Insulin Cancer Research Results

Insulin, Insulin: Click to Expand ⟱

Source:

Type:

Insulin, traditionally known for its role in regulating blood glucose levels, also exerts potent mitogenic (cell division–promoting) effects.

Insulin exerts its effects primarily through binding to the insulin receptor (IR), a receptor tyrosine kinase. Upon binding, the receptor undergoes autophosphorylation and activates several downstream signaling cascades, including:
-PI3K/Akt Pathway: Overactivation of this pathway is often observed in cancers.
-RAS/MAPK Pathway: aberrant activation can lead to tumorigenesis.

IR-A: Often predominates in fetal tissues and some cancer cells. It has a higher affinity for insulin-like growth factors (IGFs) and is more mitogenic.
IR-B: More involved in metabolic regulation.

Studies have shown that many cancers (such as breast, colon, and lung cancers) preferentially overexpress the IR-A isoform.

Scientific Papers found: Click to Expand⟱

2761-

BetA,

Betulinic acid increases lifespan and stress resistance via insulin/IGF-1 signaling pathway in Caenorhabditis elegans

in-vivo,

Nor,

Insulin↓, BA improves insulin sensitivity in metabolic syndrome rats (51), but inhibits insulin/IGF-1 receptor signaling to suppress de novo lipogenesis in HepG2 cells
IGF-1↓,
*SOD↑, figure 4
*Catalase↑,
*GSH↑,
*MDA↓,
*antiOx?, Betulinic acid has robust antioxidant activity in vivo.

5780-

CRMs,

HCAs,

RES,

Sper,

ASA

Caloric Restriction Mimetics against Age-Associated Disease: Targets, Mechanisms, and Therapeutic Potential

Review,

Var,

*OS↑, The permanent or periodic reduction of calorie intake without malnutrition (caloric restriction and fasting) is the only strategy that reliably extends healthspan in mammals including non-human primates.
*AntiAge↑, CRMs will become part of the pharmacological armamentarium against aging and age-related cardiovascular, neurodegenerative, and malignant diseases.
*cardioP↑,
*neuroP↑,
AntiCan↑,
*TNF-α↓, In healthy humans, CR also decreases the levels of circulating tumor necrosis factor-α
*Weight↓, In obese humans, CR promotes significant weight loss and improves general health
*BP↓, Figure 1
*Inflam↓,
*Insulin↓,
*ROS↓,
*AMPK↑,
*mTOR↓,
*SIRT1↑, Resveratrol and Other SIRT1 Activators
CRM↑, Figure2: HCA, Resveratrol, Spermidine, Aspirin, Berberine, EGCG, QC, etc

1863-

dietFMD,

Chemo,

Effect of fasting on cancer: A narrative review of scientific evidence

Review,

Var,

eff↑, recommend combining prolonged periodic fasting with a standard conventional therapeutic approach to promote cancer‐free survival, treatment efficacy, and reduce side effects in cancer patients.
ChemoSideEff↓, lowered levels of IGF1 and insulin have the potential to protect healthy cells from side effects
ChemoSen↑,
Insulin↓, causes insulin levels to drop and glucagon levels to rise
HDAC↓, Histone deacetylases are inhibited by ketone bodies, which may slow tumor development.
IGF-1↓, FGF21 rises during intermittent fasting, and it plays a vital role in lowering IGF1 levels by inhibiting phosphorylated STAT5 in the liver
STAT5↓,
BG↓, Fasting suppresses glucose, IGF1, insulin, the MAPK pathway, and heme oxygenase 1
MAPK↓,
HO-1↓,
ATG3↑, while increasing many autophagy‐regulating components (Atgs, LC3, Beclin1, p62, Sirt1, and LAMP2).
Beclin-1↑,
p62↑,
SIRT1↑,
LAMP2↑,
OXPHOS↑, Fasting causes cancer cells to release oxidative phosphorylation (OXPHOS) through aerobic glycolysis
ROS↑, which leads to an increase in reactive oxygen species (ROS), p53 activation, DNA damage, and cell death in response to chemotherapy.
P53↑,
DNAdam↑,
TumCD↑,
ATP↑, and causes extracellular ATP accumulation, which inhibits Treg cells and the M2 phenotype while activating CD8+ cytotoxic T cells.
Treg lymp↓,
M2 MC↓,
CD8+↑,
Glycolysis↓, By lowering glucose intake and boosting fatty acid oxidation, fasting can induce a transition from aerobic glycolysis to mitochondrial oxidative phosphorylation in cancerous cells, resulting in increased ROS
GutMicro↑, Fasting has been shown to have a direct impact on the gut microbial community's constitution, function, and interaction with the host, which is the complex and diverse microbial population that lives in the intestine
GutMicro↑, Fasting also reduces the number of potentially harmful Proteobacteria while boosting the levels of Akkermansia muciniphila.
Warburg↓, Fasting generates an anti‐Warburg effect in colon cancer models, which increases oxygen demand but decreases ATP production, indicating an increase in mitochondrial uncoupling.
Dose↝, Those patients fasted for 36 h before treatment and 24 h thereafter, having a total of 350 calories per day. Within 8 days of chemotherapy, no substantial weight loss was recorded, although there was an improvement in quality of life and weariness.

1853-

dietFMD,

Impact of Fasting on Patients With Cancer: An Integrative Review

Review,

Var,

*toxicity∅, Data suggest overall good compliance, no malnutrition, minimal side effects. No significant changes were identified to suggest increased harm.
QoL∅, unchanged quality of life (QOL),
eff↑, improved endocrine parameters
eff↝, mixed results for cancer outcomes
ChemoSideEff↓, decreasing chemotherapy-related side effects
TumCG↓, limiting tumor growth
Dose↑, When fasting is used as an adjunct to chemotherapy, a minimum fasting period of at least 48 hours is currently recommended for nutritional interventions in order to achieve a measurable metabolic response at the cellular level
toxicity↝, The increased risk for poor outcomes associated with malnutrition, weight loss, and cachexia poses an obvious safety concern for patients with cancer who participate in calorie-restricted fasting
eff↑, short-term fasting involving water-only or limited daily calorie consumption for less than a week has the potential to achieve positive metabolic changes while avoiding malnutrition and significant weight loss
IGF-1↑, statistically significant decrease in IGF-1 among participants compliant with fasting compared with regular diet during the middle of therapy
*OXPHOS↑, Healthy cells also use mitochondrial oxidative phosphorylation for metabolism while cancer cells use aerobic glycolysis, also known as the Warburg effect
BG↓, statistically significant decrease in glucose among participants compliant with fasting compared with controls
Insulin↓, statistically significant decrease in insulin among participants compliant with fasting compared with regular diet before the first cycle of chemotherapy (p = .001), as well as during the middle of therapy
RadioS↑, A complete or partial radiographic response was also noted more often among fasting participants compared with normal diet participants

1855-

dietFMD,

Impact of modified short-term fasting and its combination with a fasting supportive diet during chemotherapy on the incidence and severity of chemotherapy-induced toxicities in cancer patients - a controlled cross-over pilot study

Trial,

NA,

ChemoSideEff↓, total toxicities’ score were significantly reduced. reported significantly fewer chemotherapy-induced side effects, including asthenia, fatigue and gastrointestinal problems such as vomiting and diarrhoea
QoL↑, We also observed significantly fewer chemotherapy postponements post-mSTF, reflecting improved tolerance of chemotherapy
IGF-1↓, On average, Insulin [− 169.4 ± 44.1; 95% CI -257.1 – (− 81.8); P < 0.001] and Insulin-like growth factor 1 levels [− 33.3 ± 5.4; 95% CI -44.1 – (− 22.5); P < 0.001] dropped significantly during fasting.
Insulin↓,

2269-

dietMet,

Mechanisms of Increased In Vivo Insulin Sensitivity by Dietary Methionine Restriction in Mice

in-vivo,

Nor,

mice

*adiP↑, metabolic responses include reduced adiposity, reduced circulating and tissue lipid levels, increased plasma adiponectin and fibroblast growth factor 21 (FGF-21), and reduced fasting insulin and blood glucose
*FGF↑,
*Insulin↓,
*glucose↓,
*Akt↑, activation of Akt was significantly higher in methionine-restricted HepG2 cells
*GSH↓, MR produces a significant decrease in hepatic GSH
*PTEN↓, MR in HepG2 cells limits the capacity of the cells to reactivate oxidized PTEN, resulting in amplification of insulin activation of Akt by increasing PIP3.
*FGF21↑, MR produced a threefold increase in FGF-21 mRNA that was mirrored by a fourfold increase in serum FGF-21.
*PIP3↑,

2263-

dietMet,

Methionine Restriction and Cancer Biology

Review,

Var,

AntiCan↑, dependence of many tumor cells on an exogenous source of the sulfur amino acid, methionine, [9,10,11] makes dietary methionine restriction (MR) an exciting potential tool in the treatment of cancer.
TumCP↓, Proliferation and growth of several types of cancer cells are inhibited by MR,
TumCG↓,
selectivity↑, while normal cells are unaffected by limiting methionine as long as homocysteine is present
ChemoSen↓, MR has been shown to enhance efficacy of chemotherapy and radiation therapy in animal models
RadioS↑,
Insulin↓, MR may work by inhibiting prostate cancer cell proliferation, inhibiting the insulin/IGF-1 axis
*GlucoseCon↑, increase in tissue-specific glucose uptake measured during a hyperinsulinemic-euglycemic clamp
*ROS↓, MR does not increase oxidative stress, in part because MR enhances antioxidant capacity and increases proton leak in the liver, likely decreasing ROS production
*antiOx↑,
*GSH↑, ability of MR to increase GSH levels in red blood cells. Surprisingly, when methionine was restricted by 80% in the diet of rats, the level of GSH in the blood actually increased due to adaptations in sulfur-amino acid metabolism
GSH↑, However, GSH concentrations were reduced in the liver
eff↑, Of note, methionine restriction is effective when the non-essential amino acid, cysteine, is absent from the diet or media.
polyA↓, MR may work by inhibiting prostate cancer cell proliferation, inhibiting the insulin/IGF-1 axis, or by reducing polyamine synthesis. MR-induced depletion of polyamines
TS↓, MR selectively reduces TS activity in prostate cancer cells by ~80% within 48 h, but does not affect TS activity in normal prostate epithelial cells
Raf↓, MR inhibits Raf and Akt oncogenic pathways, while increasing caspase-9 and the mitochondrial pro-apoptotic protein, Bak
Akt↓,
Casp9↑,
Bak↑,
P21↑, MR upregulating p21 and p27 (cell cycle inhibitors that halt cell cycle progression) in LNCaP cells
p27↑,
Insulin↓, MR-induced reduction in circulating insulin and IGF1, which have both been linked to tumor growth
IGF-1↓,

2265-

dietMet,

Cysteine supplementation reverses methionine restriction effects on rat adiposity: significance of stearoyl-coenzyme A desaturase

in-vivo,

Nor,

Rats

*SCD1↓, Dietary methionine restriction in rats decreases hepatic Scd1 mRNA and protein,
*Weight↓, MR markedly lowered weight gain, as previously reported (21, 22, 28), despite food intake/g body weight being consistently higher than CF group throughout the study
*Insulin↓, MR significantly decreased serum concentrations of insulin, leptin, IGF-1, and raised adiponectin compared with CF.
*IGF-1↓,
*adiP↑,
*eff↓, these effects were reversed by cysteine

5066-

dietSTF,

Intermittent and Periodic Fasting, Hormones, and Cancer Prevention

Review,

Var,

IGF-1↓, Long-term CR is reported to reduce IGF-1 serum levels in rodents by ~30–40%, protecting them against several types of cancers
OS↑, effects of CR in retarding aging, by increasing lifespan by ~35%, reducing the incidence of kidney disorders, chronic pneumonia and tumors [
AntiAge↑,
glucose↓, underline mechanisms could be mediated by the decrease in blood glucose, IGF-1 and insulin levels
Insulin↓,

5069-

dietSTF,

The Role of Intermittent Fasting in the Activation of Autophagy Processes in the Context of Cancer Diseases

Review,

Var,

Risk↓, IF has shown potential for reducing cancer risk and enhancing therapeutic efficacy by sensitizing tumor cells to chemotherapy and radiotherapy.
ChemoSen↑, intermittent fasting (IF) may enhance the effectiveness of chemotherapy and targeted therapies by activating autophagy. IF enhances the effectiveness of chemotherapy, including drugs such as cisplatin, cyclophosphamide, and doxorubicin
RadioS↑, disease stabilization, improved response to radiotherapy patients with glioma
*Dose↝, 16:8—16 h of fasting with an 8 h eating window;
*Dose↝, 5:2—consuming a standard number of calories for 5 days and reducing intake to 25% of daily requirements for 2 days;
*Dose↝, Eat–Stop–Eat—complete fasting for 24–48 h.
*LDL↓, IF during Ramadan (approximately 18 h of fasting for 29–30 days) reduces LDL cholesterol levels and increases HDL cholesterol in women, as well as reducing inflammatory markers such as CRP and TNF-α
*CRP↓,
*TNF-α↓,
TumAuto↓, Intermittent fasting activates autophagy as an adaptive mechanism to nutrient deprivation, which may modulate tumor development and treatment
GLUT1↓, fasting reduces the expression of glucose transporters GLUT1/2, which slow down cancer metabolism and increase the susceptibility of cancer cells to oxidative stress
GLUT2↓,
glucose↓, studies on cell and animal models have shown that intermittent fasting reduces glucose and insulin-like growth factor (IGF-1) levels [103], as well as insulin [104,105], resulting in the inhibition of the mTOR kinase pathway (PI3K/Akt/mTOR), suppress
IGF-1↓,
Insulin↓,
mTOR↓,
mTORC1↓, suppression of mTORC1 [22], and activation of AMPK through increased ADP/ATP ratio in cells, which supports autophagy and induces apoptosis
AMPK↑,
Warburg↓, Moreover, IF counteracts the Warburg effect by promoting oxidative phosphorylation, leading to an increase in the production of reactive oxygen species (ROS) and enhanced oxidative stress in cancer cells [106,108], causing DNA damage and the activati
OXPHOS↑,
ROS↑,
DNAdam↑,
JAK1↓, fasting reduces the production of adenosine by cancer cells, inhibiting the activation of the JAK1/STAT pathway, thereby reducing cancer cell proliferation
STAT↓,
TumCP↓,
QoL↑, reduction in IGF-1 levels, improved quality of life patients with multiple cancer types

3708-

dietSTF,

Fasting as a Therapy in Neurological Disease

*PGC-1α↑, figure 1
*AMPK↑,
*adiP↑,
*glucose↓,
*Insulin↓,
*mTOR↓,
*IL6↓,
*TNF-α↓,
*cognitive↑, or even enhanced—cognitive performance
*Inflam↓, fasting suppresses inflammation, reducing the expression of pro-inflammatory cytokines such as interleukin 6 (IL6) and tumor necrosis factor α (TNFα)
*eff↑, mice fasted on alternate days can eat twice as much on the feeding day, such that their net weekly calorie intake remains similar to mice fed ad libitum; despite the lack of overall calorie restriction, the former still display beneficial metabolic e
*neuroP↑, Fasting can also prevent and treat many neurological disorders in animals;
ChemoSen↑, fasting has been shown to improve the therapeutic responses of a variety of rodent cancer models, including gliomas, to chemotherapy
eff↓, shorter nightly fasts were associated with an increased recurrence of cancer
chemoP↑, fasting before or after chemotherapy decreased chemotherapy-related adverse effects, such as weakness, fatigue, and gastrointestinal upset
*eff↑, implementation of a fasting regimen after a traumatic brain injury confers neuroprotection and improves functional recovery

5064-

Ex,

Insulin,_Igfs.996.aspx">Effect Of Exercise Intervention On Insulin, Igfs And Igfbps In Cancer Patients

Review,

Var,

IGF-1↓, All but one study showed that exercise resulted in significant reduction or no change in circulating levels of IGF-1 and IGF-2.
IGF-2↓,
Insulin↓, Aerobic exercise training lowers the levels of insulin and IGF in healthy people.

5235-

Ex,

Effect of Low-Intensity Aerobic Exercise on Insulin-Like Growth Factor-I and Insulin-Like Growth Factor-Binding Proteins in Healthy Men

Trial,

Nor,

 Fourteen healthy men participated in cycle ergometer training at lactate threshold intensity for 60 min/day, 5 days/week for 6 weeks.

Insulin↓, fasting insulin levels decreased by 13%.
IGF-1↓, low-intensity aerobic training decreased the circulating levels of IGF-I by 9%, while IGFBP-1 levels increased by 16%.
IGFBP1↑,
eff↑, An interesting finding was that higher pretraining level of IGF-I was associated with greater decline in IGF-I with training.

5795-

MET,

Metformin: A Review of Potential Mechanism and Therapeutic Utility Beyond Diabetes

Review,

AD,

Review,

Park,

Review,

Diabetic,

*AntiDiabetic↑, Metformin has been designated as one of the most crucial first-line therapeutic agents in the management of type 2 diabetes mellitus.
*AMPK↑, acts majorly by activating AMPK (Adenosine Monophosphate-Activated Protein Kinase) in the cells and reducing glucose output from the liver.
*glyC↓, It also decreases advanced glycation end products and reactive oxygen species production in the endothelium apart from regulating the glucose and lipid metabolism
*ROS↓,
*cardioP↑, hence minimizing the cardiovascular risks.
*neuroP↑, Preclinical studies have also shown some evidence of metformin’s neuroprotective role in Parkinson’s disease, Alzheimer’s disease, multiple sclerosis and Huntington’s disease.
*Half-Life↝, The plasma half-life of metformin is 2–3 hours, and the active duration is about 6–10hrs.
*toxicity↝, Metformin use for an extended period is linked to a deficiency of vitamin B12.
*BioAv↑, Absolute bioavailability 50–60% in healthy individuals
*glucose↓, Conventionally, it is quite established that metformin lowers blood glucose primarily by its action on the liver
*AGEs↓, Metformin decreases the synthesis of AGE (“Advanced Glycation End”) product formation and hyperglycaemic-induced ROS (“Reactive Oxygen Species”) production
AntiCan↑, There is growing evidence that metformin has anti-cancer effects based on clinical and preclinical studies.
Risk↓, reported that metformin use might decrease the risk of lung cancer within T2D patients as compared to other conventional agents.
TumCP↓, Several studies on cancer cell lines have observed that metformin treatment leads to inhibition of development and proliferation and induces apoptosis of the cancer cells
Apoptosis↑,
TumCCA↑, Metformin was found to block the cell cycle in the “G(0)/G(1)” phase
cycD1/CCND1↓, and this was observed with a sharp drop in the cyclin D1 levels, pRb phosphorylation, and elevated p27(kip) expression.
pRB↓,
p27↓,
mTOR↓, as well as inhibits the mTOR pathway that is activated by insulin.
Casp↑, Metformin is also responsible for inducing caspase-dependent apoptosis along with c- JNK (“Jun N-Terminal Kinase”) activation, oxidative stress and mitochondrial depolarization.
ROS↑,
MMP↓,
ChemoSen↑, patients who received metformin along with the chemotherapy had better pathologic responses as compared to the group without metformin
*hepatoP↑, effects including cardioprotective, hepatoprotective, anti-malignant, and geroprotective effects
*CRM↑, mechanism behind the process of calorie restriction is a reduction in insulin
*Insulin↓,

2248-

MF,

Magnetic fields modulate metabolism and gut microbiome in correlation with Pgc-1α expression: Follow-up to an in vitro magnetic mitohormetic study

in-vivo,

Nor,

1.5 mT, 10 min/week

mice

*PGC-1α↑, The combination of PEMFs and exercise for 6 weeks enhanced running performance and upregulated muscular and adipose Pgc-1α transcript levels, whereas exercise alone was incapable of elevating Pgc-1α levels.
*GutMicro↑, The gut microbiome Firmicutes/Bacteroidetes ratio decreased with exercise and PEMF exposure, alone or in combination, which has been associated in published studies with an increase in lean body mass.
*FAO↓, >4 months PEMF treatment alone enhanced oxidative muscle expression, fatty acid oxidation, and reduced insulin levels.
*Insulin↓,

2333-

RES,

Resveratrol regulates insulin resistance to improve the glycolytic pathway by activating SIRT2 in PCOS granulosa cells

in-vitro,

Nor,

SD rats received a high-fat diet and letrozole for 30 days to
establish the PCOS model

*glucose↓, RES played a protective role on the IR in PCOS rats, which significantly decreased the levels of blood glucose and serum insulin, up regulated the expression of IGF1R, and down regulated the expression of IGF1.
*Insulin↓,
*IGFR↓,
*IGF-1↓,
*LDHA↑, RES overtly repaired the glycolysis process by reversing the levels of lactic acid and pyruvate, together with up regulating the expression level of LDHA, HK2, and PKM2, after AGK2 treatment.
*HK2↑,
*PKM2↑,
*Glycolysis↝, RES could eectively improve insulin resistance and restore the glycolysis pathway by regulating SIRT2, which may contribute to attenuating the ovarian damage of PCOS rat
*SIRT2↑, activating SIRT2 in PCOS granulosa cells

Showing Research Papers: 1 to 16 of 16

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 16

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

CD8+↑, 1,
Total Targets: 73

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx?, 1, antiOx↑, 1, Catalase↑, 1, GSH↓, 1, GSH↑, 2, MDA↓, 1, OXPHOS↑, 1, ROS↓, 3, SOD↑, 1,

Mitochondria & Bioenergetics ⓘ

Insulin↓, 7, PGC-1α↑, 2,

Core Metabolism/Glycolysis ⓘ

adiP↑, 3, AMPK↑, 3, CRM↑, 1, FAO↓, 1, FGF21↑, 1, glucose↓, 4, GlucoseCon↑, 1, glyC↓, 1, Glycolysis↝, 1, HK2↑, 1, LDHA↑, 1, LDL↓, 1, PIP3↑, 1, PKM2↑, 1, SCD1↓, 1, SIRT1↑, 1, SIRT2↑, 1,

Cell Death ⓘ

Akt↑, 1,

Proliferation, Differentiation & Cell State ⓘ

FGF↑, 1, IGF-1↓, 2, IGFR↓, 1, mTOR↓, 2, PTEN↓, 1,

Immune & Inflammatory Signaling ⓘ

CRP↓, 1, IL6↓, 1, Inflam↓, 2, TNF-α↓, 3,

Protein Aggregation ⓘ

AGEs↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↑, 1, Dose↝, 3, eff↓, 1, eff↑, 2, Half-Life↝, 1,

Clinical Biomarkers ⓘ

BP↓, 1, CRP↓, 1, GutMicro↑, 1, IL6↓, 1,

Functional Outcomes ⓘ

AntiAge↑, 1, AntiDiabetic↑, 1, cardioP↑, 2, cognitive↑, 1, hepatoP↑, 1, neuroP↑, 3, OS↑, 1, toxicity↝, 1, toxicity∅, 1, Weight↓, 2,
Total Targets: 58

Scientific Paper Hit Count for: Insulin, Insulin

3 diet FMD Fasting Mimicking Diet
3 diet Methionine-Restricted Diet
3 diet Short Term Fasting
2 Resveratrol
2 Exercise
1 Betulinic acid
1 Calorie Restriction Mimetics
1 Hydroxycinnamic-acid
1 Spermidine
1 Aspirin -acetylsalicylic acid
1 Chemotherapy
1 Metformin
1 Magnetic Fields

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#:%  Target#:1190  State#:%  Dir#:1
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Insulin Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Proliferation, Differentiation & Cell State ⓘ

Immune & Inflammatory Signaling ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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