LFS is a hereditary genetic condition. This means that the cancer risk can be passed from generation to generation in a family. This condition is most commonly caused by a mutation (alteration) in a gene called TP53, which is the genetic blueprint for a protein called p53.

The standard classification used to define the various cancer genes confines tumor protein p53 (TP53) to the role of a tumor suppressor gene. However, it is now an indisputable fact that many p53 mutants act as oncogenic proteins.

The p53 proto-oncogene can act as a suppressor of transformation. Cell 57, 1083–1093 (1989). Funk, W. D., Pak, D. T., et al. A transcriptionally active DNA-binding site for human p53 protein complexes.

The TP53 gene provides instructions for making a protein called tumor protein p53 (or p53). This protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing (proliferating) too fast or in an uncontrolled way.

p53 mutants are recessive for transactivation of p21WAF1/CIP1 but dominant negative for transactivation of Bax. p53 mutants previously found in human cancers were analyzed for the ability to perform wild-type p53-associated functions.

p53 is maintained at low protein levels during times of homeostasis, when the cell is not exposed to stress or DNA-damaging events, by its predominant negative regulator Mdm2 through the ubiquitin-proteasome pathway. Initial stabilization of p53 occurs through the targeted disruption of the p53 and Mdm2 interaction.

(A) In a wildtype p53 environment, p21 acts as a genome guardian. The activation of the p53/p21 pathway can trigger momentary G1 cell cycle arrest or lead to a chronic state of senescence or apoptosis.

ras-p21 is a G protein that becomes activated when GDP, bound to the protein in its inactive state, is exchanged for GTP. This process of activation is set in motion when a specific growth factor, such as epidermal growth factor (EGF), itself a polypeptide, binds to its receptor.

A P21 is a statement of total income, tax credit and tax paid for a particular tax year for people in paid employment who pay all of their income tax under PAYE (Pay As You Earn). You do not automatically receive a P21 statement from Revenue; you must request this document.

Tumor protein p53 is a nuclear transcription factor that regulates the expression of a wide variety of genes involved in apoptosis, growth arrest, or senescence in response to genotoxic or cellular stress.

In our clinical analysis, a negative (normal) p53 status proved to be associated with resistance to paclitaxel, whereas response was supported by deficient p53. Functional p53 has been found to arrest cell cycle in G1 phase to prevent transition into subsequent phases in the presence of DNA damage (26) .

little genetic variability

Caris Life Sciences® utilizes MI Exome™ (whole exome sequencing) to analyze 250,000 evenly-spaced single nucleotide polymorphisms (SNP) to measure genomic instability in the tumor.