Cancer

Research

Cancer
Index
Unique features of Cancer cells
Database Access
Links for Summary of Research Papers

Go to UREBS Reference Design: Uniform Rotary Exciter Burst Sine

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Unique features (Hallmarks) of Cancer cells:

By understanding the differences of Normals cells and Cancer cells, we can understand how Cancer cells can be targeted for cell death and not normal cells. This is the concept of "selectivity", and is a parameter in the cancer database that can be filtered on. The best therapeutic approach would be a treatment that improves the health of normal cells (or does not affect them) and selectively targets the cancer cells for death. Chemotherapy for example tries to target Cancers, but also affects normal cells which is why people get so sick from Chemotherapy. Hence the selectivity is considered poor. Selectivity is closely related to the concept of “differential stress sensitization”.

1. High ROS
Elevated levels of reactive oxygen species (ROS) are a hallmark of cancer.
A change in ROS lower or higher can kill cancer cells.

2. Warburg effect (meaning glucose[sugar] addiction)
Cancer cells exhibit aerobic glycolysis: derive most of their energy from glycolysis that is glucose is converted to lactate for energy followed by lactate fermentation, even when oxygen is available.
    Glutamine and Glucose
Many tumours require glutamine as well as glucose for their proliferation and survival. This means the preferred nutrient of cancer cells is glucose.

3. Higher iron and demand
Tumor cells generally have higher iron than that of normal cells

4. Higher Copper
Cancers can have raised serum and tumor copper levels. Tumor cells depend on more copper for their metabolism than normal cells, and a decrease in copper or copper overload can have a detrimental effect on tumor cells.

5.Lack Catalase activity
Cancer cells generally lack catalase activity, making them vulnerable to oxidative stress.

6. Hypoxia
Regions within solid tumours experience mild to severe O2 deprivation owing to aberrant vascular function.

7. Higher GSH (Glutathione) Levels
Cancer cells can have high antioxidant levels, especially with GSH, whose appearance at an elevated concentration of ∼10 mM (10 times less in normal cells) detoxifies the cancer cells.
GSH depletion can be a key strategy to amplify the oxidative stress in cancer cells, enhancing the destruction of cancer cells.

8. MMP, mitochondrial membrane potential
In cancer cells, MMP is often decreased, which can lead to increased glycolysis, and increased reactive oxygen species (ROS) production.

9. pH differences
Normal tissues have a higher extracellular pH than intracellular pH, in cancer it is exactly the opposite. This is called the inversion of the pH gradient and is considered a hallmark of malignancy.

10. Other differences
There are numerous cancer pathways that are modulated by cancer.

Research that might be obvious and simple.

1.Vitamin D supplement/sunlight
  - excessive sunlight is well known to pose a skin cancer risk
  - BUT lower vitamin D levels (low sunlight) increases risk for basically all other cancers.
  - intake/levels is inversely associated with the incidence of cancer
2.Vitamin K2
  - inverse association between dietary intake of VK and overall cancer incidence
3.Boron supplement - food intake levels might be low
  - boron intake is inversely associated with the incidence of cancer
5. Diet Plant based
 a)FMD (Fasting Mimicking diet) variations
  - nightly fasting Example research
 b)Diet
 c)Methionine-Restricted Diet
6. Physical Exercise
7. Diet changes: fibre, green juicing

Examples of using the Cancer Database to access information.

- the database is pathway based. Searchs based on pathways are useful, as well as searches based on common pathways between products (possible synergy)
For example to see research on the ROS (Reactive Oxygen Species) pathway you would filter the database for the ROS target.
ROS filter
You can directly access the filtering (for you own selections) for the database here.

Calcium, and Magnetic Fields Database Query
Note from the above database query that the sum of the targets(at the bottom of the linked page) shows:
1. The Ca+2↑ target shows a significant count. Which indicates Ca+ is increased on applied magnetic field.
-note that at least one report claims a differential effect on Ca+ for normal cells and cancerous cells.
" > 15 min promoted Ca(2+) influx" and "Non-malignant cells did not show any EMF-dependent changes in Ca(2+) influx or cell growth"
2. Ca+2↑ coincides with ROS↑ (cancer cells). Increased ROS may lead to apoptosis of the cancer cells.
3. Notice on normal cells there are a few reports of both Ca+2↓ and ROS↓ and SOD↑, which is good for normal cells.
Calcium, and Rotary Magnetic Fields Database Query
Lots of debate over frequency and intensity. The induction intensity (dB/dt) may well be more critical than the field maximum amplitude.
Some reports try to explain the effect thru the Radical Pair Mechanism (RPM)

ROS and Magnetic Field
The above query strongly indicates an increase in ROS with applied magnetic field.
Lower time limits and lower power of field seems to correlate with a drop in ROS
One report even states: "Even a slight elevation in ROS levels within cancer cells relative to that in normal cells can surpass a critical threshold, inducing cancer cell death and suppressing tumor development". Since cancer cells have higher iron and H2O2, it is logical that the applied magnetic field induces the Fenton reaction, and would have a greater detrimental effect on cancer cells. Also cancer cells typically have less anti-oxidant defences than normal cells.
HSP70 is also typically upregulated by magnetic fields but greater effeicacy might be acheived if combined with HSP70 inhibitor, and combining with hyperthermia
ROS and Rotary Magnetic Fields
Some of the most interesting information is the OncoMagnetic device (motor pulsing the spinning of a magnet)
- Oscillating Magnetic fields on GBM cells
- sOMF on GBM cells
- sOMF causes ROS in GBM cells
- Oncomagnetic safety in mice
- Case Report: Oncomagnetic human GBM treatment 31% tumor volume reduction
- Update Release comparing efficacy to dose of radiation
- Patent for Oncomagnetic device has much information on pathways
- duplicated in China

Ascorbic Acid + Cancer
-generally considered an antioxidant, but at higher concentrations (like IV) and/or higher iron/copper levels (like in cancer cells) many research papers reflect the ProOxidant effect
Ascorbic Acid + Magnetic Fields (same reseach paper)
Compare: Ascorbic Acid + Magnetic Fields (different reseach papers)
- observe that pathways such as ROS↑ and DNA damage↑ are common
Vit K2 + Cancer
Vit K3 + Cancer
Vit K3 + Vit C (same research paper)
Vit K3 + Vit C (comparison/different papers)
Iron + Cancer
Iron + Magnetic Fields (same reseach paper)
Iron + Rotary Magnetic Fields (same reseach paper)
Compare: Iron + Magnetic Fields (different reseach papers)
Copper and Cancer Research
Blood flow circulation and Magnetic Fields
Magnetic Field Research and Cancer
Rotating Magnetic Fields and Cancer
FMD (Fasting Mimicking diet) and Cancer Research
Alkalization Therapy (pH)
Alpha-Lipoic-Acid (ALA)
Boron
Hydroxycitric Acid
Curcumin
Heat/Hyperthermia
Magnesium
Oxygen, Hyperbaric
Peppermint
Photodynamic Therapy
Propyl gallate
Quercetin
Conflicting Research of Selenium and Cancer
Vitamin K2
Vitamin K3 (with toxic warnings)
Whole Body Vibration
There are over 280 products in the database, so many more queries are possible.

Pathways/Targets information from Database:.

ATP (adenosine triphosphate): source of energy
2 possible ways available for cancer cells to generate ATP: glycolysis and OXPHOS
Glycolysis
OXPHOS, Oxidative phosphorylation: source of energy
ROS
Catalase
GSH Glutathione
Hydrogen Peroxide (H2O2)
Warburg Effect
There are about 1200 pathways listed in the database, so many more queries are possible.
You may also include the Target direction in the search. For example suppose you are looking for:
HDAC inhibitors
or
Research on Glycolysis downregulators
or another example that includes the Target notes(which is possible for any target query)
Efficacy Improvement with Target Notes

Focusing on ROS research: ProOxidant strategy

All Research mentioning ROS
* - indicate citations using chat AI

Products that seems to UNCONDITIONALLY raise ROS in Cancer Cells
FMD diet that increases ROS
- notice also in the targets that FMD may be a chemosensitizer, reduces chemo-Side-Effects, improves gut microbiota and has selectivity between normal and cancer cells .
Methionine-Restricted Diet
- inhibits growth of cancer cells, with no effect on normal cells (as long as homocysteine is present)
-might need to combine with cystine restriction .
-might raise ROS in cancer cells while lowering ROS in normal cells (research)
- usually combined with other ROS raising therapies. chemo-sensitization or RadioSensitizer
Vitamin K2
- notice that the tendency is to ROS↑ in cancer cells and ROS↓ in normal cells
Vitamin K3(considered more toxic/less unavailable)
Silver NanoParticles(self made)
- may ROS↑ in cancer and normal cells but antioxidant system in normal cells may reduce toxicity? Example ALA
ART/DHA, Artemisinin
DCA, Dichloroacetate
RetA, Retinoic Acid
Auranofin(gold base)
Sulfasalazine
Gambogic Acid
Parthenolide but seems to lower ROS in normal cells?
Juglone (seems mostly only available as black walnut husks)
TQ, Thymoquinone might be only Pro-Oxidant for cancer cells, as normal cells reduce ROS
*Piperlongumine - selectivity, - Borneol might enhance cellular uptake
Plumbagin -no selectivity between normal and cancer cells here, and here too but not always
*Emodin hum, a few examples of raising ROS in normal cells too

Then there are many products that CONDITIONALLY increase cellular ROS (typically dose dependent)
You may search for products that may raise ROS
Here are some possibilities of search preconfigured for you:
ALA -Pro-Oxidant only in cancer cells, Pro-Oxidant Dose margin >100uM, ALA with Silver NanoParticle
Allicin IC50 12-30um/mL, might mean 30g consumption?:#1069
- example report of ROS in cancer cells but not normal cells
Apigenin likely need Apigenin Pro Liposomal to get theraputic dose
- may protect normal cells from oxidative damage while only be proOxidant capable in cancer cells
- see protective anti-Oxidant effect from Chemo on normal cells
*Ashwagandha high selectivity only raising ROS in cancer cells not normal cells, here, here, and here too
Baicalein -cancer vs normal cells, selectivity
*Berberine -cancer vs normal cells, selectivity
Boswellia -cancer vs normal cells, selectivity
Caffeic acid -cancer vs normal cells, selectivity
Capsaicin -cancer vs normal cells, selectivity
citrate -cancer vs normal cells, selectivity
Copper - mostly takes nanoParticles to have selectivity
*Curcumin
Ellagic acid
*EGCG
Ferulic acid
Garinol
Galloflavin
Luteolin
Lycopene
Magnetic Fields PEMF
Melatonin
PDT
Piperine
Propolis
Propyl gallate (PG)
*Quercetin
Reservatol
Rosmarinic acid
Scoulerine
Selinite
Sanguinarine
Shikonin (Shikonin Pro Liposomal from mcsformulas.com)
- seems to generate ROS and any dose for cancer cells
- good selectivity, - hepatoprotective - renoprotective
- some evidence of lowering ROS in normal cells and raising NRF2
- also may inhibit glycolysis and GPX4 and have chemosensitation properties
Sulforaphane (brocolli)
Vitamin C (Ascorbic Acid)

Looking at ProOxidant from pathway approach
Inhibit NRF2 to reduce anti-Oxidant defense.
NRF2 inhibition
Inhibit the Melavonate Pathway
HCA
Atorvastatin
Dipyridamole
Lycopene
Metabolic/Fermentation Inhibiting
3BP (Metabolic/Fermentation/HKII Inhibition)
Products used to increase efficacy with other targets
2DG (Glycolysis Inhibition)

Inhibit the Trx/Trx1/Trx2/TrxR Pathway (which increase ROS)
Auranofin (gold)
Gold Nanoparticles
Silver Nanoparticles
PL, Piperlongumine
Gambogic Acid inhibits Trx - TrxR
EGCG inhibit Trx - Trx1 - TrxR but opposite effect on normal cells?
Curcumin inhibit Trx - Trx1 - Trx2 - TrxR - TrxR1
Parthenolide inhibit Trx - TrxR - TrxR2 - TrxR1 some opposing effects on normal vs Cancer cells?


Pathways to inhibit Glycolysis/Warburg Effect:
Chat AI citations: Curcumin(Hif1a↓), Res(Hif1a↓), Quercetin, EGCG, Berberine(Hif1a↓), Sulforaphane(Hif1a↓)

Direct Enzyme Inhibition in Glycolysis
HK2 inhibitors: Ex 2DG
PFK1 via citrate, ATP, AMP
PKM2 inhibitors
LDH inhibitors
Upstream PI3K/Akt/mTOR Pathways:
PI3K inhibition
Akt inhibition - Trends: Glycolysis↓, PI3K↓,Akt↓,mTOR↓, Hif1a↓, cMyc↓, AMPK↑, GLUT1↓, ROS↑, VEGF↓, selectivity↑ and for Normal Cells: ROS↓
mTOR inhibition
HIF-1α Inhibitors - notice the trend for ROS to increase in cancer cells, while decreasing in normal cells.
c-Myc Suppression - aligns with COX2↓ ?
Active AMPK can Inhibit PI3K/Akt/mTOR pathway
AMPK activation - possible trend for ROS to increase in cancer cells, while decreasing in normal cells?
Downregulate GLUT1
GLUT1 downregulation - possible trend for ROS to increase in cancer cells, while decreasing in normal cells?

Here is an example of a multi product query, based on a selection of targets. We are using the "Breast Pack" of natural products offered by MCS Formulas as an example

There are 2 basic types of synergies between products:
1. alignment of targets increasing the overall effect.
2. corrections of some target directions, increasing the overall effect.
- an example of this is the FMD (Fasting Mimicking diet) and high dose Vitamin C(HDVC) (Ascorbic Acid)
- HDVC raises ROS but its activity is limited by the up-regulation HO-1. FMD reverses vitamin C-induced up-regulation of HO-1, hence improving the effect.

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