P53 Cancer Research Results

P53, P53-Guardian of the Genome: Click to Expand ⟱
Source: TCGA
Type: Proapototic
TP53 is the most commonly mutated gene in human cancer. TP53 is a gene that encodes for the p53 tumor suppressor protein ; TP73 (Chr.1p36.33) and TP63 (Chr.3q28) genes that encode transcription factors p73 and p63, respectively, are TP53 homologous structures.
p53 is a crucial tumor suppressor protein that plays a significant role in regulating the cell cycle, maintaining genomic stability, and preventing tumor formation. It is often referred to as the "guardian of the genome" due to its role in protecting cells from DNA damage and stress.
TP53 gene, which encodes the p53 protein, is one of the most frequently mutated genes in human cancers.
Overexpression of MDM2, an inhibitor of p53, can lead to decreased p53 activity even in the presence of wild-type p53.
In some cancers, particularly those with mutant p53, there may be an overexpression of the p53 protein.
Cancers with overexpression: Breast, lung, colorectal, overian, head and neck, Esophageal, bladder, pancreatic, and liver.
PSA, Psoriasis: Click to Expand ⟱
Psoriasis is an autoimmune skin disease.
This section mainly deals with PsA which is psoriatic arthritis

PsA evidence based approach

Rank Approach Evidence Mechanism / Rationale Notes
1 Weight loss if overweight/obese Best direct evidence in PsA Reduces metabolic inflammation, adipokine burden, and joint inflammatory load; may improve treatment response. Highest-yield natural strategy when excess weight is present.
2 Regular exercise / physical activity Good supportive evidence Improves pain, stiffness, function, fatigue, muscle support, and cardiometabolic health. Strong adjunct for joint symptoms and overall health.
3 Mediterranean-style diet / antioxidant-rich whole-food diet Moderate evidence May reduce systemic inflammatory tone; provides polyphenols, fiber, unsaturated fats, and better metabolic support. Best antioxidant strategy is diet pattern rather than antioxidant pills.
4 Intermittent fasting / time-restricted eating Early limited evidence May improve inflammatory signaling and metabolic regulation; possible benefit for CRP, enthesitis, and disease activity. Promising but still exploratory.
5 Omega-3 (fish / fish oil) Mixed evidence Shifts eicosanoids toward less inflammatory profiles and may modestly reduce inflammatory tone. Reasonable adjunct, but not a top-tier PsA joint intervention.
6 Vitamin D Weak PsA-specific treatment evidence More relevant for deficiency correction, bone support, and immune modulation than for direct joint control. Most relevant when levels are low.

PsA pathways to modulate

Rank Pathway / Axis Why It Matters in PsA Joints Helpful Modulation Support Level
1 IL-23 → Th17/Tc17 → IL-17A/F Core inflammatory axis in psoriatic arthritis; active in synovium, enthesis, and related tissues. Reduce excessive IL-23 / IL-17 signaling and downstream cytokine/chemokine output. Very high
2 TNF-α / NF-κB inflammatory axis Major validated cytokine pathway driving inflammation, tissue injury, and amplification of disease activity. Reduce TNF / NF-κB-driven inflammatory signaling and matrix damage. Very high
3 JAK / STAT3 signaling Supports cytokine signaling relevant to synovial and entheseal inflammation. Dampen excessive JAK / STAT3 inflammatory activity. High
4 Myeloid / inflammasome amplification (IL-1β, IL-6, GM-CSF) Amplifies synovitis, pain, recruitment of inflammatory cells, and osteoclastogenic signaling. Reduce IL-1β, IL-6, and GM-CSF inflammatory amplification. High
5 RANKL / M-CSF / osteoclastogenesis Important for bone erosions and osteoclast-mediated damage. Reduce osteoclast differentiation and bone resorption pressure. High
6 DKK1 / Wnt / BMP bone-remodeling balance PsA involves both erosions and abnormal new bone formation. Rebalance remodeling rather than simply suppress all bone formation. Moderate to high
7 COX-2 / 5-LOX / eicosanoid signaling Contributes to inflammatory pain, swelling, and leukocyte recruitment. Reduce excess prostaglandin and leukotriene inflammatory tone. Moderate
8 KEAP1-NRF2 / oxidative stress-redox balance Oxidative imbalance may reinforce inflammatory signaling and tissue injury. Improve antioxidant defense and redox resilience. Moderate
9 Obesity / adipokine / metabolic inflammation axis Obesity is linked to worse disease activity and poorer response. Reduce metabolic inflammation and adverse adipokine signaling. Moderate
10 Gut microbiome / barrier / immune-metabolite axis Gut dysbiosis and barrier changes may influence systemic immune activation. Support gut barrier function and more favorable immune-metabolic signaling. Moderate

Natural products that might help PsA — mechanistic HTML table

Natural Product / Class Main PsA-Relevant Pathways Mechanistic Rationale Direct PsA Joint Evidence Practical Read
Omega-3 (EPA/DHA) IL-17-related signaling; TNF/NF-κB tone; eicosanoids / resolution pathways May shift lipid mediators toward less inflammatory profiles and reduce inflammatory signaling. Mixed / weak Most practical food/supplement adjunct, but not a strong standalone PsA joint therapy.
Curcumin / Turmeric NF-κB; JAK/STAT3; MAPK; IL-17 / IFN-γ; redox signaling Broad anti-inflammatory and signaling-modulating effects relevant to psoriatic disease biology. Very limited direct evidence Reasonable mechanistic adjunct; stronger biology than clinical PsA proof.
Boswellia / Boswellic acids 5-LOX; NF-κB; COX-2; leukotrienes Notable leukotriene / 5-LOX angle with broader anti-inflammatory effects. No strong direct PsA joint trials Plausible adjunct, especially for eicosanoid-driven inflammation.
Ginger NF-κB; COX / LOX; inflammatory pain pathways Anti-inflammatory and antioxidant actions with arthritis-relevant pathway effects. Indirect only Plausible low-to-moderate adjunct; evidence is not PsA-specific.
EGCG / Green tea catechins IL-17 / IL-23-related inflammation; oxidative stress; keratinocyte hyperproliferation Immune-regulatory and antioxidant effects; mainly supported in psoriasis/preclinical models. Mostly psoriasis / preclinical Interesting adjunct, but not proven for PsA joints.
Sulforaphane KEAP1-NRF2; oxidative stress; TH17-related inflammation; autoimmune signaling Strong redox / NRF2 rationale with anti-inflammatory effects in preclinical models. Preclinical / indirect Good mechanistic candidate for the NRF2-redox tier.
Quercetin NF-κB; PI3K/AKT/GLUT1; inflammatory cell signaling Multi-target anti-inflammatory effects with arthritis relevance. Weak direct PsA evidence Mechanistically attractive, clinically still speculative for PsA.
Resveratrol NF-κB; oxidative stress; inflammatory mediators; SIRT1/AMPK-linked effects May reduce inflammatory signaling and support metabolic/redox regulation. Very limited for PsA Interesting but not near the top for real-world PsA use.
Piperlongumine NLRP3 inflammasome; ROS-sensitive inflammatory signaling; FLS proliferation/migration; MMPs Research-stage anti-inflammatory candidate with RA/psoriasis-model relevance. Research-stage only Experimental; not a practical PsA supplement at present.
Shikonin JAK/STAT; TNF-driven synoviocyte signaling; macrophage polarization; psoriasis inflammation Biologically interesting for synovitis and immune-cell signaling. Research-stage only Experimental; mainly of mechanistic interest.


Scientific Papers found: Click to Expand⟱
6164- Cin,    Advances in pharmacological effects and mechanism of action of cinnamaldehyde
- Review, Var, NA - Review, PSA, NA
*glucose↑, *cardioP↑, *Inflam↓, *lipid-P↓, GutMicro↑, TumCP↓, Apoptosis↑, TumCI↓, TumCMig↓, BAX↑, P53↑, Bcl-2↓, IAP1↓, PI3K↓, Akt↓, *ROS↓, *NRF2↑, *NF-kB↓, NF-kB↑,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   IAP1↓, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,  

Migration ⓘ

TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↑, 1,  

Clinical Biomarkers ⓘ

GutMicro↑, 1,  
Total Targets: 12

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

lipid-P↓, 1,   NRF2↑, 1,   ROS↓, 1,  

Core Metabolism/Glycolysis ⓘ

glucose↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   NF-kB↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,  
Total Targets: 7

Scientific Paper Hit Count for: P53, P53-Guardian of the Genome
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:74  Cells:%  prod#:%  Target#:236  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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