Nestronics
Nestronics
Index
Research that might be obvious and simple
Things that can lower Cancer Risk (Chemopreventive)
Direct Cancer Database Access
Unique Cancer Cell Features Relevant to Selective Targeting
Examples of using the Cancer Database to access information
OncoMagnetic device details
Sample of Pathways/Targets information from Database
Focusing on ROS research: ProOxidant strategy
ProOxidant strategy: pathways
Debate of AntiOxidants during ProOxidant strategy
Pathways to inhibit Glycolysis/Warburg Effect
Cancer Clinical Biomarkers
Go to UREBS Reference Design: Uniform Rotary Exciter Burst Sine
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
8. Selenium Levels:
- deficiency correlates with higher cancer incidence
- Selenium nanoparticles may inhibit tumor growth.
- may reduce chemotherapy/radiation side effects. (chemoprotective)
(radioprotective)
(radiosensitizer)
- To make Selenium Nanoparticles.
Risk: by definition reduces risk of disease or cancer.
Down Target direction of risk indicates lower cancer risk.
ChemoPreventive also mean lower cancer risk.
But for Chemopreventive an up arrow indicates more preventive.
Cancer Risk Impact Score (CRIS) CRIS scale: –5 = very strong risk reduction –4 = strong risk reduction –3 = moderate risk reduction –2 = modest risk reduction –1 = weak / context-dependent 0 = neutral
| CRIS | Exposure / Compound | Evidence | Cancers | Notes |
|---|---|---|---|---|
| -5 | Exercise (overall) | VStrong Hum | BC, CRC, Endo, PCa, Liv | i Notes |
| -5 | Aerobic + resistance | VStrong Hum | Broad inc + mort | i Notes |
| -4 | Aerobic exercise (mod–vig) | VStrong Hum | BC, CRC, Endo | i Notes |
| -4 | Resistance training (alone) | Strong Hum | BC, CRC | i Notes |
| -3 | High-intensity interval training | Mod–Strong Hum | BC, CRC | i Notes |
| -2 | NEAT / low-intensity activity | Moderate Hum | CRC | i Notes |
| -5 | Cruciferous vegetable pattern | Strong Hum | Lung, CRC, BC, PCa | i Notes |
| -5 | Sunlight exposure (physiologic) | Strong Hum | CRC, BC, PCa | i Notes |
| -4 | Fasting (metabolic pattern) | Strong Mech + Hum | BC, CRC, PCa | i Notes |
| -4 | Curcumin | Hum + Pre | GI, BC, PCa | i Notes |
| -4 | Sulforaphane | Hum + Pre | Lung, CRC, BC | i Notes |
| -4 | PEITC | Hum + Pre | Lung, CRC, PCa | i Notes |
| -4 | EGCG (tea matrix) | Strong Hum | GI, PCa, BC | i Notes |
| -4 | Lycopene | Strong Hum | PCa | i Notes |
| -4 | Apigenin | Pre + Diet Hum | BC, PCa, CRC | i Notes |
| -4 | Luteolin | Pre + Diet Hum | Lung, CRC, BC | i Notes |
| -4 | Kaempferol | Diet Hum | Ov, Panc, Lung | i Notes |
| -4 | Fisetin | Pre + Early Hum | CRC, PCa, Mel | i Notes |
| -4 | Ellagic acid → Urolithin A | Hum (microbiome) | CRC, PCa, BC | i Notes |
| -3 | Omega-3 (EPA/DHA) | Strong Hum | CRC, BC | i Notes |
| -3 | Vitamin D3 (supp) | Obs + RCT | CRC, BC | i Notes |
| -3 | Garlic (allicin) | Mod Hum | GI | i Notes |
| -3 | Mushroom beta-glucans | Hum adjunct | GI, BC | i Notes |
| -3 | Melatonin | Hum + Mech | BC, PCa | i Notes |
| -3 | Coffee (whole) | Strong Hum | Liv, Endo | i Notes |
| -2 | Quercetin | Limited Hum | Lung, CRC | i Notes |
| -2 | Resveratrol | Limited Hum | CRC, BC | i Notes |
| -2 | I3C / DIM | Mod Hum | BC, Cerv | i Notes |
| -2 | Thymoquinone | Early Hum | BC, CRC | i Notes |
| -2 | Beta-carotene (food) | Hum | Lung | i Notes |
| -1 | Vitamin K2 (MK-4/7) | Limited Hum | Liv, PCa | i Notes |
| -1 | Boron | Obs | PCa, Lung | i Notes |
| 0 | Vitamin C (oral) | Strong Hum | — | i Notes |
| 0 | Genistein (soy) | Strong Hum | BC, PCa | i Notes |
| 0 | Selenium (diet) | Mixed Hum | PCa | i Notes |
| 0 | Capsaicin | Mixed | Gastric | i Notes |
| +2 | Vitamin E (alpha only) | Strong RCT | PCa | i Notes |
| +2 | Green tea extract (high-dose) | Case reports | Liv | i Notes |
| +4 | Beta-carotene (supplement) | Strong RCT | Lung (smokers) | i Notes |
| +5 | Alcohol (ethanol) | Strong Hum | BC, Liv, Eso | i Notes |
Cancer cells differ from normal cells in ways that can be exploited for selective targeting. The core idea is differential stress sensitization: cancer cells are pushed beyond their stress tolerance while normal cells remain viable. The hallmarks below are grouped into major stress domains that directly inform pro-oxidant (ProOx) pathway strategies.
Tip: Hover over underlined terms to see a concise explanation.
How to use this framework: Selective ProOx strategies typically combine (A) reduced antioxidant capacity (NRF2/Trx/GSH axis) with (B) a ROS source (mitochondrial stress, metal-catalyzed ROS, or physical modalities), while accounting for oxygenation and tumor-specific dependencies.
Direct Cancer Database Access
View Complete List Products
View Complete List Targets/Pathways
View Complete List of Cancers / Illness covered in Database
Filtering tips:
1. To see how to improve the efficacy of a product, filter on the
efficacy target in the up direction ,
and click the check box to include the target notes in the results. Listed at the bottom is the
Scientific Paper hit counts and links for each product.
2. To see the things that decrease the efficacy, filter on
efficacy in the down direction,
(include check box for target notes).
Note: that is also shows experimental results such as when anti-oxidants (NAC) are used to purposely test if the effect is attenuated (such as ROS).
You may optionally use the browser search and highlight all function to find all the occurances of
NAC
3. For BioAvailability
information on a product, filter on the "bioavailability" target, (optionally specify direction)
and click the check box to include the target notes in the results.
3b. For BioEnhancers you need to look at the target notes
as the search result may be for a product that benefits from a bioEnchancer.
Sonoporation is effectively a bioenhancer too.
4. You can narrow the search down to only
Trials or
Case Reports
by selecting it in the Research Model.
5. Other interesting targets to query:
RadioProtective,
RadioSensitizer,
ChemoProtective,
ChemoSensitizer
Addition Requests and Corrections:
1. If you found a Research Paper that should be added,
1st do a title search to verify if it is in the database.
2. If you found an Addition or Data Entry Error, Contact us thru this email form.
with the full information.
Personal Favorite Research Topics based on DIY principles.
SDT(Sonoporation),
PEMF rotating fields,
PEMF,
Silver Nano Particles,
Hydrogen,
Apigenin(Parsley),
Sulforaphane (mainly Broccoli)
- 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 efficacy might be acheived if combined with HSP70 inhibitor,
and combining with hyperthermia
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 389 products in the database, so many more queries are possible.
The OncoMagnetic rotary magnetic field generator was invented by the Houston Methodist Hospital
and is being used for compassionate treatment of GBM brain tumors.
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
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 over 1400 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
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 |
|---|---|---|---|---|---|
| Piperlongumine | +++ | ↓ | [D][T] | ROS-dominant | i Notes |
| Shikonin | +++ | ↓/± | [D][T] | ROS-dominant | i Notes |
| Vitamin K3 (menadione) | +++ | ↓ | [D] | ROS-dominant | i Notes |
| Copper (ionic / nano) | +++ | ↓ | [Fe][F] | ROS-dominant | i Notes |
| Selenite | +++ | ↓ | [D] | ROS-dominant | i Notes |
| Juglone | +++ | ↓ | [D] | ROS-dominant | i Notes |
| Auranofin | +++ | ↓ | [D] | ROS-dominant | i Notes |
| Photodynamic Therapy (PDT) | +++ | 0 | [L][O₂] | ROS-dominant | i Notes |
| Radiotherapy / Radiation | +++ | 0 | [O₂] | ROS-dominant | i Notes |
| Doxorubicin | +++ | ↓ | [D] | ROS-dominant | i Notes |
| Cisplatin | ++ | ↓ | [D][T] | ROS-dominant | i Notes |
| Salinomycin | ++ | ↓ | [D][T] | ROS-dominant | i Notes |
| Artemisinin / DHA | ++ | ↓ | [Fe][T] | ROS-dominant | i Notes |
| Sulfasalazine | ++ | ↓ | [C][T] | ROS-dominant | i Notes |
| FMD / fasting | ++ | ↓ | [M][C][O₂] | ROS-dominant | i Notes |
| Vitamin C (pharmacologic) | ++ | ↓ | [Fe][D] | ROS-dominant | i Notes |
| Silver nanoparticles | ++ | ± | [F][D] | ROS-dominant | i Notes |
| Gambogic acid | ++ | ↓ | [D][T] | ROS-dominant | i Notes |
| Parthenolide | ++ | ↓ | [D][T] | ROS-dominant | i Notes |
| Plumbagin | ++ | ↓ | [D] | ROS-dominant | i Notes |
| Allicin | ++ | ↓ | [D] | ROS-dominant | i Notes |
| Ashwagandha (Withaferin A) | ++ | ↓ | [D][T] | ROS-dominant | i Notes |
| Berberine | ++ | ↓ | [D][M] | ROS-dominant | i Notes |
| PEITC | ++ | ↓ | [D][C] | ROS-dominant | i Notes |
| Methionine restriction | + | ↓ | [M][C][T] | ROS-secondary | i Notes |
| DCA | + | ± | [M][T] | ROS-secondary | i Notes |
| Capsaicin | + | ± | [D][T] | ROS-secondary | i Notes |
| Galloflavin | + | 0 | [D] | ROS-secondary | i Notes |
| Piperine | + | ± | [D][F] | ROS-secondary | i Notes |
| Propyl gallate | + | ↓ | [D] | ROS-secondary | i Notes |
| Scoulerine | + | ? | [D][T] | ROS-secondary | i Notes |
| Thymoquinone | ± | ± | [D][T] | Dual redox | i Notes |
| Emodin | ± | ± | [D][T] | Dual redox | i Notes |
| Alpha-lipoic acid (ALA) | ± | ↑ | [D][M] | NRF2-dominant | i Notes |
| Curcumin | ± | ↑/↓ | [D][F] | NRF2-dominant | i Notes |
| EGCG | ± | ↑/↓ | [D][O₂] | NRF2-dominant | i Notes |
| Quercetin | ± | ↑/↓ | [D][Fe] | NRF2-dominant | i Notes |
| Resveratrol | ± | ↑ | [D][M] | NRF2-dominant | i Notes |
| Sulforaphane | ± | ↑↑ | [D] | NRF2-dominant | i Notes |
| Lycopene | 0 | ↑ | — | Antioxidant | i Notes |
| Rosmarinic acid | 0 | ↑ | — | Antioxidant | i Notes |
| Citrate | 0 | 0 | — | Neutral | i Notes |
A practical way to organize “pro-oxidant” cancer approaches is by which redox-control pathway is being stressed. Most interventions that raise ROS in cancer cells do so by (1) reducing antioxidant capacity, (2) forcing ROS production, or (3) both. Importantly, many agents are condition-dependent (dose, formulation, oxygenation, tumor type, or combination therapy).
Chemotherapy raises the ROS in cancer cells (and normal cells) in an attempt to kill the cancer cells.
Hence there is a debate on the use of antioxidants for Chemotherapy (or any pro-oxidant therapy).
The debate is logical as it well known that anti-oxidants will reduce ROS. In fact it is common
for anti-oxidants to be used in the lab to test reversal of the killing action of cancer compounds that
are being tested. If the reversal happens then they conclude the ROS was a major contributor to the killing
action in the cancer cells.
You can see many examples in this
cancer database query,
if you look for the highlighted word NAC (an anti-oxidant). One example of the wording is
"Allicin significantly induced ROS overproduction, whereas NAC pretreatment decreased the ROS induction by allicin exposure in Hep 3B cells"
The argument for the use of anti-oxidants during chemo, is to protect normal cells from the rise in ROS,
and hence reduce the side effects caused by chemotherapy.
The debate is not simple because the compounds classified as anti-oxidants are not pure anti-oxidants.
That is only one of their properties. Each of them will have other properties that will come into play.
Another factor is some anti-oxidant compounds can have a pro-oxidant effect depending on dose and other factors.
An interesting example of this is a
report
that selenium when combined with oxygen can lower NRF2 (master anti-oxidant regulator)
in cancer cells.
From a research perspective there appears that there may be some compounds that can raise ROS in cancer cells,
and some that can do it selectively. Review
Focusing on ROS research: ProOxidant strategy and query the database
Curcumin is one such example
that may selectively lower ROS in normal cells, but raise it in cancer cells (dose depend?).
Curcumin is often considered as an anti-oxidant. Timing can matter.
"Antioxidants are compounds that inhibit oxidation, a chemical reaction that can produce free radicals."
For example Vitamin C (normally Antioxidant), Vitamin e, and Trolox are anti-oxidants.
Berries: Blueberries, Strawberries, Raspberries, Blackberries
Fruits: Grapes, Pomegranates, Oranges, Apples
Vegetables: Spinach and other leafy greens, Kale, Broccoli, Brussels sprouts
Nuts and Seeds: Walnuts, Almonds, Flaxseeds, Chia seeds
Beverages: Green tea, Black tea
Spices and Herbs: curcumin, Ginger, Garlic, Cinnamon
Other: Dark chocolate (with high cocoa content), Beans and legumes, Tomatoes (rich in lycopene)
Antioxidants are compounds that help neutralize free radicals—unstable molecules that can damage cells and contribute to the development of chronic diseases including cancer.
Cancer Prevention:
Mechanism: Antioxidants protect cells from oxidative damage caused by free radicals, which can lead to mutations in DNA. Over time, these mutations might initiate or promote the growth of cancer cells.
Dietary Role: Eating a diet rich in antioxidants (fruits, vegetables, and other plant-based foods) has been associated with a lower risk of some cancers. Many epidemiological studies suggest that diets high in natural antioxidants are linked to a reduced risk of cancer.
During Cancer Treatment:
Controversy: There is debate about whether taking antioxidant supplements during chemotherapy or radiation therapy is beneficial or harmful. Many therapies such as Chemotherapy raise the ROS(Reactive oxygen Species) intentionally to kill cancer cells. Some theory applies that antioxidants might prevent the ROS from being raised, and hence reduce treatment effectiveness. Some laboratory and clinical studies indicate that antioxidants might protect not only healthy cells but also cancer cells against the oxidative damage intentionally induced by these treatments. This could potentially reduce the effectiveness of cancer therapies. Another theory is there is a differential effect from taking antioxidants. Meaning the antioxidants help protect normal cells, but not the cancer cells.
Recommendation: Many oncologists recommend caution with high-dose antioxidant supplements during active cancer treatment. Instead, a balanced diet with naturally occurring antioxidants is typically advised.
thiol-containing antioxidants: -Contain a functional –SH (sulfhydryl) group
-Can undergo oxidation to form disulfide bonds. This reversible redox behavior allows these molecules to neutralize reactive oxygen species (ROS).
-Thiol antioxidants (like N‑acetylcysteine or glutathione) are potent because the –SH group can directly scavenge ROS.
-There is concern that supplementation with thiol antioxidants during chemotherapy could neutralize some of the ROS generated by the treatment, potentially reducing the intended cytotoxic effects on cancer cells.
Examples:
-NAC
-GSH
-NMPG
-dihydrolipoic acid (reduced form of ALA)
-Cysteamine
-Ergothioneine
-Thioredoxin
Non-thiol ROS scavengers:
-Act by donating electrons or hydrogen atoms to free radicals, thereby stabilizing them or converting them into less reactive species.
-Non‑thiol antioxidants (like vitamin C, vitamin E, flavonoids, etc.) have different mechanisms of action and may not interact as directly with ROS in the specific context of chemotherapy-induced cell death.
-That said, even non‑thiol antioxidants could potentially interfere with chemotherapy in some cases. For example, high doses of vitamin C or vitamin E might also diminish the oxidative stress essential for the efficacy of some chemotherapeutics.
Examples
-Ascorbic Acid(VitC)
-Vitamin E
-Flavoniods (Quercetin)
-Carotenoids(beta-carotene)
-Resveratrol
-Coenzyme Q10 (ubiquinone)
-Curcumin (indirectly disrupt thiol systems)
-Polyphenols (ferulic acid and caffeic acid)
-manganese(III)
-tetrakis( (4-benzoic acid)
-porphyrin chloride (MnTBAP)
-SOD
*** NOTE:
Thiol AntiOxidants could block ROS generation caused by Gambogic Acid, but not NON-Thiol AntiOxidants.
-Thiol-based antioxidants directly support glutathione and thioredoxin buffering and are most likely to protect cancer cells from ROS- or thiol-dependent therapies. Non-thiol antioxidants may act as radical scavengers, redox modulators, or—under certain tumor-specific conditions—pro-oxidants. Therefore, the likelihood that an antioxidant interferes with cancer therapy depends less on whether it ‘scavenges ROS’ and more on whether it restores thiol redox homeostasis or activates cytoprotective signaling pathways such as NRF2.
OTHER CLASSES of antioxidants
1. Enzymatics Antioxidants (SOD, Catalase, GPXs)
-proteins that catalyze reactions to detoxify reactive oxygen species (ROS).
2. Non-Enzymatic (Small-Molecule) Antioxidants.
Further divided to Thiol-Based Antioxidants, vs Non-Thiol Based Antioxidants.
3. Metal-Binding Proteins and Chelators (Ferritin, Transferrin)
These compounds limit oxidative damage indirectly by sequestering transition metals (like iron and copper) that catalyze reactive oxygen species formation via the Fenton reaction.
4. Indirect Antioxidants (Nrf2 Activators): (Sulforaphane, Curcumin)
enhance the body’s own antioxidant defenses by upregulating the expression of antioxidant enzymes.
Cancer-Relevant Antioxidant Matrix (Oral/achievable doses)
| AntiOxidant | Oral | Pro-ox. | Thiol | Effect | Effect on | NRF2 up | NRF2 up | Cancer | Chemo | Mechanism |
|---|---|---|---|---|---|---|---|---|---|---|
| Compound | Dose/day | Cancer | Buffer | on ROS | ROS | risk | in | Redox. | Compatibility | and |
| Idx 0-4 | cancer | Normal | Cancer | Normal | Buffer | Notes | ||||
| Salinomycin | 0.2–1 mg | Yes | 0 | ↑3 | ↓1 | 0 | 0 | 0 | Compatible | |
| Disulfiram (+Cu) | 250–500 mg | Yes | 1 | ↑3–4 | ↓1–2 | 0–1 | 0–1 | 0–1 | Cond.[M][D] | |
| PEITC | 40–100 mg | Yes | 3 | ↑3 | ↓1–2 | 0–1 | 0–1 | 1–2 | Compatible | |
| Withaferin A | 5–20 mg | Yes | 1–2 | ↑3 | ↓1–2 | 1 | 1 | 1–2 | Cond.[D][M] | |
| Betulinic Acid | 200–600 mg | Yes | 0–1 | ↑2–3 | ↓1–2 | 0 | 0 | 0–1 | Compatible | |
| Ursolic Acid | 150–450 mg | Yes | 1 | ↑2–3 | ↓2 | 1 | 1 | 1 | Cond.[D][M] | |
| Thymoquinone (TQ) | 100–400 mg | Yes | 2–3 | ↑2–3 | ↓2 | 2–3 | 2–3 | 1–2 | Cond.[D][M] | |
| Curcumin | 1–4 g | Yes | 2 | ↑2–3 | ↓2 | 3 | 2 | 1 | Cond.[T][D][M] | |
| Quercetin | 500–1000 mg | Yes | 2 | ↑2–3 | ↓2 | 1–2 | 2–3 | 1 | Cond.[D][M] | |
| EGCG (green tea) | 400–800 mg | Yes | 2 | ↑2–3 | ↓2 | 2–3 | 1–2 | 1–2 | Cond.[T][D][M] | |
| Honokiol | 200–600 mg | Yes | 1–2 | ↑2–3 | ↓2–3 | 1 | 1 | 1–2 | Compatible | |
| Berberine | 500–1500 mg | Yes | 2 | ↑2–3 | ↓2 | 1–2 | 1–2 | 1–2 | Cond.[D][M] | |
| Resveratrol | 500–2000 mg | Yes | 1 | ↑1–2 | ↓2 | 2 | 1–2 | 1–2 | Cond.[D][M] | |
| Pterostilbene | 100–300 mg | Yes | 1 | ↑1–2 | ↓2 | 1 | 1 | 1 | Compatible | |
| Lycopene | 15–75 mg | Context | 0–1 | ↔1–2 | ↓2–3 | 1 | 1–2 | 0–1 | Compatible | |
| Selenium (org.) | 200–400 µg | Yes(sel.) | 3 | ↑1–2 | ↓2–3 | 1–2 | 2–3 | 2–3 | Compatible[F] | |
| SeNPs (oral) | 50–200 µg | Yes(tumor) | 3 | ↑2–3 | ↓2–3 | 0–1 | 1–2 | 2–3 | Compatible[F] | |
| Vitamin C (oral) | ≤2–3 g | Limited | 2 | ↔1 | ↓2–3 | 1 | 2 | 2 | Compatible | |
| β-Carotene | 20–30 mg | High-risk | 1 | ↔1–2 | ↓2 | 1 | 1–2 | 1 | Caution[D][M] | |
| Sulforaphane | 30–100 mg | Indirect | 2 | ↑1 | ↓3–4 | 3–4 | 3–4 | 3–4 | Caution[M] | |
| Melatonin | 10–50 mg | Selective | 1 | ↑1 | ↓3–4 | 1–2 | 1–2 | 1–2 | Compatible | |
| CoQ10 (oxidized) | 100–300 mg | Possible | 2 | ↔1 | ↓2–3 | 1–2 | 2 | 2 | Cond.[M][F] | |
| Luteolin | 50–200 mg | Yes | 1 | ↑1 | ↓2–3 | 1–2 | 1–2 | 1 | Compatible | |
| Apigenin | 50–200 mg | Yes | 1 | ↑1 | ↓2–3 | 1–2 | 1–2 | 1 | Compatible | |
| Kaempferol | 50–200 mg | Yes | 1 | ↑1 | ↓2–3 | 1–2 | 1–2 | 1 | Compatible | |
| Genistein | 30–100 mg | Yes | 1 | ↑1 | ↓2–3 | 1–2 | 1–2 | 1–2 | Cond.[D][H][M] | |
| Fisetin | 100–500 mg | Yes | 1 | ↑1 | ↓2–3 | 1–2 | 1–2 | 1 | Compatible[D][M] | |
| Myricetin | 50–250 mg | Yes | 1 | ↑1–2 | ↓2–3 | 1–2 | 1–2 | 1 | Compatible[D][M] | |
| Ellagic Acid | 200–800 mg | Yes | 0–1 | ↑1–2 | ↓2–3 | 1 | 1 | 0–1 | Compatible | |
| Urolithin A (UA) | 250–1000 mg | Yes (sel.) | 0–1 | ↑1–2 | ↓2–3 | 0–1 | 1 | 0–1 | Compatible | |
| Spermidine | 5–20 mg | Context | 0–1 | ↔1 | ↓1–2 | 0–1 | 1 | 0–1 | Compatible | |
| α-Lipoic acid (ALA) | 300–600 mg | Limited | 2 | ↑1 | ↓2–3 | 1–2 | 1–2 | 1 | Cond.[D][M] | |
| Caffeic / Ferulic | 100–500 mg | Context | 0–1 | ↔1 | ↓2–3 | 1 | 1 | 0–1 | Compatible | |
| Naringenin / Hesp. | 50–200 mg | Limited | 0–1 | ↔1 | ↓3–4 | 0–1 | 0–1 | 0–1 | Compatible | |
| Astaxanthin (ASTX) | 4–12 mg | No | 0 | ↔0 | ↓3–4 | 0 | 0 | 0 | Cond.[M] | |
| Vitamin E (α-toc.) | 200–800 IU | No | 2 | ↔0–1 | ↓3–4 | 0 | 2–3 | 2–3 | Caution[M][D] | |
| Trolox (Vit E) | 20–200 mg | No | 2 | ↔0–1 | ↓3–4 | 0 | 2–3 | 2–3 | Caution[M][D] | |
| N-acetylcysteine | 600–1800 mg | No | 4 | ↓1–2 | ↓3–4 | 2 | 3–4 | 4 | Caution[M][D] | |
| Glutathione (oral) | 250–1000 mg | No | 4 | ↓1 | ↓3–4 | 2 | 3–4 | 3–4 | Caution[M][D] | |
| Lutein / Zeaxanthin | 10–20 mg | No | 0 | ↔0 | ↓3–4 | 0 | 0 | 0 | Compatible |
Compatible – No known interference at oral doses Cond. (Conditional) – Timing, dose, or regimen dependent Caution – Likely to interfere with ROS-dependent therapies [T] = Timing-sensitive (avoid peri-infusion / ROS-dependent window) [D] = Dose-dependent (low vs high dose behave differently) [M] = Mechanism-dependent (NRF2, ETC, thiol buffering, metal chelation) [H] = Hormone- or receptor-dependent [F] = Form-dependent (chemical form matters)(organic vs nano) *NFR2 Explanation not necessarily reflected in ratings (example Quercetin) -NRF2↑ in normal cells is the dominant pattern -In cancer cells, NRF2 upregulation is possible, but not dominant, and often context-suppressed by stronger pro-oxidant mechanisms. Smaller <50 nm SeNPs generate ROS more efficiently; may interfere with ROS-dependent chemo if given concurrently Chemo compatibility assumes ROSs-dependent cytotoxic modalities (e.g., anthracyclines, platinum agents, radiation). Non-ROS-dependent therapies may not share these constraints. *β-carotene is incompatible primarily in smokers / high-oxygen tissues. Arrows show whether ROS increases (↑), decreases (↓), or neutral/variable (↔) Thiol Buffering Index (0–4): | TBI Score | Meaning | | --------- | ------------------------------------------------------------------------------------------------------ | | 0 | No effect on thiol pools; does not buffer redox stress (mostly non-thiol antioxidants) | | 1 | Minimal indirect thiol effect; may slightly modulate thiol-dependent enzymes | | 2 | Moderate indirect thiol effect; may perturb thiols or partially modulate GSH/Trx system | | 3 | Significant thiol buffering; contributes to redox stabilization in cancer cells | | 4 | Strong direct thiol donor; substantially increases GSH/thioredoxin pools; high chemo interference risk | Note the table is very general, and database searches and details should be researched for each compound of interest. Example: Luteolin can show NRF2 down in cancer cells
A) Direct disruption of glycolytic flux (energy stress ± ROS)
HK step disruption: 2-DG (substrate analog; blocks glycolysis; also affects glycosylation)
PFK regulation (note: citrate/ATP/AMP are endogenous regulators; actionable nodes include PFKFB3)
PKM2 modulation (context-dependent effects on glycolysis vs biosynthetic routing)
LDH-A inhibition (Warburg output suppression: pyruvate → lactate)
MCT1 / MCT4 inhibition (lactate transport; acid stress)
B) Shift away from fermentation toward mitochondrial oxidation (often ROS↑)
HIF-1α inhibition (context-dependent; oxygenation and tumor type matter)
PDK inhibition (e.g., DCA → pyruvate into mitochondria; OXPHOS↑; mito ROS may rise)
C) Upstream growth signaling that drives glycolysis
PI3K inhibition
AKT inhibition
- Often decreases glycolysis via PI3K/AKT/mTOR and HIF-1α programs; ROS effects are model-dependent and may increase if cells are forced toward OXPHOS or lose antioxidant compensation.
mTOR inhibition
c-Myc suppression
- Frequently reduces glycolysis and glutamine programs; relationship to COX-2 is context-dependent.
D) Metabolic regulators and nutrient entry points
AMPK activation
- Typically opposes anabolic glycolysis; ROS direction is context-dependent (can rise if OXPHOS is increased, or fall if antioxidant programs dominate).
GLUT1 downregulation (glucose import)
- Model-dependent; ROS may increase if cells are forced toward OXPHOS or lose antioxidant compensation.
GLS (glutaminase) / glutamine dependency
PPP / G6PD (NADPH supply for redox defense)
ROS interpretation note: glycolysis/Warburg inhibition does not always mean ROS↑. ROS is more likely to rise when interventions force a shift toward mitochondrial respiration or simultaneously reduce antioxidant capacity (often [C][M][T]).
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.
(Example query demonstration only; this does not imply clinical benefit.)
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.
|Rank| Biomarker | Primary Clinical Decision Impact | Clinical Class | Why This Rank | | ---| ------------- | -------------------------------- | ---------------- | ---------------------------------------------- | | 1 | EGFR | Determines TKI therapy | Target selection | Binary, life-altering therapy choice | | 2 | HER2 | Anti-HER2 therapy | Target selection | Mandatory in breast/gastric cancer | | 3 | KRAS | Excludes EGFR therapy | Target selection | Negative predictor with major impact | | 4 | PD-L1 | Immunotherapy eligibility | Immunotherapy | Gatekeeper for checkpoint use | | 5 | MSI | Tumor-agnostic immunotherapy | Immunotherapy | One of the strongest predictors of IO response | | 6 | BRAF | Targeted therapy | Target selection | Direct, mutation-specific action | | 7 | BRCA1 / BRCA2 | PARP inhibitor use | Target selection | Therapy + inherited risk | | 8 | ALK | Fusion-targeted therapy | Target selection | Dramatic response when positive | | 9 | AR | Prostate therapy backbone | Target selection | Defines entire disease class | | 10 | ESR1 | Endocrine therapy | Target selection | Absolute requirement in breast cancer | Mid-Tier: Strong but Contextual Decision Impact | Rank | Biomarker | Primary Use | Clinical Class | Notes | | ---- | ------------- | ----------------------- | ---------------- | ----------------------------- | | 11 | NTRK (fusion) | Tumor-agnostic therapy | Target selection | Rare but decisive | | 12 | PSA | Monitoring, progression | Monitoring | Drives treatment timing | | 13 | B2M | Staging & prognosis | Immunotherapy | Used in myeloma/lymphoma | | 14 | TP53 | Risk stratification | Aggressiveness | Alters intensity, trials | | 15 | WT1 | MRD monitoring | Monitoring | Highly actionable in leukemia | | 16 | Ki-67 | Growth rate | Aggressiveness | Influences therapy escalation | | 17 | CA-125 | Therapy response | Monitoring | Standard ovarian tracking | | 18 | CEA | Recurrence detection | Monitoring | Common but nonspecific | Lower-Tier: Indirect / Emerging / Contextual Impact | Rank |Biomarker| Primary Role | Clinical Class | Why Lower | | ---- | ------- | ---------------------- | ---------------- | -------------------------- | | 19 | AFP | Diagnosis/monitoring | Monitoring | Cancer-specific contexts | | 20 | CA 19-9 | Disease burden | Monitoring | Prognostic, not directive | | 21 | MYC | Risk biology | Aggressiveness | Not directly actionable | | 22 | TERT | Prognosis | Aggressiveness | Rarely changes therapy | | 23 | EZH2 | Epigenetic state | Aggressiveness | Select indications | | 24 | SUZ12 | PRC2 dependency | Aggressiveness | Indirect | | 25 | RBM3 | Prognostic | Aggressiveness | Informative, not directive | | 26 | OPG | Bone microenvironment | Microenvironment | Supportive info | | 27 | RAGE | Inflammation state | Microenvironment | Research-stage | | 28 | XIST | Epigenetic instability | Aggressiveness | Not yet clinical | | 29 | FOXM1 | High-risk biology | Aggressiveness | No routine testing | | 30 | TRIB3 | Stress adaptation | Aggressiveness | Mechanistic, not clinical | Core Liver & Systemic Biomarkers in Oncology | Marker | What It Reflects | Main Use in Cancer | Decision Impact | | --------- | ----------------------------------- | ----------------------------------------- | ----------- | | ALT | Hepatocellular injury | Baseline eligibility, toxicity monitoring | High | | AST | Liver + systemic injury | Detect liver injury, muscle involvement | High | | ALP | Cholestasis, bone turnover | Liver mets vs bone mets | High | | bilirubin | Hepatic clearance | Chemotherapy dosing | Critical | | albumin | Synthetic liver function, nutrition | Prognosis, frailty | High | | LDH | Tumor burden, hypoxia | Aggressiveness, prognosis | High | | INR | Liver synthetic failure | Treatment safety | High | Key Inflammatory / Host-Response Biomarkers Used in Oncology | Biomarker | What It Reflects | Main Use in Cancer | Clinical Decision Impact | | ------------------ | -------------------------------- | ---------------------------- | -------------------- | | C-reactive protein | Systemic inflammation | Prognosis, therapy tolerance | High | | ESR | Chronic inflammation | Disease activity trend | Moderate | | ferritin | Inflammation + iron status | Cachexia, cytokine load | High | | IL-6 | Cytokine signaling | Aggressiveness, cachexia | High (specialty use) | | LDH | Tumor burden + hypoxia | Risk stratification | Very high | | albumin | Nutritional & inflammatory state | Frailty, survival | Very high |
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