The p53, p63 and p73 genes is the heart of the war on Breast Cancer

October 25, 2010 By Robert Graham -- Washington DC /Businesswire/
The p53, p63 and p73 genes is the heart of the war on Breast Cancer.When p53 is suppressed, as it is in many cancers, defective cells multiply, fueling Breast Cancer. p53 can't order a bad cell to kill itself without p63 and p73 also being active.

When metastatic Breast Cancer occurs p63 is inactive.The reactivation of TAp63 could benefit patients with metastatic breast cancer.

Viral transduction of a few genes for the reprogramming of
human somatic cells into induced pluripotent stem (iPS) cells.Identifying conditions that can replace viral transduction of oncogenic transcription factors (TFs) and enhance reprogramming efficiency. Hybrid Pharma have found that neural progenitor cells can be reprogrammed with fewer genetic manipulations than previously reported somatic cells, and in the other we have found
that small molecules may be able to replace viral integration of
certain transcription factors and promote the reprogramming process.

Genomic Science indicates that we have to change the breast cancer culture to find a cure. Stem cells and progenitor cells has shown promise. Like stem cells, progenitor cells have a tendency to differentiate into a specific type of cell. In contrast to stem cells,
however, they are already far more specific: they are pushed to
differentiate into their "target" cell. The most important difference
between stem cells and progenitor cells is that stem cells can
replicate indefinitely, whereas progenitor cells can only divide a
limited number of times. Controversy about the exact definition
remains and the concept is still evolving.

Hybrid Medical first direction of research aims to determine
what cell becomes transformed; in other words, the cell of
origin of a breast tumor. In the mammary gland, mammary stem
cells, which can self-renew and differentiate, generate rapidly
dividing progenitors that in turn generate differentiated cells
of the mammary gland epithelial lineages: the luminal and myoepithelial lineages. Cancer is thought to originate in these stem cells or in progenitor cells that have acquired self-renewal. Thus, a first degree of heterogeneity comes from whether a tumor comes from a stem cell or a progenitor cell.

Hybrid second direction aims to determine what genetic alterations
transform a normal breast cell and make it cancerous. The repertoire of genetic alterations can be found by using high-throughput, large-scale methods, such as mass sequencing and array comparative genomic hybridization (aCGH) . These have
revealed a number of alterations – mutations, deletions,
amplifications and fusions – that target hundreds of genes,
suggesting a high level of heterogeneity. Some tumors can
have a high level of genetic instability whereas others can
have an apparently normal genome.


Panoincell qX also uses a Visualize Real-Time Breast Cancer
Data using Signal Stochastic Resonance Units Neurons
Detection and Analysis for Breast Cancer model after McCulloch-Pitts.
Panoincell qX computer-assisted diagnosing of breast cancer from mammograms. How Panoincell qX works is a genetic network simulation trained with tumor incidence data from knockout experiments.

The genetic network is implemented using a neural
network; knockout genotypes are simulated by removing
nodes in the neural network. Two analyses are used to
interpret the resulting network weights. We use a novel
approach of fixing the network topology that allows knockout
TSG (tumor suppressor gene) data from multiple studies to
overlap and indirectly inform one another. The trained
simulation is validated by reproducing qualitative mammary
cancer susceptibilities of ATM, BRCA1, and p53,p63 TSGs. The work
Panoincell qx is valuable because it allows TSG mammary cancer
susceptibility to be quantified using genetic network
topology and in vivo knockout data.