The Dallas Cowboys Tony Dorsett Is losing His Memory Because Tony Has Neuroblastoma And Gene TDP-43

Barron’s Medical Journal Reporting From Baylor College Of Medicine In The Texas Medical Center Houston, Texas USA

---

The Dallas Cowboys Tony Dorsett Is losing His Memory Because Tony Has Neuroblastoma And Gene TDP-43 

---

Houston, Texas ( AP ) Barron’s Medical Journal Sports was concerned after seeing Tony Dorsett the famous running back for The Dallas Cowboys announced that he was losing his memory. Barron’s

decided to ask the question, can some football players have a gene that would cause football players to lose their memory while playing Football?

The Gene TDP-43 In Adults And Gene MYCN or CD44 In Kids has shown some amazing results. Neuroblastoma is a malignant (cancerous) tumor that develops from nerve tissue. It usually occurs in infants and children.

Barrons Medical Journal ask Sam Houston Biotech CEO for answers. To our surprise Rose Conrad Sam Houston CEO says that it has been known for years that some football players have a gene called TDP- 43. TAR DNA-binding protein of 43kDa (TDP-43). Genomics is again the key to equalize a patient’s risk. Conrads says new Genomics genetic risk factor for amyotrophic lateral sclerosis, commonly known as ALS or Lou Gehrig's disease.

There is no cure for ALS and the current treatment only slows disease progression. The identification of pathological interactions between ataxin 2 and TDP-43, another ALS-associated disease protein, together with the strong genetic association of ataxin 2 intermediate-length polyQ expansions and ALS, should aid in the development of biomarkers and empower the development of new therapies for this disease.

Barron’s Medical Journal Researched Joshua M. Shulman, M.D., Ph.D. of Laboratory for Integrative Functional Genomics Departments of Neurology and Molecular & Human Genetics Baylor College of Medicine. Their mission is to offer clinical manifestation of neurodegenerative disease is the culmination of a multi-tiered pathogenic cascade that evolves over decades—understanding how genetic variants impact this causal chain is essential. Although 2% of the population over age 65 are clinically diagnosed with Parkinson's disease, the defining pathology of disease (alpha-synuclein Lewy bodies) is discovered in 20% of brains from population-based autopsy studies. We are therefore investigating the impact of genomic variation on directly measured Lewy pathology, neuronal loss in the midbrain substantia nigra, and progressive motor impairment, leveraging human subject cohorts with detailed clinical and pathological data. We also participate in collaborative studies for the functional genetic dissection of Alzheimer's disease, focusing on the responsible neuropathology, amyloid neuritic plaques and Tau neurofibrillary tangles.

Despite the promise of current human genetic methods, such as genome-wide association studies, they often fail to identify disease susceptibility genes with certainty, instead highlighting broad genomic regions. We are taking advantage of the rapid and powerful genetics available in the fruit fly Drosophila melanogaster in order to accelerate the validation of responsible genes and an understanding of their functions in disease pathogenesis. Expression of human amyloid-beta, Tau, or alpha-synuclein proteins in the fly nervous system recapitulates many core features of Alzheimer's disease and Parkinson's disease pathogenesis. We are testing candidate human susceptibility genes for functional genetic interactions in these fly models of neurodegeneration. Implicated molecular pathways are probed in greater depth, using both Drosophila and human genetic approaches. Our strategy has recently identified cell adhesion converging on the cytoskeleton as likely important for Tau-mediated neurodegeneration and Alzheimer's disease susceptibility, and we are now following up these insights to elucidate the detailed mechanisms.

Chronic traumatic encephalopathy (CTE) is the term coined for the neurodegenerative disease often suspected in athletes with histories of repeated concussion and progressive dementia. Histologically, CTE is defined as a tauopathy with a distribution of tau-positive neurofibrillary tangles (NFTs) that is distinct from other tauopathies, and usually shows an absence of beta-amyloid deposits, in contrast to Alzheimer's disease (AD). Although the connection between repeated concussions and CTE-type neurodegeneration has been recently proposed, this causal relationship has not yet been firmly established. Also, the prevalence of CTE among athletes with multiple concussions is unknown.

All participants had progressive neurocognitive decline prior to death; however, only 3 cases had post-mortem neuropathological findings consistent with CTE. The other 3 participants had pathological diagnoses

of AD, amyotrophic lateral sclerosis (ALS), and Parkinson's disease (PD). Moreover, the CTE cases showed co-morbid pathology of cancer, vascular disease, and AD

Parents can look for in their kids disease called Neuroblastoma. 8% of 30 Million Uninsured has Familial Cancer 1% of the 8% Kids has the ALK Gene on Chromosome2 that results in Neuroblastoma Cancer. Sam Houston Biotech Analytics Business Intelligence CIO Reports - 50% of the Moms with the Gene MYCN or CD44 Kids will have Neuroblastoma Cancer. The way Moms can recognized Neuroblastoma is a Abdominal Mass. The symptoms in high-risk patients are due to this tumor mass or bone pain from the cancer metastases. Extensive bone marrow metastasis may result in pancytopenia. Abdominal distention with respiratory compromise due to massive liver metastases may occur in infants. Because they originate in paraspinal ganglia, neuroblastomas may invade through neural foramina and compress the spinal cord extradurally, causing paralysis. The survival rate is twice as high if diagnosed in infants less that one years old. Genes that encode RNA-binding proteins (RBPs) such as PTB, hnRNP L, and SRSF1 are auto regulated to maintain a constant level of mRNA (Buratti and Baralle 2011).This autoregulatory process may be achieved in part by selective alternative splicing events that trigger nonsense-mediated decay (NMD)-mediated RNA degradation (Lejeune and Maquat 2005). The general termRUST (regulated unproductive splicing and translation) has been proposed to describe this category of gene regulation (Lareau et al. 2007a). Conrad also says that science labs use Genomics to generated multiple antibodies specific to phosphorylated TDP-43 by immunizing phosphopeptides of TDP-43, and analyzed

FTLD-U and ALS brains by immunohistochemistry, immunoelectron microscopy, and immunoblots. In addition, we performed investigations aimed at identifying the responsible kinases, and we assessed the effects of phosphorylation on TDP-43 oligomerization and fibrillization.

As we see in the above picture of A Future National Football League (NFL ) Quarter Back Greyson Dean Secades Of Pope John XXIII High School In Houston, Texas playing is his State Championship Game and planning on being a "Pre-Med-Major" will have the benefit of having a Genomic Science Test to ensure that player thirty years from now will remain healthy after their Football playing days are over.

http://www.hudl.com/athlete/o/520388/highlights/31158406

Is Amy Robach Making The Right Breast Cancer Treatment Choice At 40

Barron's Medical Journal Reporting From Duke University Medical School Durham, NC USA (Global Newswire )(AP News)

---

Is Amy Robach Making The Right Breast Cancer Treatment Choice At 40 

---

Durham, NC (AP) After Good Morning America’s Amy Robach was diagnosed with Breast Cancer Barron’s Medical Journal Asked The CEO Of Sam Houston Biotech Inc Rose Conrad what she taught of the announcement ? Rose was happy to see that so many Women will now take notice and be willing to take a test at forty years of age to see if they are candidates for breast cancer. Conrad went on to say, why did Good Morning America not include A Genomic Test as part of the breast cancer testing process.

Genomics is a discipline in genetics that applies recombinant DNA, DNA sequencing methods, and bioinformatics to sequence, assemble, and analyze the function and structure of genomes (the complete set of DNA within a single cell of an organism). We then ask Rose is her company Doing any work with Genomics for breast cancer and if so explain the process. Genomics is the Gaussian processes in action, to predict the likelihood of chemotherapy benefit as well as recurrence, for patients with node-negative breast cancer that is estrogen-receptor positive and/or progesterone-receptor positive. Additionally, physicians use Sam Houston to make treatment recommendations for certain node-positive breast cancer patients, and the test report also provides quantitative scores for select individual genes. Sam Houston has been extensively evaluated in thirteen clinical studies involving more than 4,000 breast cancer patients worldwide, including a large validation study published in The New England Journal of Medicine and a chemotherapy benefit study published in the Journal of Clinical Oncology. Both Medicare and private health plans covering over 90 percent of U.S. insured lives provided reimbursement for Sam Houston for patients with node-negative breast cancer that is estrogen-receptor positive and/or progesterone-receptor positive through contracts, agreements or policy decisions.

Breast Cancer Researchers and Scientist are ahead of the curve with several new technologies based on Nanoparticles and Semi Conductors Namely Genomics and treatments. The field of genomics is caught ina data deluge. Targeted breast cancer DNA sequencing is becoming faster and cheaper at a pace far outstripping Moore’s law, which describes the rate at which computing gets faster and cheaper.

The result is that the ability to determine Targeted breast cancer DNA sequences is starting to outrun the ability of researchers to store, transmit and especially to analyze the data.

The cost of sequencing a human genome — all three billion bases of DNA in a set of human chromosomes — plunged to $10,000.00 which means genomics breast cancer DNA sequencing is around $3000.00.

The lower cost, along with increasing speed, has led to a huge increase in how much breast Cancer sequencing data is being produced.

Numerous investigations have shown that both tissue and cell distribution profiles of anticancer drugs can be controlled by their entrapment in submicronic colloidal systems (nanoparticles). The rationale behind this approach is to increase antitumor efficacy, while reducing systemic side-effects. This review provides an update of tumor targeting with conventional or long-circulating nanoparticles. The in vivo fate of these systems, after intravascular or tumoral administration, is discussed, as well as the mechanism involved in tumor regression. Nanoparticles are also of benefit for the selective delivery of oligonucleotides to tumor cells. Moreover, certain types of nanoparticles showed some interesting capacity to reverse MDR resistance, which is a major problem in chemotherapy. The first experiments, aiming to decorate nanoparticles with molecular ligand for active targeting of cancerous cells

Miniaturization will allow the tools for many different tests to be situated together on the same small device. Hybrid Sam Houston Researchers Say that nanotechnology will allow them to run many diagnostic tests simultaneously.

Nanoparticles nanoshells is use to antibodies that recognize cancer cells. Sam Houston scientist envision letting these nanoshells seek out their cancerous targets, then applying near-infrared light. The heat generated by the light-absorbing nanoshells can successfully killed breast cancer tumor cells while leaving neighboring cells intact.

A nanometer is a billionth of a meter. It's difficult to imagine anything so small, but think of something only 1/80,000 the width of a human hair. Ten hydrogen atoms could be laid side-by-side in a single nanometer.

Sam Houston minuscule molecule that will be used to detect breast cancer is a quantum dot. Quantum dots are tiny crystals that glow when they are stimulated by ultraviolet light. The wavelength, or color, of the light depends on the size of the crystal. Latex beads filled with these crystals can be designed to bind to specific DNA sequences. Hybrid Sam Houston understands that Hyperthermia gold nanoshell Targeted breast cancer genomics at 40 for high risk women will reduce breast cancer at 60 years of Age. Training Genomics Counselor and Storing DNA Analysis in the cloud will allow Hybrid Sam Houston to say that Chemotherapy will help their breast cancer outcome or if Chemotheraphy and Hyperthermia will extend their life.

The impact of genomics and pharmacogenomics in the current arena of clinical oncology is well-established. In breast cancer, mutations in the BRCA1 and BRCA2 genes have been well-characterized to carry a high risk of the disease during a woman's lifespan. However, these high risk genes contribute to only a small proportion of the familial cases of breast cancer. Hence, further efforts aimed to study the contribution of genetic mutations in other genes, including the estrogen receptor gene, TP53, CYP19, and mismatch repair genes to further investigate the genetic component of breast cancer.

Multiple pharmacogenomic studies have previously linked genetic variants in known pathways with treatment response in cancer patients. Currently, polymorphisms in drug metabolizing enzymes, efflux transporters, as well as, drug targets have shown correlations to variations in response and toxicity to commonly prescribed chemotherapeutic treatments of breast cancer. CYP2D6 variants have been correlated with tamoxifen response and interindividual variability seen. An emerging application of cancer genetics and pharmacogenetics involves the use of inherited or acquired genetic abnormalities to predict treatment toxicity or outcomes. Recently, methods that involve the scanning of entire genomes for common variants have begun to influence studies of cancer causation. Currently, treatment individualization for breast cancer can take place on the basis of few molecular targets including the estrogen receptor and the overexpression of the HER2 receptor. Overall, the current review summarizes the recent findings in the genetic and pharmacogenetic research of breast cancer and the advances made in personalization of treatment.

Women that use a Genomic Breast Cancer Test at 40 has a eighty seven percent chance to make sixty

Want To Know The Power Of Breast Cancer Research Funding Perjeta

Want To Know The Power Of Breast Cancer Research Funding Perjeta 

---

Barron’s Medical Journal Reporting from The University Of Texas Medical School Houston, Texas USA

---

Houston ( AP ) Barron’s Medical Journal is at The University of Texas Medical School to bring you the latest in breast cancer research. Yes there is a new kid on the block for breast cancer Perjeta. Perjeta was only used for Women that had stage four breast cancer and now thanks to millions of dollars spent on breast cancer research the FDA has approved Perjeta to be use in Stage one breast cancer. This is fantastic news and the power of genomics science what use to take years now companies like Roche and other are using genomic to speed up their research.

United States (U.S.) Food and Drug Administration (FDA) granted accelerated approval of a Perjeta (pertuzumab) regimen for neoadjuvant treatment (use before surgery) in people with high-risk, HER2-positive early stage breast cancer. This approval is based primarily on data from a Phase II study showing that nearly 40 percent of people receiving the combination of Perjeta, Herceptin (trastuzumab) and docetaxel chemotherapy had no evidence of tumour tissue detectable at the time of surgery (known as a pathological complete response, or pCR). The Perjeta regimen is the first neoadjuvant breast cancer treatment approved by the FDA and also the first to be approved based on pCR data.

The approval of pertuzumab for neoadjuvant treatment of breast cancer is based on a randomized, multicenter, open-label trial in patients with HER2-positive, operable, locally advanced or inflammatory breast cancer

Brought To You By Singer & Song Writer Kristen Mills (T2-4d). Breast tumor samples were required to show HER2 overexpression (IHC 3+ or FISH amplification ratio of at least 2.0 determined by a central laboratory). The trial enrolled 417 patients who were randomly assigned to receive 1 of 4 neoadjuvant regimens prior to surgery as follows: trastuzumab plus docetaxel; pertuzumab plus trastuzumab and docetaxel; pertuzumab plus trastuzumab; or pertuzumab plus docetaxel.

Pertuzumab, trastuzumab, and docetaxel were administered preoperatively by intravenous infusion (IV) every 3 weeks for a total of 4 cycles. Following surgery all patients received 3 cycles of fluorouracil, epirubicin, and cyclophosphamide (FEC) IV every 3 weeks and trastuzumab was administered IV every 3 weeks to complete 1 year of therapy. The trial’s primary endpoint was pathologic complete response (pCR) rate defined as the absence of invasive cancer in the breast (ypT0/is). The FDA-preferred definition of pCR is the absence of invasive cancer in the breast and lymph nodes (ypT0/is ypN0). PERJETA is a sterile, clear to slightly opalescent, colorless to pale brown liquid for intravenous infusion. Each single use vial contains 420 mg of pertuzumab at a concentration of 30 mg/mL in 20 mM L-histidine acetate (pH 6.0), 120 mM sucrose and 0.02% polysorbate 20.

Some breast cancers have large amounts of a protein called HER2 on the surface of the cells. These cancers are ‘HER2 positive’ and can be treated with a drug called trastuzumab which targets the HER2 protein. You may have trastuzumab with chemotherapy. Paclitaxel anddocetaxel are drugs that doctors often use.

Sam Houston Biotech A Houston Based cancer Research Organization has found that genomic science has advanced. Sections of microarray provide targets for parallel in situ detection of DNA, RNA and protein targets in each specimen on the array. The better News is that Genomics is on the Clock. Genomics provide a faster cheaper more effective way to detect the Her2 gene by using Semiconductor Sequencing. A example of this technique is Gennxeix Biotech Inc Semiconductor Sequencing. "Quantum Theory" In Action for Breast Cancer Patients. One of the major player and touch down makers for breast cancer is Houston Texas Methodist Hospital. In A clinical Trial A Rev. Noel Denison, a retired Methodist minister, was diagnosed with locally advanced HER2-positive breast cancer and is enrolled in the study at Methodist, one of only two locations in the United States. The clinical trial is for locally advanced or metastatic HER2-positive breast cancer and combines standard chemotherapy with trastuzumab emtansine, better known in the breast cancer world as T-DM1, and pertuzumab, a monoclonal antibody that also attaches to HER2 on cancer cells. Using Genomics and semiconductors to detect breast cancer plus T-DM1 to treat breast cancer is a winning combination. What is T-DM1? T-DM1 is in a new class of cancer-fighting agents called antibody drug conjugates. By combining the antibody trastuzumab directly with docetaxel (standard chemotherapy) and/or pertuzumab, the T-DMI is designed to attack the tumor cells directly and deliver the chemotherapy. Trastuzumab emtansine (T-DM1) consists of our proprietary DM1 cancer-killing agent attached to the HER2-binding antibody, trastuzumab, developed by Genentech (a member of the Roche Group) using our linker and methods of attachment. Trastuzumab emtansine is in global development by Roche under a collaboration agreement between ImmunoGen and Genentech. Marketing applications for trastuzumab emtansine are under review in the US and Europe. The Defense and the most dangerous aspect of breast cancer is its ability to spread to distant sites, most tumors are initially unable to do that Learning more specifically what triggers metastases may provide additional targets for preventing and treating the malignant process that causes cancer deaths.

It’s widely accepted that cancers acquire the ability to spread through the gradual accumulation of genetic changes, and experiments have also shown that these changes occur in parallel with changes in the protein content and 3-dimensional patterning of the protein meshwork that creates their immediate surroundings Gene that stops the growth of KCNK9 Genes is gene is p53. p53 is a fundamental determinant of cancer susceptibility, p53 integrates stress signals and elicits apoplectic responses that maintain genomic stability. When cells sense a decrease in oxygen availability (hypoxia), they develop adaptive responses in order to sustain this condition and survive. If hypoxia lasts too long or is too severe, the cells eventually die. Hypoxia is also known to modulate the p53 pathway, in a manner dependent or not of HIF-1 (hypoxia-inducible factor-1), the main transcription factor activated by hypoxia. The p53 protein is a transcription factor, which is rapidly stabilized by cellular stresses and which has a major role in the cell responses to these stresses. This process is why it is important Conrad says for people that are first degree relatives of breast cancer patients, must take a genomic test to see if they are the carrier of gene KCNK9. By identifying this gene we can direct patients with the correct advise as to deal with the fact that they have a lunp on the breast to they are going to get a lump on their breast. Often what happens is that a breast cancer patients dose not go to the doctor or take important test to see if there is a lump on the breast. what happens is the spread of breast cancer is responsible for more than 90 percent of breast cancer deaths.

Pertuzumab is a type of biological therapy called a monoclonal antibody. It works by targeting the HER2 protein but in a different way to trastuzumab. We know from research that having both pertuzumab and trastuzumab together may be better than having just one of them alone.

TDM1 is a combination of trastuzumab and a chemotherapy drug called DM1. Trastuzumab finds the cancer cells and delivers the DM1 to them. This type of drug is called a conjugated monoclonal antibody.

It is clear to Barron’s Medical Journal first year oncologist will have a new way of treating breast cancer all before the end of President Obama second Term

How Susan G. Komen And Personalized Medicine--Genomics Is A Breast Cancer Game Changer

Barron’s Medical Journal Reporting From Boston At Harvard University Beth Israel Medical Center

---

 How Susan G. Komen And Personalized Medicine--Genomics Is A Breast Cancer Game Changer 

---

Boston MA ( AP )Barron’s Medical Journal investigative report on breast cancer fundraising series starts with The Susan G Komen March. With only fifteen percent of the research dollars spent on Personalized Medicine, Barron's wants to make all of the new patient’s that is going to get to go the Doctors now that they have Affordable Health Care Act ( Obama Care )BMJ want to make sure that patients are asking about genomics for breast cancer. DNA methylation patterns can discover three hundred times faster than a mammogram can breast cancer. Breast cancer is one of the most prevalent human malignancies and is a major cause of cancer-related morbidity and mortality. Invasive ductal carcinoma (IDC) of the breast is a phenotypically diverse disease, consisting of tumors with varying pathologic and molecular characteristics. The primary biological subtypes of IDC include estrogen receptor (ER)– and progesterone receptor (PR)–positive tumors (luminal A and B), tumors that are human epidermal growth factor receptor 2 (HER2)–enriched, and tumors that are ER/PR-negative (basal-like). These molecular determinants have significant effects on metastatic behavior and clinical outcome. For example, ER/PR+tumors are generally associated with better clinical prognosis, whereas basal-like (ER/PR− and HER2−, triple-negative) tumors are associated with higher rates of metastasis and death The genomic alterations, including both genetic and epigenetic aberrations, underlying these differing metastatic potentials are ill-defined.

Significant effort has been undertaken to more accurately define the molecular alterations underlying breast cancer. For example, it has been shown that hormone receptor (HR) status is prognostic for clinical outcome. Mutations in genes such asBRCA1, PTEN, and PIK3CA help promote breast cancer oncogenesis and are enriched in specific subgroups of IDC in breast cancers). These data demonstrate that there exists substantial biological heterogeneity between and within the ER/PR+ and ER/PR− subgroups for which the molecular foundations remain obscure In addition, gene expression classifiers have been developed to help predict metastatic risk). Despite their increasing use in the clinic, the genomic root causes of the transcriptome differences that underlie metastatic potential are unclear.

Genome-wide sequencing surveys have been performed to identify the scope of mutations

It is well established that widespread changes in DNA methylation patterns occur during oncogenesis and tumor progression Cancer-specific changes in DNA methylation can alter genetic stability, genomic structure, and gene expression). Promoter CpG island methylation can result in transcriptional silencing and plays an important role in the oncogenic process A CpG island methylator phenotype (CIMP), which is associated with a strong tendency to hypermethylate specific loci, has been described in a subset of colorectal cancers, and recently in a subgroup of gliomas Aberrations in DNA methylation have been reported in human breast cancer, but the impact of the methylome on metastasis and the presence of a B-CIMP have remained elusive To resolve these questions, we conducted a systematic, genome-wide characterization of the breast cancer methylome in breast cancers with diverse metastatic behavior.

Cancer cells undergo massive alterations to their DNA methylation patterns that result in aberrant gene expression and malignant phenotypes. However, the mechanisms that underlie methylome changes are not well understood nor is the genomic distribution of DNA methylation changes well characterized.

Here, we performed methylated DNA immunoprecipitation combined with high-throughput sequencing (MeDIP-seq) to obtain whole-genome DNA methylation profiles for eight human breast cancer cell (BCC) lines and for normal human mammary epithelial cells (HMEC). The MeDIP-seq analysis generated non-biased DNA methylation maps by covering almost the entire genome with sufficient depth and resolution. The most prominent feature of the BCC lines compared to HMEC was a massively reduced methylation level particularly in CpG-poor regions. While hypomethylation did not appear to be associated with particular genomic features, hypermethylation preferentially occurred at CpG-rich gene-related regions independently of the distance from transcription start sites. We also investigated methylome alterations during epithelial-to-mesenchymal transition (EMT) in MCF7 cells. EMT induction was associated with specific alterations to the methylation patterns of gene-related CpG-rich regions, although overall methylation levels were not significantly altered. Moreover, approximately 40% of the epithelial cell-specific methylation patterns in gene-related regions were altered to those typical of mesenchymal cells, suggesting a cell-type specific regulation

of DNA methylation. Cancer-specific alterations in DNA methylation are hallmarks of human malignancies; however, the nature of the breast cancer epigenome and its effects on metastatic behavior remain obscure. To address this issue, we used genome-wide analysis to characterize the methylomes of breast cancers with diverse metastatic behavior. Groups of breast tumors were characterized by the presence or absence of coordinate hypermethylation at a large number of genes, demonstrating a breast CpG island methylator phenotype (B-CIMP).

The B-CIMP provided a distinct epigenomic profile and was a strong determinant of metastatic potential. Specifically, the presence of the B-CIMP in tumors was associated with low metastatic risk and survival, and the absence of the B-CIMP was associated with high metastatic risk and death. B-CIMP loci were highly enriched for genes that make up the metastasis transcriptome. Methylation at B-CIMP genes accounted for much of the transcriptomal diversity between breast cancers of varying prognosis, indicating a fundamental 

Pharmaceutical Lobbyist Is Trying To Stop The Breast Cancer Cure Barron’s Medical Journal Second Call For First Lady Michele Obama To Be The Breast Cancer Czar

Barron’s Medical Journal reporting from the Houston Medical Center at Marriott Medical Center the Site of Lori Sumako Meeting on A Breast Cancer Cure

---

Pharmaceutical Lobbyist is trying to stop The Breast cancer Cure Barron’s Medical Journal Second Call for First Lady Michele Obama To Be The Breast Cancer Czar

---

Houston ( AP )The Pharmaceutical Lobbyist is trying to stop The Breast cancer Cure. Just as we are on the door step to a cure we now have a wave of science reports trying to make genomics

science too broad. Roche Names Lufthansa CEO Franz to Replace their present CEO Humer. " Their Stock Price Drops" In the New York Times Today An Article on Mosaicism . Mosaicism by definition is the presence of two or more populations of cells with different genotypes in one individual. We contain genetic multitudes. Not long ago, researchers had thought it was rare for the cells in a single healthy person to differ genetically in a significant way. But scientists are

finding that it’s quite common for an individual to have multiple genomes. Some people, for example, have groups of cells with mutations that are not found in the rest of the body. Some have genomes that came from other people. “There have been whispers in the matrix about this for years, even decades, but only in a very hypothetical sense,” said Alexander Urban,

Brought To You By The Dalmore Single Malt a geneticist at Stanford University. Even three years ago, suggesting that there was widespread genetic variation in a single body would have been met with skepticism, he said. “You would have just run against the wall.”But a series of recent papers by Dr. Urban and others has demonstrated that those whispers were not just hypothetical. The variation in the genomes found in a single

person is too large to be ignored. “We now know it’s there,” Dr. Urban said. “Now we’re mapping this new continent.”NIH In Nature Journal talk about how Francis Collins and other are making President Obama BRAIN Initiative goals for 2014 too broad. The NIH is one of three government partners in the BRAIN Initiative, and the first to announce research goals; the report will guide the agency's spending of the $40 million it has committed for 2014. The Defense Advanced Research Projects Agency in Arlington,

Virginia, has said that it does not intend to release a road map for its $50-million contribution to the project, and the National Science Foundation, also in Arlington, has not yet finalized plans for its $20-million commitment in the next year.Fifteen leading neuroscientists selected by Collins — nicknamed the 'Dream Team' — prepared the NIH plan after holding four workshops around the country since May. The resulting report calls for molecular characterization of cell types in the brain, with

the eventual goal of manipulating specific neuronal populations of interest. It says that better diagrams of neural circuits are needed to accompany the deluge of data that will be enabled

by large-scale recording techniques. The NIH committee also recommends the development of theoretical and computational approaches to deal with the massive data sets that such research is expected to produce.We need to stay focus on the breast cancer cure prize In the Houston Chronicle Today

Lori Sumako received her second cancer diagnosis in October 2007, when her doctor suggested she simply enjoy what time she had left. Sumako looked at her in disbelief, and vowed to find a new oncologist.She and husband Rick Mitchell wandered into a breast cancer conference a few days later, and Sumako spotted a man wearing a suit and a stethoscope. Yes, he was an oncologist, and he told her exactly what she needed to hear. “I don’t believe in palliative care,” Dr. Khaled Jabboury said to her. “The goal is complete remission.”
As Sumako and Jabboury talked, Mitchell interviewed radiation oncologist Dr. Karl King. The two physicians became the leaders of Sumako’s cancer-fighting team. First came chemotherapy, a cocktail of six drugs. One had to be discontinued because of painful side effects. But the others worked so well that her small tumors disappeared. That left one, which was blasted into nothingness by radio-frequency ablation. Then came four months of radiation.
Early phase of biomarker discovery in three clinically important types of breast cancer using a panel of human cell lines: HER2 positive, hormone receptor positive and HER2 negative, and triple negative (HER2-, ER-, PR-). We identified and characterized the most abundant secreted, sloughed, or leaked proteins released into serum free media from these breast cancer cell lines using a combination of protein fractionation methods before LC-MS/MS mass spectrometry analysis.

A total of 249 proteins were detected in the proximal fluid of 7 breast cancer cell lines. The expression of a selected group of high abundance and/or breast cancer-specific potential biomarkers including thromobospondin 1, galectin-3 binding protein, cathepsin D, vimentin, zinc-α2-glycoprotein, CD44, and EGFR from the breast cancer cell lines and in their culture media were further validated by Western blot analysis. Interestingly, mass spectrometry identified a cathepsin D protein single-nucleotide polymorphism (SNP) by alanine to

valine replacement from the MCF-7 breast cancer cell line. Comparison of each cell line media proteome displayed unique and consistent biosignatures regardless of the individual group classifications, demonstrating the potential for stratification of breast cancer. On the basis of the cell line media proteome, predictive Tree software was able to categorize each cell line as HER2 positive, HER2 negative, and hormone receptor positive and triple negative based on only two proteins, muscle fructose 1,6-bisphosphate aldolase and keratin 19. In addition, the predictive Tree software clearly identified MCF-7 cell line overexpresing the HER2 receptor with the SNP cathepsin D biomarker.Approximately 30% of malignant breast cancers demonstrate overamplification of the human epidermal receptor type 2 (HER2) gene. HER-2 can be resistant to low-doses of anthracycline-based chemotherapy. The Good News is that science has advanced. Sections of microarray provide targets for parallel in situ detection of DNA, RNA and protein targets in each specimen on the array. The better News is that Genomics is on the Clock. Genomics provide a faster cheaper more effective way to detect the Her2 gene by using Semiconductor Sequencing. A example of this technique is Gennxeix Biotech Inc Semiconductor Sequencing. "Quantum Theory" In Action for Breast Cancer Patients. One of the major player and touch down makers for breast cancer is Houston Texas Methodist Hospital. In A clinical Trial A Rev. Noel Denison, a retired Methodist minister, was diagnosed with locally advanced HER2-positive breast cancer and is enrolled in the study at Methodist, one of only two locations in the United States. The clinical trial is for locally advanced or metastatic HER2-positive breast cancer and combines standard chemotherapy with trastuzumab emtansine, better known in the breast cancer world as T-DM1, and pertuzumab,a monoclonal antibody that also attaches to HER2 on cancer cells. Using

Genomics and semiconductors to detect breast cancer plus T-DM1 to treat breast cancer is a winning combination. What is T-DM1? T-DM1 is in a new class of cancer-fighting agents called antibody drug conjugates. By combining the antibody trastuzumab directly with docetaxel (standard chemotherapy) and/or pertuzumab,

the T-DMI is designed to attack the tumor cells directly and deliver the chemotherapy. Trastuzumab emtansine (T-DM1) consists of our proprietary DM1 cancer-killing agent attached to the HER2-binding antibody, trastuzumab, developed by Genentech (a member of the Roche Group)The Science and Medical communities must stay focus on the gifts that genomic science has given 

National Football League Where Should Your Breast Cancer Research Funding Go To Stop Epithelial-Mesenchymal

Barron’s Medical Journal Reporting from the US Open Tennis Championships in New York City, USA.

---

National Football League Where Should Your Breast Cancer Research Funding Go To Stop Epithelial-Mesenchymal Transition Process

---

Brought To You By Skyline Deli/Cafe- Houston Medical Center:

---

New York City ( AP) At this year’s US Open -- Genomics is now a house hold name. Barron’s Medical Journal Interviewed Rose Conrad Ph.D. The C.E.O Of Sam Houston Biotech

A Houston Based Biotech Clinical Research Company. What is the first object of genomics and breast cancer research. Conrad’s said right away that we must stop the Epithelial-mesenchymal transition process. No One Dies Of Breast Cancer Only When Breast Cancer Spreads to the Lungs. This process is called Epithelial-mesenchymal transition (EMT). Epithelial-mesenchymal is a process by which epithelial cells lose their cell polarity and cell-cell adhesion, and gain migratory and invasive properties to become mesenchymal cells. EMT was not recognized as a distinct process until 1982.Breast cancer is the most common cancer in women, and approximately 90% of breast cancer deaths are caused by local invasion and distant metastasis of tumor cells. Epithelial-mesenchymal transition (EMT) is a vital process for large-scale cell movement during morphogenesis at the time of embryonic development.

Tumor cells usurp this developmental program to execute the multi-step process of tumorigenesis and metastasis. Several transcription factors and signals are involved in these events Metastasis,is the spread of a cancer

from one organ or part to another non-adjacent organ or part Cancer development and metastasis are multistep processes that involve local tumor growth and invasion followed by dissemination to and re-establishment at distant sites. The ability of a tumor to metastasize is the major determinant of the mortality of cancer patients. Thus, elucidating the molecular pathways essential for tumor metastasis is of high priority in cancer biology and provides a basis for novel therapeutic targets for the development of antimetastatic cancer treatmentsSeveral molecular mechanisms contribute directly and mechanically to the loss of epithelial phenotype. During epithelial–mesenchymal transition (EMT), adherens junctions and desmosomes are at least partially dissociated. At the same time, a massive cytoskeleton reorganization takes place, involving the rho family and the remodeling of the actin microfilament mesh. Numerous pathways have been described in vitro that control phenotype transition in specific cell models stromal- and epithelial-specific cre-transgenic mice to directly visualize epithelial-mesenchymal transition (EMT) during cancer progression in vivo.

Using three different oncogene-driven mouse mammary tumor models and cell-fate mapping strategies, we show in vivo evidence for the existence of EMT in breast cancer and show that myc can specifically elicit this process. Hierarchical cluster analysis of genome-wide loss of heterozygosity reveals that the incidence of EMT in invasive human breast carcinomas is rare, but when it occurs it is associated with the amplification of MYC.Histological analysis of metastasis assays, lungs were immersed in 10% neutral buffered formalin before paraffin embedding and sectioning. Sections 5 μm in thickness were processed for hematoxylin and eosin staining and histological evaluation. When we can detect or predict when a patients has or is going to get breast cancer is the goal all clinical research organization are looking to achieve.
Early phase of biomarker discovery in three clinically important types of breast cancer using a panel of human cell lines: HER2 positive, hormone receptor positive and HER2 negative, and triple negative (HER2-, ER-, PR-). We identified and characterized the most abundant secreted, sloughed, or leaked proteins released into serum free media from these breast cancer cell lines using a combination of protein fractionation methods before LC-MS/MS mass spectrometry analysis. A total of 249 proteins were detected in the proximal fluid of 7 breast cancer cell lines. The expression of a selected group of high abundance and/or breast cancer-specific potential biomarkers including thromobospondin 1, galectin-3 binding protein, cathepsin D, vimentin, zinc-α2-glycoprotein, CD44, and EGFR from the breast cancer cell lines and in their culture media were further validated by Western blot analysis. Interestingly, mass spectrometry identified a cathepsin D protein single-nucleotide polymorphism (SNP) by alanine to valine replacement from the MCF-7 breast cancer cell line. Comparison of each cell line media proteome displayed unique and consistent biosignatures regardless of the individual group classifications, demonstrating the potential for stratification of breast cancer. On the basis of the cell line media proteome, predictive Tree

software was able to categorize each cell line as HER2 positive, HER2 negative, and hormone receptor positive and triple negative based on only two proteins, muscle fructose 1,6-bisphosphate aldolase and keratin 19. In addition, the predictive Tree software clearly identified MCF-7 cell line overexpresing the HER2 receptor with the SNP cathepsin D biomarker.Approximately 30% of malignant breast cancers demonstrate overamplification of the human epidermal receptor type 2 (HER2) gene. HER-2 can be resistant to low-doses of anthracycline-based chemotherapy.
The Good News is that science has advanced. Sections of microarray provide targets for parallel in situ detection of DNA, RNA and protein targets in each specimen on the array. The better News is that Genomics is on the Clock. Genomics provide a faster cheaper more effective way to detect the Her2 gene by using Semiconductor Sequencing. A example of this technique is Gennxeix Biotech Inc Semiconductor Sequencing. "Quantum Theory" In Action for Breast Cancer Patients. One of the major player and touch down makers for breast cancer is Houston Texas Methodist Hospital. In A clinical Trial A Rev. Noel Denison, a retired Methodist minister, was diagnosed with locally advanced HER2-positive breast cancer and is enrolled in the study at Methodist, one of only two locations in the United States. The clinical trial is for locally advanced or metastatic HER2-positive breast cancer and combines standard chemotherapy with trastuzumab emtansine, better known in the breast cancer world as T-DM1, and pertuzumab,a monoclonal antibody that also attaches to HER2 on cancer cells. Using Genomics and semiconductors to detect breast cancer plus T-DM1 to treat breast cancer is a winning combination. What is T-DM1? T-DM1 is in a new class of cancer-fighting agents called antibody drug conjugates. By combining the antibody trastuzumab directly with docetaxel (standard chemotherapy) and/or pertuzumab, the T-DMI is designed to attack the tumor cells directly and deliver the chemotherapy. Trastuzumab emtansine (T-DM1) consists of our proprietary DM1 cancer-killing agent attached to the HER2-binding antibody, trastuzumab, developed by Genentech (a member of the Roche Group)

Who Purchased The Washington Post And How Can Breast Cancer Patients Benefit

Barron’s Medical Journal Robert Graham Ph.D. Reporting from Rice University Houston, Texas USA (Global Newswire ) ( PRNewswire )

---

Who Purchased The Washington Post And How Can Breast Cancer Patients Benefit

---

Brought To You By Skyline Deli/Cafe- Houston Medical Center:

---

Houston ( AP )

Who is this person that has purchased one of the most prestigious News Papers in The United States and around the World, The Washington Post? How can breast cancer patients benefit from this transaction? Jeff Bezos. Yes Jeff Bezos, founder and chief executive officer of Amazon.com. The Washington Post along with another one of the Bezos Transactions ,Bezos Center for Neural Circuit Dynamics. Before Barron’s Medical Journal get in to the benefits of this transaction for breast cancer, here is some background on the Bezos Center for Neural Circuit Dynamics. Jeff and his wife MacKenzie Bezos, both graduates of Princeton University, donated $15

million to the school’s neuroscience institute. By purchasing the Washington Post, Bezos now has reporters in Washington DC that will have firsthand knowledge of President Obama New Brain Activity Mapping program which in turn, will be great for when the Washington Post Incorporate Amazon digital cloud computing, that will send information out to the science communities around the world. To accomplish this The Washing Post is going to have to upgrade their science reporting. One way to accomplish this is to partner with News Organizations like Barron’s Medical Journal and The Nature Magazine. The gift will establish the Bezos Center for Neural Circuit Dynamics. Reason for this epic quest is to unravel one of humankind’s greatest challenges — understanding the brain. “New tools and techniques are making possible discoveries that would have been unthinkable just

two decades ago. We can hope for advancements that lead to understanding deep behaviors, more effective learning methods for young children, and cures for neurological diseases. MacKenzie and I are delighted and excited to support Princeton in their focus on fundamental neuroscience.” Breast Cancer Patients often struggle with Neurogenesis. Neurogenesis is prolonged chemotherapy decreases the development of new brain cells, a process known as neurogenesis. Neurogenesis disrupts ongoing brain rhythms in the part of the brain responsible for making new memories. That affected by learning and in some cases are necessary for learning to occur.
"One of the things that these brain rhythms do is to connect information across brain

regions "Scientist are starting to have a better understanding of how these natural rhythms are used in the process of communication and how they change with experience." A substantial proportion of breast cancer survivors report significant, long-lasting impairments in cognitive function, often referred to as "chemobrain." Advances in detection and treatment mean that many more patients are surviving long-term following diagnosis of invasive breast cancer. Thus, it is important to define the types, extent, and persistence of cognitive impairments following treatment with cytotoxic cancer drugs. Sam Houston Biotech examined the effects of chronic treatment with two agents commonly used in patients with breast cancer, cyclophosphamide and doxorubicin (Adriamycin). Athymic nude rats were given 50 mg/kg cyclophosphamide, 2 mg/kg doxorubicin, or saline injections once per week for 4 weeks. A novel place recognition task and contextual and cued fear conditioning were used to characterize learning and memory ability. Immunofluorescence staining for immature and mature neurons and activated microglia was used to assess changes in neurogenesis and neuroinflammation.
Cyclophosphamide- and doxorubicin-treated rats showed significantly impaired performance on the novel place recognition task and the contextual fear conditioning task compared with untreated controls, suggesting disrupted hippocampal-based memory function. Chemotherapy-treated animals showed a significant decline in neurogenesis [80%-90% drop in bromodeoxyuridine (BrdUrd)-labeled cells expressing NeuN]. Activated microglia (ED1-

positive) were found after cyclophosphamide but not doxorubicin treatment. Our results show that chronic treatment with either of two commonly used chemotherapeutic agents impairs cognitive ability and suggest that strategies to prevent or repair disrupted hippocampal neurogenesis may be effective in ameliorating this serious side effect in cancer survivors. The human olfactory bulb displays high morphologic dynamics changing its volume with olfactory function, which has been explained by active neurogenetic processes. Discussion continues whether the human olfactory bulb hosts a continuous turnover of neurons. Sam Houston Biotech analyzed the transcriptome via RNA quantification of adult human olfactory bulbs and intersected the set of expressed transcriptomic genes with independently available proteomic expression data. To obtain a functional genomic perspective, this intersection was analyzed for higher-level organization of gene products into biological pathways established in the gene ontology database.Sam Houston Biotech reports that a fifth of genes expressed in adult human olfactory bulbs serve functions of nervous system or neuron development, half of them functionally converging to axonogenesis but no other non-neurogenetic biological processes. Other genes were expectedly involved in signal transmission and response to chemical stimuli. This provides a novel, functional genomics perspective supporting the existence of neurogenesis in the adult human olfactory bulb.
Neurogenesis and Epidermal Growth Factor Receptor genes can partner with , Genomics and President Obama Brain Acivity Mapping all working hand in hand will look for tumors identified recurrent genomic aberrations in each molecular subtype. The classical subtype was characterised by frequent EGFR amplification and EGFRvIII mutations, CDKN2A deletion, and a lack of TP53mutations, whereas the mesenchymal subtype was characterised by NF1, TP53, and PTEN mutations. Consensus neuropathological review of a subset of TCGA cases has shown that the proneural, classical, and mesenchymal subtypes are enriched for GBM with oligodendroglial features, small-cell GBM, and gliosarcoma (a morphological variant of GBM with mesenchymal differentiation (Miller and Perry, 2007)), respectively (Cameron Brennan, personal communication). Moreover, pseudopalisading necrosis and to a lesser extent florid microvascular proliferation are frequent in mesenchymal GBM, but the proneural subtype typically lacks necrosis. These findings suggest that mesenchymal GBM may be uniquely susceptible to angiogenesis inhibitors, a hypothesis currently being tested in the RTOG 0825 trial discussed below. The proneural subtype, which like previous studies (Phillips et al, 2006; Lee et al, 2008) was found in younger patients, harboured frequent PDGFRAamplification and mutations in IDH1, TP53, andPIK3CA/PIK3R1, suggesting susceptibility to PDGFRA- and PI3K-targeted therapies. A recent proteomic analysis confirmed protein- and phosphorylation-level signalling abnormalities in the EGFR, PDGFR, and NF1 pathways in classical, proneural, and mesenchymal subtypes of GBM, respectively, further suggesting that these GBM subtypes may be uniquely susceptible to targeted agents (Brennan et al, 2009).
It is a great day for Science and News organization around The World