hTERT/TERT Cancer Research Results

hTERT/TERT, human telomerase reverse transcriptase: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
A key component of the enzyme telomerase, which is responsible for maintaining the length of telomeres at the ends of chromosomes.
In most somatic cells, telomerase activity is low or absent, leading to progressive telomere shortening with each cell division, which eventually triggers cellular senescence or apoptosis. many cancer cells exhibit reactivation of telomerase, primarily through the upregulation of hTERT. This reactivation allows cancer cells to maintain their telomere length, enabling them to divide indefinitely and contributing to the immortality characteristic of cancer cells. The expression of hTERT is often associated with various types of cancer, including melanoma, breast cancer, and lung cancer.
| Cancer context | TERT biomarker                | Clinical use                             |
| -------------- | ----------------------------- | ---------------------------------------- |
| Glioma         | Promoter mutation             | **WHO classification, prognosis**        |
| Thyroid cancer | Promoter mutation             | **Aggressiveness, recurrence risk**      |
| Melanoma       | Promoter mutation             | Risk stratification                      |
| Bladder cancer | Promoter mutation (urine DNA) | **Noninvasive detection & surveillance** |
| HCC            | Promoter mutation             | Early event, prognosis                   |

Why TERT Is Valuable Despite Limited “Actionability”
-Telomere maintenance is mandatory for long-term tumor survival
-TERT activation is often an early, irreversible event
-Its presence signals a tumor that has escaped replicative limits
-That makes TERT one of the best markers of “point-of-no-return” biology.


Var, Various Cancer: Click to Expand ⟱
Cyclooxygenase (COX)-2 overexpression has been noted in various cancers. PI3Ks/AKT pathways are over-activated in several types of cancers.
EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity.
Activating protein-1 transcription factor has been associated with pathogenesis including cancer.
Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics.
The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors.
The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50.
Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25].
The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell.
Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.
Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer.
Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research.
Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy.
Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer.
Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis.
More than 50% of human cancers have a mutated nonfunctional p53.


Scientific Papers found: Click to Expand⟱
2782- CHr,    Broad-Spectrum Preclinical Antitumor Activity of Chrysin: Current Trends and Future Perspectives
- Review, Var, NA - Review, Stroke, NA - Review, Park, NA
*antiOx↑, *Inflam↓, *hepatoP↑, *neuroP↑, *BioAv↓, *cardioP↑, *lipidLev↓, *RenoP↑, *TNF-α↓, *IL2↓, *PI3K↓, *Akt↓, *ROS↓, *cognitive↑, eff↑, cycD1/CCND1↓, hTERT/TERT↓, VEGF↓, p‑STAT3↓, TumMeta↓, TumCP↓, eff↑, eff↑, IL1β↓, IL6↓, NF-kB↓, ROS↑, MMP↓, Cyt‑c↑, Apoptosis↑, ER Stress↑, Ca+2↑, TET1↑, Let-7↑, Twist↓, EMT↓, TumCCA↑, Casp3↑, Casp9↑, BAX↑, HK2↓, GlucoseCon↓, lactateProd↓, Glycolysis↓, SHP1↑, N-cadherin↓, E-cadherin↑, UPR↑, PERK↑, ATF4↑, eIF2α↑, RadioS↑, NOTCH1↑, NRF2↓, BioAv↑, eff↑,
2783- CHr,    Apoptotic Effects of Chrysin in Human Cancer Cell Lines
- Review, Var, NA
TumCP↓, Apoptosis↑, Casp↑, PCNA↓, p38↑, NF-kB↑, DNAdam↑, XIAP↓, Cyt‑c↑, Casp3↑, Akt↓, SCF↓, hTERT/TERT↓, COX2↓, *Inflam↓, *antiOx↑, *chemoPv↑, AR-V7?, CYP19?,
2784- CHr,    Chrysin targets aberrant molecular signatures and pathways in carcinogenesis (Review)
- Review, Var, NA
Apoptosis↑, TumCMig↓, *toxicity↝, ChemoSen↑, *BioAv↓, Dose↝, neuroP↑, *P450↓, *ROS↓, *HDL↑, *GSTs↑, *SOD↑, *Catalase↑, *MAPK↓, *NF-kB↓, *PTEN↑, *VEGF↑, ROS↑, MMP↓, Ca+2↑, selectivity↑, PCNA↓, Twist↓, EMT↓, CDKN1C↑, p‑STAT3↑, MMP2↓, MMP9↓, eff↑, cycD1/CCND1↓, hTERT/TERT↓, CLDN1↓, TumVol↓, OS↑, COX2↓, eff↑, CDK2↓, CDK4↓, selectivity↑, TumCCA↑, E-cadherin↑, HK2↓, HDAC↓,
2785- CHr,    Emerging cellular and molecular mechanisms underlying anticancer indications of chrysin
- Review, Var, NA
*NF-kB↓, *COX2↓, *iNOS↓, angioG↓, TOP1↓, HDAC↓, TNF-α↓, IL1β↓, cardioP↑, RenoP↑, neuroP↑, LDL↓, BioAv↑, eff↑, cycD1/CCND1↓, hTERT/TERT↓, MMP-10↓, Akt↓, STAT3↓, VEGF↓, EGFR↓, Snail↓, Slug↓, Vim↓, E-cadherin↑, eff↑, TET1↑, ROS↑, mTOR↓, PPARα↓, ER Stress↑, Ca+2↑, ERK↓, MMP↑, Cyt‑c↑, Casp3↑, HK2↓, NRF2↓, HO-1↓, MMP2↓, MMP9↓, Fibronectin↓, GRP78/BiP↑, XBP-1↓, p‑eIF2α↑, *AST↓, ALAT↓, ALP↓, LDH↓, COX2↑, Bcl-xL↓, IL6↓, PGE2↓, iNOS↓, DNAdam↑, UPR↑, Hif1a↓, EMT↓, Twist↓, lipid-P↑, CLDN1↓, PDK1↓, IL10↓, TLR4↓, NOTCH1↑, PARP↑, Mcl-1↓, XIAP↓,
2790- CHr,    Chrysin: Pharmacological and therapeutic properties
- Review, Var, NA
*hepatoP↑, *neuroP↓, *ROS↓, *cardioP↑, *Inflam↓, eff↑, hTERT/TERT↓, cycD1/CCND1↓, MMP9↓, MMP2↓, TIMP1↑, TIMP2↑, BioAv↑, HK2↓, ROS↑, MMP↓, Casp3↑, ADP:ATP↑, Apoptosis↑, ER Stress↑, UPR↑, GRP78/BiP↝, eff↑, Ca+2↑,
5148- GamB,    Gambogic acid: A shining natural compound to nanomedicine for cancer therapeutics
- Review, Var, NA
AntiCan↑, angioG↓, ChemoSen↑, RadioS↑, VEGF↓, MMP2↓, MMP9↓, Telomerase↓, TrxR↓, ERK↓, HSP90↓, ROS↑, SIRT1↑, survivin↓, cFLIP↓, Casp3↑, Casp8↑, Casp9↑, BAD↓, BID↓, Bcl-2↓, BAX↑, STAT3↓, hTERT/TERT↓, NF-kB↓, Myc↓, Hif1a↓, FOXD3↑, BioAv↓, BioAv↑, P53↑, eff↓, OCR↓, MMP↓, PI3K↓, Akt↓, BBB↑, TumCG↓, TumMeta↓, BioAv↑,
2912- LT,    Luteolin: a flavonoid with a multifaceted anticancer potential
- Review, Var, NA
ROS↑, TumCCA↑, TumCP↓, angioG↓, ER Stress↑, mtDam↑, PERK↑, ATF4↑, eIF2α↑, cl‑Casp12↑, EMT↓, E-cadherin↑, N-cadherin↓, Vim↓, *neuroP↑, NF-kB↓, PI3K↓, Akt↑, XIAP↓, MMP↓, Ca+2↑, BAX↑, Casp3↑, Casp9↑, Bcl-2↓, Cyt‑c↑, IronCh↑, SOD↓, *ROS↓, *LDHA↑, *SOD↑, *GSH↑, *BioAv↓, Telomerase↓, cMyc↓, hTERT/TERT↓, DR5↑, Fas↑, FADD↑, BAD↑, BOK↑, BID↑, NAIP↓, Mcl-1↓, CDK2↓, CDK4↓, MAPK↓, AKT1↓, Akt2↓, *Beclin-1↓, Hif1a↓, LC3II↑, Beclin-1↑,
2914- LT,    Therapeutic Potential of Luteolin on Cancer
- Review, Var, NA
*antiOx↑, *IronCh↑, *toxicity↓, *BioAv↓, *BioAv↑, DNAdam↑, TumCP↓, DR5↑, P53↑, JNK↑, BAX↑, cl‑Casp3↑, cl‑Casp8↑, cl‑Casp9↑, cl‑PARP↑, survivin↓, cycD1/CCND1↓, CycB/CCNB1↓, CDC2↓, P21↑, angioG↓, MMP2↓, AEG1↓, VEGF↓, VEGFR2↓, MMP9↓, CXCR4↓, PI3K↓, Akt↓, ERK↓, TumAuto↑, LC3B-II↑, EMT↓, E-cadherin↑, N-cadherin↓, Wnt↓, ROS↑, NICD↓, p‑GSK‐3β↓, iNOS↓, COX2↓, NRF2↑, Ca+2↑, ChemoSen↑, ChemoSen↓, IFN-γ↓, RadioS↑, MDM2↓, NOTCH1↓, AR↓, TIMP1↑, TIMP2↑, ER Stress↑, CDK2↓, Telomerase↓, p‑NF-kB↑, p‑cMyc↑, hTERT/TERT↓, RAS↓, YAP/TEAD↓, TAZ↓, NF-kB↓, NRF2↓, HO-1↓, MDR1↓,
2916- LT,    Antioxidative and Anticancer Potential of Luteolin: A Comprehensive Approach Against Wide Range of Human Malignancies
- Review, Var, NA - Review, AD, NA - Review, Park, NA
proCasp9↓, CDC2↓, CycB/CCNB1↓, Casp9↑, Casp3↑, Cyt‑c↑, cycA1/CCNA1↑, CDK2↓, APAF1↑, TumCCA↑, P53↑, BAX↑, VEGF↓, Bcl-2↓, Apoptosis↑, p‑Akt↓, p‑EGFR↓, p‑ERK↓, p‑STAT3↓, cardioP↑, Catalase↓, SOD↓, *BioAv↓, *antiOx↑, *ROS↓, *NO↓, *GSTs↑, *GSR↑, *SOD↑, *Catalase↑, *lipid-P↓, PI3K↓, Akt↓, CDK2↓, BNIP3↑, hTERT/TERT↓, DR5↑, Beclin-1↑, TNF-α↓, NF-kB↓, IL1↓, IL6↓, EMT↓, FAK↓, E-cadherin↑, MDM2↓, NOTCH↓, MAPK↑, Vim↓, N-cadherin↓, Snail↓, MMP2↓, Twist↓, MMP9↓, ROS↑, MMP↓, *AChE↓, *MMP↑, *Aβ↓, *neuroP↑, Trx1↑, ROS↓, *NRF2↑, NRF2↓, *BBB↑, ChemoSen↑, GutMicro↑,
1666- PBG,    Molecular and Cellular Mechanisms of Propolis and Its Polyphenolic Compounds against Cancer
- Review, Var, NA
ChemoSen↑, TumCCA↑, TumCP↓, Apoptosis↑, antiOx↓, ROS↑, COX2↑, ER(estro)↓, cycA1/CCNA1↓, CycB/CCNB1↓, CDK2↓, P21↑, p27↑, hTERT/TERT↓, HDAC↓, ROS⇅, Dose?, ROS↓, ROS↑, DNAdam↑, ChemoSen↑, LOX1↓, lipid-P↓, NO↑, Igs↑, NK cell↑, MMPs↓, VEGF↓, Hif1a↓, GLUT1↓, HK2↓, selectivity↑, RadioS↑, GlucoseCon↓, lactateProd↓, eff↓, *BioAv↓,
1730- SFN,    Sulforaphane: An emergent anti-cancer stem cell agent
- Review, Var, NA
BioAv↓, BioAv↑, GSTA1↑, P450↓, TumCCA↑, HDAC↓, P21↑, p27↑, DNMT1↓, DNMT3A↓, cycD1/CCND1↑, DNAdam↑, BAX↑, Cyt‑c↑, Apoptosis↑, ROS↑, AIF↑, CDK1↑, Casp3↑, Casp8↑, Casp9↑, NRF2↑, NF-kB↓, TNF-α↓, IL1β↓, CSCs↓, CD133↓, CD44↓, ALDH↓, Nanog↓, OCT4↓, hTERT/TERT↓, MMP2↓, EMT↓, ALDH1A1↓, Wnt↓, NOTCH↓, ChemoSen↑, *Ki-67↓, *HDAC3↓, *HDAC↓,
1508- SFN,    Nrf2 targeting by sulforaphane: A potential therapy for cancer treatment
- Review, Var, NA
*BioAv↑, HDAC↓, TumCCA↓, eff↓, Wnt↓, β-catenin/ZEB1↓, Casp12?, Bcl-2↓, cl‑PARP↑, Bax:Bcl2↑, IAP1↓, Casp3↑, Casp9↑, Telomerase↓, hTERT/TERT↓, ROS?, DNMTs↓, angioG↓, VEGF↓, Hif1a↓, cMYB↓, MMP1↓, MMP2↓, MMP9↓, ERK↑, E-cadherin↑, CD44↓, MMP2↓, eff↑, IL2↑, IFN-γ↑, IL1β↓, IL6↓, TNF-α↓, NF-kB↓, ERK↓, NRF2↑, RadioS↑, ChemoSideEff↓,
2095- TQ,    Review on the Potential Therapeutic Roles of Nigella sativa in the Treatment of Patients with Cancer: Involvement of Apoptosis
- Review, Var, NA
TumCCA↑, Apoptosis↑, ROS↑, Cyt‑c↑, Bax:Bcl2↑, Casp3↑, Casp9↑, cl‑PARP↑, P53↑, P21↑, cMyc↓, hTERT/TERT↓, cycD1/CCND1↓, CDK4↓, NF-kB↓, IAP1↓, IAP2↓, XIAP↓, Bcl-xL↓, survivin↓, COX2↓, MMP9↓, VEGF↓, eff↑,
1740- VitD3,    Vitamin D and Cancer: An Historical Overview of the Epidemiology and Mechanisms
- Review, Var, NA
Risk↓, eff↑, eff↑, Risk↓, Risk↓, ChemoSen↑, RadioS↑, Cyt‑c↑, Casp3↑, Casp9↑, hTERT/TERT↓, eff↑, E-cadherin↑, CLDN2↑, ZO-1↑, Snail↓, Zeb1↓, Vim↓, VEGF↓, NK cell↑, Risk↓, eff↑,

Showing Research Papers: 1 to 14 of 14

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 14

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   Catalase↓, 1,   GSTA1↑, 1,   HO-1↓, 2,   lipid-P↓, 1,   lipid-P↑, 1,   NRF2↓, 4,   NRF2↑, 3,   ROS?, 1,   ROS↓, 2,   ROS↑, 12,   ROS⇅, 1,   SOD↓, 2,   Trx1↑, 1,   TrxR↓, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

ADP:ATP↑, 1,   AIF↑, 1,   BOK↑, 1,   CDC2↓, 2,   MMP↓, 6,   MMP↑, 1,   mtDam↑, 1,   OCR↓, 1,   XIAP↓, 4,  

Core Metabolism/Glycolysis ⓘ

AKT1↓, 1,   ALAT↓, 1,   cMyc↓, 2,   p‑cMyc↑, 1,   GlucoseCon↓, 2,   Glycolysis↓, 1,   HK2↓, 5,   lactateProd↓, 2,   LDH↓, 1,   LDL↓, 1,   PDK1↓, 1,   PPARα↓, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 5,   Akt↑, 1,   p‑Akt↓, 1,   APAF1↑, 1,   Apoptosis↑, 8,   BAD↓, 1,   BAD↑, 1,   BAX↑, 6,   Bax:Bcl2↑, 2,   Bcl-2↓, 4,   Bcl-xL↓, 2,   BID↓, 1,   BID↑, 1,   Casp↑, 1,   Casp12?, 1,   cl‑Casp12↑, 1,   Casp3↑, 11,   cl‑Casp3↑, 1,   Casp8↑, 2,   cl‑Casp8↑, 1,   Casp9↑, 8,   cl‑Casp9↑, 1,   proCasp9↓, 1,   cFLIP↓, 1,   Cyt‑c↑, 8,   DR5↑, 3,   FADD↑, 1,   Fas↑, 1,   hTERT/TERT↓, 14,   IAP1↓, 2,   IAP2↓, 1,   iNOS↓, 2,   JNK↑, 1,   MAPK↓, 1,   MAPK↑, 1,   Mcl-1↓, 2,   MDM2↓, 2,   Myc↓, 1,   NAIP↓, 1,   NICD↓, 1,   p27↑, 2,   p38↑, 1,   survivin↓, 3,   Telomerase↓, 4,   YAP/TEAD↓, 1,  

Kinase & Signal Transduction ⓘ

FOXD3↑, 1,  

Protein Folding & ER Stress ⓘ

eIF2α↑, 2,   p‑eIF2α↑, 1,   ER Stress↑, 5,   GRP78/BiP↑, 1,   GRP78/BiP↝, 1,   HSP90↓, 1,   PERK↑, 2,   UPR↑, 3,   XBP-1↓, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 2,   BNIP3↑, 1,   LC3B-II↑, 1,   LC3II↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 5,   DNMT1↓, 1,   DNMT3A↓, 1,   DNMTs↓, 1,   P53↑, 4,   PARP↑, 1,   cl‑PARP↑, 3,   PCNA↓, 2,  

Cell Cycle & Senescence ⓘ

CDK1↑, 1,   CDK2↓, 6,   CDK4↓, 3,   cycA1/CCNA1↓, 1,   cycA1/CCNA1↑, 1,   CycB/CCNB1↓, 3,   cycD1/CCND1↓, 6,   cycD1/CCND1↑, 1,   P21↑, 4,   TumCCA↓, 1,   TumCCA↑, 7,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 1,   ALDH1A1↓, 1,   AR-V7?, 1,   CD133↓, 1,   CD44↓, 2,   cMYB↓, 1,   CSCs↓, 1,   EMT↓, 7,   ERK↓, 4,   ERK↑, 1,   p‑ERK↓, 1,   p‑GSK‐3β↓, 1,   HDAC↓, 5,   Let-7↑, 1,   mTOR↓, 1,   Nanog↓, 1,   NOTCH↓, 2,   NOTCH1↓, 1,   NOTCH1↑, 2,   OCT4↓, 1,   PI3K↓, 4,   RAS↓, 1,   SCF↓, 1,   SHP1↑, 1,   STAT3↓, 2,   p‑STAT3↓, 2,   p‑STAT3↑, 1,   TAZ↓, 1,   TOP1↓, 1,   TumCG↓, 1,   Wnt↓, 3,  

Migration ⓘ

AEG1↓, 1,   Akt2↓, 1,   Ca+2↑, 6,   CDKN1C↑, 1,   CLDN1↓, 2,   CLDN2↑, 1,   E-cadherin↑, 8,   FAK↓, 1,   Fibronectin↓, 1,   MMP-10↓, 1,   MMP1↓, 1,   MMP2↓, 9,   MMP9↓, 8,   MMPs↓, 1,   N-cadherin↓, 4,   Slug↓, 1,   Snail↓, 3,   TET1↑, 2,   TIMP1↑, 2,   TIMP2↑, 2,   TumCMig↓, 1,   TumCP↓, 5,   TumMeta↓, 2,   Twist↓, 4,   Vim↓, 4,   Zeb1↓, 1,   ZO-1↑, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 5,   ATF4↑, 2,   EGFR↓, 1,   p‑EGFR↓, 1,   Hif1a↓, 5,   LOX1↓, 1,   NO↑, 1,   VEGF↓, 9,   VEGFR2↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,   GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 4,   COX2↑, 2,   CXCR4↓, 1,   IFN-γ↓, 1,   IFN-γ↑, 1,   Igs↑, 1,   IL1↓, 1,   IL10↓, 1,   IL1β↓, 4,   IL2↑, 1,   IL6↓, 4,   NF-kB↓, 8,   NF-kB↑, 1,   p‑NF-kB↑, 1,   NK cell↑, 2,   PGE2↓, 1,   TLR4↓, 1,   TNF-α↓, 4,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,   CYP19?, 1,   ER(estro)↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 6,   ChemoSen↓, 1,   ChemoSen↑, 8,   Dose?, 1,   Dose↝, 1,   eff↓, 3,   eff↑, 16,   MDR1↓, 1,   P450↓, 1,   RadioS↑, 6,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   ALP↓, 1,   AR↓, 1,   EGFR↓, 1,   p‑EGFR↓, 1,   GutMicro↑, 1,   hTERT/TERT↓, 14,   IL6↓, 4,   LDH↓, 1,   Myc↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   cardioP↑, 2,   ChemoSideEff↓, 1,   neuroP↑, 2,   OS↑, 1,   RenoP↑, 1,   Risk↓, 4,   TumVol↓, 1,  
Total Targets: 238

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 4,   Catalase↑, 2,   GSH↑, 1,   GSR↑, 1,   GSTs↑, 2,   HDL↑, 1,   lipid-P↓, 1,   NRF2↑, 1,   ROS↓, 5,   SOD↑, 3,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↑, 1,  

Core Metabolism/Glycolysis ⓘ

LDHA↑, 1,   lipidLev↓, 1,  

Cell Death ⓘ

Akt↓, 1,   iNOS↓, 1,   MAPK↓, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC↓, 1,   HDAC3↓, 1,   PI3K↓, 1,   PTEN↑, 1,  

Migration ⓘ

Ki-67↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,   VEGF↑, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL2↓, 1,   Inflam↓, 3,   NF-kB↓, 2,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 6,   BioAv↑, 2,   P450↓, 1,  

Clinical Biomarkers ⓘ

AST↓, 1,   Ki-67↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 2,   chemoPv↑, 1,   cognitive↑, 1,   hepatoP↑, 2,   neuroP↓, 1,   neuroP↑, 3,   RenoP↑, 1,   toxicity↓, 1,   toxicity↝, 1,  
Total Targets: 47

Scientific Paper Hit Count for: hTERT/TERT, human telomerase reverse transcriptase
5 Chrysin
3 Luteolin
2 Sulforaphane (mainly Broccoli)
1 Gambogic Acid
1 Propolis -bee glue
1 Thymoquinone
1 Vitamin D3
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:26  Cells:%  prod#:%  Target#:150  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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