| 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. -Hypoxia (low oxygen levels) within tumors is a major cause of resistance to radiotherapy |
| Source: CGL-CS |
| Type: oncogene |
| Family of RAS proteins (KRAS, NRAS, and HRAS) have been well described to cause oncogenic transformation. - The expression and mutational status of RAS isoforms are critical in several cancers and are generally linked with a poorer prognosis when mutated. RAS is one of the most frequently activated oncogenic drivers in human cancer. Mutations lock RAS in its GTP-bound active state, making signaling: -Constitutive -Growth-factor independent -Resistant to normal feedback control Key framing: RAS is a true driver oncogene, not just an amplifier. Core Oncogenic Pathways Downstream of RAS RAS sits at the apex of multiple essential signaling cascades: a. MAPK Pathway (RAF–MEK–ERK) -Drives proliferation -Induces cell-cycle genes (Cyclin D, MYC, FOS/AP-1) -Supports invasion and differentiation blockade b. PI3K–AKT–mTOR -Promotes survival and metabolic reprogramming -Enhances resistance to apoptosis -Supports protein synthesis and growth c. RAL-GDS and Others -Cytoskeletal remodeling -Vesicle trafficking -Metastatic behavior Together, these create a multi-axis growth and survival program. |
| 3487- | MF, | Rad, | High-specificity protection against radiation-induced bone loss by a pulsed electromagnetic field |
| - | Review, | Var, | NA |
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#:269 State#:% Dir#:2
wNotes=0 sortOrder:rid,rpid