contribute to cancer development and progression.
Scientific Papers found: Click to Expand⟱
948- Fuc,    Low Molecular Weight Fucoidan Inhibits Tumor Angiogenesis through Downregulation of HIF-1/VEGF Signaling under Hypoxia
- vitro+vivo, Bladder, T24/HTB-9 - in-vitro, Nor, HUVECs
p‑PI3k/Akt/mTOR↓,
p‑p70S6↓,
p‑4E-BP1↓,
angioG↓, did not affect angiogenesis under normoxic conditions (data not shown), suggesting the antiangiogenic activity of LMWF is hypoxia specific.
Hif1a↓,
VEGF↑,
TumCG↓,
TumVol↓, in mice (needed 300mg/kg/day to actually shrink tumor as opposed to slowing growth)
TumW↓, in mice
Iron∅, maintaining Fe2+ availability through suppression of hypoxia-induced ROS formation is crucial for promoting HIF-1 degradation and diminishing HIF-1 activity by preventing PHD and FIH inactivation
ROS↓, LMWF may target different levels, including inhibition of ROS formation

7699- IP6,    IP6: From Seeds to Science—A Natural Compound’s Path to Clinical Promise
- Review, Var, NA
*Iron∅, Early reports fueled concerns that high dietary phytate intake could contribute to mineral deficiencies, albeit without direct scientific evidence, particularly in populations lacking dietary diversity
ChemoSen↑, Preclinical and clinical research indicate that IP6, alone or in tandem with inositol (Ins), selectively targets cancer cells and enhances chemotherapy efficacy.
*cardioP↑, Growing evidence also suggests that IP6 plays a protective role in cardiovascular health, neurodegenerative disorders, and metabolic diseases
neuroP↑,
IronCh∅, confirmed that life-time consumption of IP6±Inositol did not cause any reduction in Ca, Mg, Fe, or Zn levels in the blood or bones of rats and mice
P21↓, IP6 downregulates cell cycle regulators such as p21 and p27, inhibits phosphorylation of retinoblastoma protein (pRB), and suppresses PI3K/protein kinase B (PI3K/Akt)
p27/CDKN1B↓,
p‑pRB↓,
PI3K↓,
Akt↓,
NF-kB↓, decreased NF-kB activity and inflammatory responses
Inflam↓,
TumW↓, After 12 days of treatment, IP6-treated mice exhibited a 3.4-fold lesser tumor weight as compared to controls
TumCI↓, figure 3
TumMeta↓,
Imm↑,
Diff↑,
selectivity↑, the growth of non-cancerous MCF-10A epithelial breast cells remained unaffected, further illustrating IP6’s capacity to differentiate between cancerous and normal cells
toxicity↓, Importantly, no adverse effects have been reported in studies administering IP6 or Ins to humans or animal models, even at high doses
RenoP↑, Plant-based food diets are often recommended to individuals with chronic kidney disease, where the protective effects of the diet are ascribed to IP6
QoL↑, Clinical trials, though still sparse, have yielded encouraging results regarding IP6’s synergistic enhancement of chemotherapy efficacy and improvement of patients’ quality of life.


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Iron∅, 1,   ROS↓, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh∅, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

p‑PI3k/Akt/mTOR↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   p27/CDKN1B↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

p‑p70S6↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

p‑pRB↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

P21↓, 1,  

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

p‑4E-BP1↓, 1,   Diff↑, 1,   PI3K↓, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

TumCI↓, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   Hif1a↓, 1,   VEGF↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Imm↑, 1,   Inflam↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   selectivity↑, 1,  

Functional Outcomes(tgid=23) ⓘ

neuroP↑, 1,   QoL↑, 1,   RenoP↑, 1,   toxicity↓, 1,   TumVol↓, 1,   TumW↓, 2,  
Total Targets: 29

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Iron∅, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 1,  
Total Targets: 2

Scientific Paper Hit Count for: Iron, Iron
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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