Radiotherapy/Radiation / ICAM-1 Cancer Research Results

Rad, Radiotherapy/Radiation: Click to Expand ⟱
Features:
Treatment of disease with radiation, especially by selective irradiation with x-rays or other ionizing radiation and by ingestion of radioisotopes.

Radiosensitizer
Atorvaqone, (mitochondria inhibitor) decrease O2 consumption making more O2 available as a radiosensitizer.
ICAM-1, Intercellular Adhesion Molecule 1: Click to Expand ⟱
Source:
Type:
ICAM-1 also known as CD54 is a protein that in humans is encoded by the ICAM1 gene. ICAM-1 is an important regulator of cell–cell interactions and recent studies have shown that it promotes malignancy in several carcinomas.
Intercellular Adhesion Molecule 1 (ICAM-1) is a cell surface glycoprotein that plays a critical role in the immune response by facilitating the adhesion of leukocytes to endothelial cells. It is part of the immunoglobulin superfamily and is involved in various cellular processes, including inflammation, immune response, and tumor progression.
Expression in Cancers: ICAM-1 is often overexpressed in various types of cancers, including breast, lung, colorectal, and melanoma. Its expression can be induced by pro-inflammatory cytokines, growth factors, and other stimuli present in the tumor microenvironment.
Prognostic Implications: The expression levels of ICAM-1 have been associated with cancer prognosis. In some studies, high levels of ICAM-1 expression correlate with poor prognosis, increased tumor aggressiveness, and a higher likelihood of metastasis.

ICAM-1 is an adhesion molecule that is often overexpressed in various cancers and is associated with poor prognosis and increased metastatic potential.
Scientific Papers found: Click to Expand⟱
2669- AL,  Rad,    Inhibition of ICAM-1 expression by garlic component, allicin, in gamma-irradiated human vascular endothelial cells via downregulation of the JNK signaling pathway
- in-vitro, Nor, HUVECs
*ICAM-1↓, *AP-1↓, *p‑cJun↓, *radioP↑, JNK↓,
3012- RosA,  Rad,    Rosmarinic Acid Prevents Radiation-Induced Pulmonary Fibrosis Through Attenuation of ROSMYPT1TGFβ1 Signaling Via miR-19b-3p
- in-vitro, Nor, IMR90
*Inflam↓, *ROS↓, *p‑NF-kB↓, *Rho↓, *ROCK1↓, *radioP↑, *MCP1↓, *RANTES↓, *ICAM-1↓, *PGC1A↑, *NOX4↓, *Dose↝,

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:


Cell Death ⓘ

JNK↓, 1,  
Total Targets: 1

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

NOX4↓, 1,   ROS↓, 1,  

Core Metabolism/Glycolysis ⓘ

PGC1A↑, 1,  

Transcription & Epigenetics ⓘ

p‑cJun↓, 1,  

Migration ⓘ

AP-1↓, 1,   Rho↓, 1,   ROCK1↓, 1,  

Immune & Inflammatory Signaling ⓘ

ICAM-1↓, 2,   Inflam↓, 1,   MCP1↓, 1,   p‑NF-kB↓, 1,   RANTES↓, 1,  

Drug Metabolism & Resistance ⓘ

Dose↝, 1,  

Functional Outcomes ⓘ

radioP↑, 2,  
Total Targets: 14

Scientific Paper Hit Count for: ICAM-1, Intercellular Adhesion Molecule 1
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#:201  Target#:419  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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