hyperG Cancer Research Results

hyperG, hyperglycemia: Click to Expand ⟱
Source:
Type:
Hyperglycemia is defined as elevated blood glucose levels and may result from diabetes mellitus, insulin resistance, or stress-induced metabolic changes.

– Elevated glucose levels provide abundant energy resources, potentially facilitating rapid tumor cell division and growth.
– Some cancers upregulate glucose transporters (such as GLUT1) to utilize the increased availability of glucose.

Oxidative Stress and DNA Damage:
– Hyperglycemia is associated with the production of reactive oxygen species (ROS) and advanced glycation end-products (AGEs).
– Both ROS and AGEs can lead to DNA damage, genomic instability, and alterations in cell signaling pathways that promote tumor progression.

– Studies have linked hyperglycemia with increased tumor aggressiveness in several cancer types, including breast, colorectal, and pancreatic cancers.
– Patients with hyperglycemia may experience more rapid disease progression and a higher likelihood of metastasis.
– In some cases, elevated glucose levels have been associated with chemotherapy resistance and decreased sensitivity to radiation therapy.

– Effective control of blood sugar through dietary interventions, medications (e.g., insulin, metformin), and lifestyle modifications may beneficially impact cancer outcomes.
– Regular monitoring of blood glucose and hemoglobin A1c (HbA1c) can inform oncologists about potential metabolic challenges during cancer treatment.
Scientific Papers found: Click to Expand⟱
1860- dietFMD,  Chemo,    Fasting-mimicking diet blocks triple-negative breast cancer and cancer stem cell escape
- in-vitro, BC, SUM159 - in-vitro, BC, 4T1
PI3K↑, FMD activates PI3K-AKT, mTOR, and CDK4/6 as survival/growth pathways, which can be targeted by drugs to promote tumor regression.
Akt↑,
mTOR↑,
CDK4↑,
CDK6↑,
hyperG↓, FMD cycles also prevent hyperglycemia and other toxicities caused by these drugs.
TumCG↓, cycles of FMD significantly slowed down tumor growth, reduced tumor size, and caused an increased expression of intratumor Caspase3
TumVol↓,
Casp3↑,
BG↓, confirming our hypothesis that lowering intracellular glucose levels (through reduced extracellular levels or reduced uptake) reduces CSC survival
eff↑, 2DG potentiated the effect of FMD both in terms of delaying tumor progression and in decreasing the number of mammospheres derived by tumor masses,
eff∅, metformin did not show any additive or synergistic antitumor effect when combined with the FMD, thus suggesting that FMD and metformin have redundant effects on blood glucose levels
PKA↓, We have previously shown that prolonged fasting reduces the activity of protein kinase A (PKA) in different types of normal cells
KLF5↓, PKA inhibition resulted in the downregulation of KLF5, a potential therapeutic target for TNBC
p‑GSK‐3β↑, (GSK3β) phosphorylation
Nanog↓, stemness-associated genes NANOG and OCT4, and KLF2 and TBX3,
OCT4↓,
KLF2↓,
eff↑, Combining FMD cycles with PI3K/AKT/mTOR inhibitors results in long-term animal survival and reduces treatment-induced side effects
ROS↑, FMD resulted in an increased expression of pro-apoptotic molecules, such as BIM, and ASK1, a critical cellular stress sensor frequently activated by ROS, whose production was previously shown to be increased by the FMD
BIM↑,
ASK1↑,
PI3K↑, FMD cycles upregulate PI3K-AKT and mTOR pathways and downregulate CCNB-CDK1 while upregulating CCND-CDK4/6 signaling axes
Akt↑,
mTOR↑,
CDK1↓,
CDK4↑,
CDK6↑,
eff↑, combining STS with pictilisib, ipatasertib, and rapamycin, selective inhibitors for PI3K, AKT, and mTOR, respectively, resulted in enhanced cancer cell death and reduction of mammosphere numbers in SUM159 cells

1681- PBG,    Propolis: Its Role and Efficacy in Human Health and Diseases
- Review, Nor, NA
*Inflam↓,
*AntiCan↑,
*antiOx↑,
*hyperG↓, flavanone glycoside found in propolis, has been reported to have insulin-like and lipid-reducing properties that reduce both insulin resistance and hyperglycemia
*BG↓, These flavonoids, including apigenin, naringin, chrysin, galangin, kaempferol, luteolin, genistein, and quercetin help to reduce blood glucose concentration
*HbA1c↓, propolis showed significant effects, reducing the blood glucose levels, serum insulin, and serum glycosylated haemoglobin (HbA1c) levels of T2DM patients
*NF-kB↓, propolis can also suppress inflammatory cascades by blocking the NF-κB pathway and reducing ROS by enhancing antioxidants
*ROS↓,
*TGF-β↑, formation of the transforming growth factor-β1 (TGF-β1) of the cells are promoted by the caffeic acid, CAPE, hesperidin, and quercetin of propolis
*selectivity↑, CAPE is a very significant compound of propolis that has anti-inflammatory properties and also acts as the selective inhibitor of NF-κB activation


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 ⓘ

hyperG↓, 1,   ROS↑, 1,  

Metal & Cofactor Biology ⓘ

KLF5↓, 1,  

Cell Death ⓘ

Akt↑, 2,   ASK1↑, 1,   BIM↑, 1,   Casp3↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK4↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

p‑GSK‐3β↑, 1,   mTOR↑, 2,   Nanog↓, 1,   OCT4↓, 1,   PI3K↑, 2,   TumCG↓, 1,  

Migration ⓘ

KLF2↓, 1,   PKA↓, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↑, 2,  

Drug Metabolism & Resistance ⓘ

eff↑, 3,   eff∅, 1,  

Clinical Biomarkers ⓘ

BG↓, 1,  

Functional Outcomes ⓘ

TumVol↓, 1,  
Total Targets: 22

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   hyperG↓, 1,   ROS↓, 1,  

Migration ⓘ

TGF-β↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

selectivity↑, 1,  

Clinical Biomarkers ⓘ

BG↓, 1,   HbA1c↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,  
Total Targets: 10

Scientific Paper Hit Count for: hyperG, hyperglycemia
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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