Bobby Graham Reporting From The Houston Galleria --- Houston, Texas USA
GlobeNewswire>< PRWire>
In the Houston Galleria two power houses merge and produce a fashion work product in which the global fashion world has taken notice. Both Vogue Magazine and Simon came together and produced a fashion show with precision, style and grace. This is the first time Vogue has participated in the Houston Fashion scene and Vogue delivered with one of the best Fashion Shows this country has ever witnessed. Take A Look:
Saturday, September 13, 2014
Breast Cancer Month: The World Geographical Fashion Map Changed Forever In Houston
Wednesday, August 13, 2014
25% Of Huntington Disease Patients Attempt Suicide
25% Of Huntington Disease Patients Attempt Suicide At Some Point In Their Illness
It was surprising to find out 70% of White Males contribute to suicide cases in the United States. Now with President Obama Health care plan in full effect and more Americans can get to a Doctor, one of the items of concern is Huntington’s disease. A genomics 
test that will find the HTT gene which maps to chromosome 4p16.3 aka (Huntington's Disease).
Huntington’s disease is an autosomal-dominant, progressive neurodegenerative disorder with a distinct phenotype, including chorea and dystonia, incoordination, cognitive decline, and behavioural difficulties. Typically, onset of symptoms is in middle-age after affected individuals have had children, but the disorder can manifest at any time between infancy and senescence. 
The mutant protein in Huntington’s disease—huntingtin—results from an expanded CAG repeat leading to a polyglutamine strand of variable length at the N-terminus. Evidence suggests that this tail confers a toxic gain of function. The precise pathophysiological mechanisms of Huntington’s disease are poorly understood, but research in transgenic animal models of the disorder is providing insight into causative factors and potential treatments.
Huntington disease affects an estimated 3 to 7 per 100,000 people of European ancestry. The disorder appears to be less common in some other populations, including people
of Japanese, Chinese, and African descent.
Mutations in the HTT gene cause Huntington disease. The HTT gene provides instructions for making a protein called huntingtin. Although the function of this protein is unknown, it appears to play an important role in nerve cells (neurons) in the brain.
The HTT mutation that causes Huntington disease involves a DNA segment known as a CAG trinucleotide repeat. This segment is made up of a series of three DNA building blocks (cytosine, adenine, and guanine)
that appear multiple times in a row. Normally, the CAG segment is repeated 10 to 35 times within the gene. In people with Huntington disease, the CAG segment is repeated 36 to more than 120 times. People with 36 to 39 CAG repeats may or may not develop the signs and symptoms of Huntington disease, while people with 40 or more repeats almost always develop the disorder.
An increase in the size of the CAG segment leads to the production of an abnormally long version of the huntingtin protein. The elongated protein is cut into smaller, 
toxic fragments that bind together and accumulate in neurons, disrupting the normal functions of these cells. The dysfunction and eventual death of neurons in certain areas of the brain underlie the signs and symptoms of Huntington disease.
Read more about the HTT gene.
Huntington’s disease. In a cross-sectional study, about 9% of asymptomatic at-risk individuals contemplated suicide at least occasionally,11 perhaps a result of being
raised by an affected parent and awareness of the disease. In the prediagnostic phase, the proportion rose to 22%, but in patients who had been recently diagnosed, suicidal
ideation was lower. Brought To You By 2014 Cadillac ELR
The frequency increased again in later stages of the illness.11 The correlation of suicidal ideation with suicide has not been studied in people with Huntington’s disease, but suicide attempts are not in common. In one study, researchers estimated that more than 25% of patients attempt suicide at some point in their illness.18 Individuals without children might be at amplifi ed risk,19,20 and for these people access to suicidal means (ie, drugs or weapons) should be restricted. The presence of affective symptoms, specific suicidal plans, or actions that increase isolation (eg, divorce, giving away pets) warrants similar precautions.20.
A single abnormal gene, the basic biological unit of heredity, produces HD. Genes are composed of deoxyribonucleic acid (DNA), a molecule shaped like a spiral ladder. Each rung of this ladder is composed of two paired chemicals called bases. There are four types of bases, adenine, thymine, cytosine, and guanine, each abbreviated by the first letter of its name: A, T, C, and G. Certain bases always "pair" together, and different combinations of base pairs join to form coded messages. A gene is a long string of this DNA in various combinations of A, T, C, and G. . 
These unique combinations determine the gene's function, much like letters join together to form words. Each person has about 30,000 genes, a billion base pairs of DNA or bits of information repeated in the nuclei of human cells, which determine individual characteristics or traits. This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. An affected person usually inherits the altered gene from one affected parent. In rare cases, an individual with Huntington disease does not have a parent with the disorder.
As the altered HTT gene is passed from one generation to the next, the size of the CAG trinucleotide repeat often increases in size. A larger number of repeats is usually associated with an earlier onset of signs and symptoms. This phenomenon is called anticipation. People with the adult-onset form of Huntington disease typically have 40 to 50 CAG repeats in the HTT gene, while people with the juvenile form of the disorder tend to have more than 60 CAG repeats.
Individuals who have 27 to 35 CAG repeats in the HTT gene do not develop Huntington disease, but they are at risk of having children who will develop the disorder. As the gene is passed from parent to child, the size of the CAG trinucleotide repeat may lengthen into the range associated with Huntington disease (36 repeats or more).uncommon. In one study, researchers estimated that more than 25% of patients attempt suicide at some point 
in their illness.18 Individuals without children might be at amplified risk,19,20 and for these people access to suicidal means (ie, drugs or weapons) should be restricted. The presence of affective symptoms, specific suicidal plans, or actions that increase isolation (eg, divorce, giving away
pets) warrants similar precautions.20.
In genetics, a chromosome translocation is a chromosome abnormality caused by rearrangement of parts between nonhomologous chromosomes. A gene fusion may be created when the translocation joins two otherwise-separated genes, the occurrence of which is common in cancer. It is detected on cytogenetics or akaryotype of affected cells. 
Translocations can be balanced (in an even exchange of material with no genetic information extra or missing, and ideally full functionality) or unbalanced (where the exchange of chromosome material is unequal resulting in extra or missing genes)
Neuropathological changes in Huntington’s disease are strikingly selective, with prominent cell loss and atrophy in the caudate and putamen.33–35 Striatal medium spiny neurons are the most vulnerable. Those that contain enkephalin and that project to the external globus pallidum are more involved than neurons that contain
substance P and project to the internal globus pallidum.33,34 Interneurons are generally spared. These findings accord with the hypothesis that chorea dominates early in the course of Huntington’s disease because of preferential involvement of the indirect pathway of basal ganglia-thalamocortical circuitry.11
Other brain areas greatly affected in people with Huntington’s disease include the substantia nigra, cortical layers 3, 5, and 6, the CA1 region of the hippocampus,36 the angular gyrus in the parietal lobe,37,38 Purkinje cells of the cerebellum,39 lateral tuberal nuclei of the hypothalamus,40,41 and the cells.
Saturday, July 26, 2014
New Gene BRCAX Help Women Live Longer With Breast Cancer
New Gene BRCAX Help Women Live Longer With Breast Cancer
HOUSTON (AP ) ----- Barron’s Medical Journal at A Susan G Komen Fundraising event in Houston Texas at the world famous Hotel ZA ZA reporting on a major concern among scientist, why is there a slight increase in breast cancer rates with Black Women ? The American Cancer Society provides an overview of female breast cancer statistics in the United States, including data on incidence, mortality, survival, and screening. Approximately 232,340 new cases of invasive 
breast cancer and 39,620 breast cancer deaths are expected to occur among US women in 2013. One in 8 women in the United States will develop breast cancer in her lifetime. Breast cancer incidence rates increased slightly among African American women; decreased among Hispanic women; and were stable among whites, Asian Americans/Pacific Islanders, and American Indians/Alaska Natives from 2006 to 2010. Historically, white women have had the highest breast cancer incidence rates among women aged 40 years and older; however, incidence rates are converging among white and African American women, particularly among women aged 50 years to 59 years. Incidence rates increased for estrogen receptor-positive breast cancers in the youngest white women, Hispanic women aged 60 years to 69 years, and all but the oldest African American women. In contrast, estrogen receptor-negative breast cancers declined among most age and racial/ethnic groups. These divergent trends may reflect etiologic heterogeneity and the differing effects of some factors, such as obesity and parity, on risk by tumor subtype. Since 1990, breast cancer death rates have dropped by 34% and this decrease was evident in all racial/ethnic groups except American Indians/Alaska Natives. Nevertheless, survival disparities persist by race/ethnicity, with African American women having the poorest breast cancer survival of any racial/ethnic group. Continued progress in the control of breast cancer will require sustained 
and increased efforts to provide high-quality screening, diagnosis, and treatment to all segments of the population.
Not all hereditary breast cancers are caused by BRCA1 and BRCA2. In fact, researchers now believe that at least half of hereditary breast cancers are not linked to these genes. Scientists also now think that these remaining cases of hereditary breast cancer are not caused by another single, unidentified gene, but rather by many genes, each accounting for a small fraction of breast cancers
In 1995 and 1996, studies of DNA samples revealed that Ashkenazi (Eastern European) Jews are 10 times more likely to have mutations in BRCA1 and BRCA 2 genes than the general population. Approximately 2.65 percent of the Ashkenazi Jewish population has a mutation in these genes, while only 0.2 percent of 
the general population carries these mutations.
Further research showed that three specific mutations in these genes accounted for 90 percent of the BRCA1 and BRCA2 variants within this ethnic group. This contrasts with hundreds of unique mutations of these two genes within the general population. However, despite the relatively high prevalence of these genetic mutations in Ashkenazi Jews, only seven percent of breast cancers in Ashkenazi women are caused by alterations in BRCA1 and BRCA2.
Researchers in Finland, Iceland and Sweden, working with scientists at the National Human Genome Research Institute (NHGRI) of the National Institutes of Health (NIH), have found evidence of a gene that appears to increase susceptibility to hereditary breast cancer. The study examined women who live in Nordic countries and who have three or more female family members with breast cancer.
Published in the August 15, 2000 issue of the
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Proceedings of the National Academy of Sciences (PNAS), this finding may help to explain why some women with a family history of hereditary breast cancer are at particularly high risk of developing the potentially fatal disease, even when they lack mutations in two previously identified breast cancer susceptibility genes, BRCA1 and BRCA2.
While scientists have not yet identified a third BRCA gene, they have succeeded in pinpointing its probable location to chromosome 13, the same chromosome that contains the previously identified BRCA2 gene. Mutations of BRCA1 and BRCA2 impair the body's cell production of tumor suppressor proteins.
"We've located what looks like a very good region in the human genome in which to search for a third breast cancer susceptibility gene," said Dr. Olli Kallioniemi, former senior scientist at NHGRI. He is one of 35 scientists in 14 laboratories in the United States, Finland, Sweden, Iceland and Germany who collaborated on the study.
Sam Houston Biotech 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) 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
Breast cancer is a common disease. Each year, approximately 200,000 women in the United States are diagnosed with breast cancer, and one in nine American women will develop breast cancer in her lifetime. But hereditary breast cancer - caused by a mutant gene passed from parents to their children -
is rare. Estimates of the incidence of hereditary breast cancer range from between 5 to 10 percent to as many as 27 percent of all breast cancers.
In 1994, the first gene associated with breast cancer - BRCA1 (for Breast Cancer1) was identified on chromosome 17. A year later, a second gene associated with breast cancer - BRCA2 - was discovered on chromosome 13. When individuals carry a mutated form of either BRCA1 or BRCA2, they have an increased risk of developing breast or ovarian cancer at some point in their lives. Children of parents with a BRCA1 or BRCA2 mutation have a 50 percent chance of inheriting the gene mutation
Wednesday, July 2, 2014
BMJ Has Under Covered How Patients Can live 14 % longer With Breast Cancer
BMJ Has Under Covered How Patients Can live 14 % longer With Breast Cancer:
New York City ( AP ) How does breast cancer get to the point where patients have to surrender to the disease. For friends and family members to be able to help breast cancer patients with treatment and other options. BMJ has under covered how patients can live 74 % longer with breast cancer. Breast
• Tissue. The cancer spreads from where it began by growing into nearby areas.
• Lymph system. The cancer spreads from where it began by getting into the lymph system. The cancer travels through the lymph vessels to other parts of the body.
Blood. The cancer spreads from where it began by getting into the blood. The cancer travels through the blood vessels to other parts of the body.
The sentinel lymph node is the first lymph node or group of nodes draining breast cancer. In case of established cancerous dissemination it is postulated that the sentinel lymph node/s is/are the target organs primarily reached by metastasizing cancer cells from the tumor. Thus, sentinel lymph nodes can be totally void of cancer, due to the fact that they were detected prior to dissemination.
Historically, complete axillary lymph node dissections had been performed with lumpectomy or mastectomy primarily for staging purposes, providing information that was used to determine adjuvant chemotherapy. The complete axillary lymph node dissection (CALND) may not change the course of the disease, although with removal of involved axillary nodes, the control of local recurrence in the axilla is easier. The morbidity associated with this procedure is substantial in terms of limitation of arm motion, arm pain, and chronic lymphedema.
The concept of a sentinel lymph node (SLN) was spawned by Cabanas his study of penile carcinoma.The pioneering studies of sentinel lymph node metastasis (SLNM) originated with the study of melanoma patients; the goal was to spare these patients the morbidity of large regional lymph node dissections.
Patients with melanomas who had SLN surgery were found to have a relatively orderly progression of lymph node metastases.
Lymphangiogenomics is an Integrated Project of the European Commission´s Sixth Framework Programme for Life Sciences, Genomics, and Biotechnology for Health (LSHG-CT-2004-503573) with 13 participating consortium members. Its aim is to thoroughly dissect the processes of lymphangiogenesis and to compare them with angiogenesis at the genetic, molecular, cellular, and functional level.
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The lymphatic vasculature is essential for the maintenance of fluid balance in the body, for immune defence, and for the uptake of dietary fat. Absent or damaged lymphatic vessels may lead to lymphedema, a chronic and disfiguring swelling of the extremities, sometimes necessitating the amputation of the affected limb. In addition, lymphatic vessels promote metastatic spread of cancer cells to distant organs - a leading cause of death in patients with cancer, and a major obstacle in the design of effective therapies. The lymphatic vessels were identified hundreds of years ago, yet very limited understanding exists of their development, function, and molecular mechanisms underlying their disease process. The aim of this project is to discover novel genes important for lymphatic vascular versus blood vascular development and function and to study the functional role and therapeutic potential of their gene products in lymphangiogenesis using state-of-the-art technologies. The methods we use
Scientist researched Genome-wide association studies looking for genetic variations known as single nucleotide polymorphisms (SNP). SNPs are alterations in the genetic code in which a single nucleotide, the individual building blocks that make up DNA, is changed. The researchers found that variations in four SNPs located in a region of
chromosome 6 were present more often in the breast cancer patients, suggesting that genes in this region might contribute to the risk of breast cancer. The researchers also confirmed the finding of previous studies indicating that the locus named FGFR2 is associated with a 20 percent increased risk of breast cancer. Panoincell uses Semiconductor Sequencing Chips that create a direct connection between Biochemical and digital
information, bringing these two languages together.Hybrid's chips are designed like any other semiconductor chips.
Pairing proprietary semiconductor technology with sequencing chemistry a nucleotide is incorporated into a strand of DNA by a polymerase, a hydrogen ion is released.
Sam Houston Biotech used a high-density array of micro-machined wells for bioctechnology process in a massive way. Each well holds a different DNA template. Beneath the wells is an ion-sensitive layer and beneath that a proprietary Ion sensor. When a nucleotide, is added to a DNA template and is then incorporated into a strand of DNA, a hydrogen ion will be released. The charge from that ion will change the pH of the solution, which can be detected. Hybrid's sequencer—essentially will call the base, going directly from Biochemical information to digital information. If there are two identical bases on the DNA strand, the voltage will be double, and the chip will record two identical bases called. This process uses no scanners, no cameras, no light—each Nucleotide incorporation is recorded in a real time process. Panoincell uppressed p53, 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.
Life Science has taken the next step. Genome, Epigenome In a paper published in Genome Medicine, a team of researchers from University College London (UCL) found an epigenetic signature that is associated with all breast cancer cases, not just those that are linked to a BRCA mutation. "We identified an epigenetic signature in women with a mutated BRCA-1 gene that was linked to increased cancer risk and lower survival rates,” said Professor Martin Widschwendter, the study's lead author and head of UCL's Department of Women's Cancer, in a press release. “Surprisingly, we found the same signature in large cohorts of women without the BRCA-1 mutation and it was able to predict breast cancer risk several years before diagnosis."
Although your DNA, called the genome, determines what proteins your body’s cells can produce, you also have an epigenome, a series of molecules that attach themselves to your DNA to increase or decrease the activity of specific genes. The most well-studied form of epigenetics is methylation, in which environmental 
factors cause methyl groups to bond to DNA.
Usually, the methyl groups bond with the promoter region of a gene, a set of DNA at the beginning of the gene that instructs the cell to turn the gene on. Methyl groups tend to down regulate genes, meaning that if a promoter normally instructed a gene to express itself 20 times, a methylated gene might only express itself 10 times instead.
In humans, most epigenetic changes occur during fetal development and early childhood, and they are influenced by any number of environmental factors.
An Epigenetic Difference
To find an epigenetic signature linked to breast cancer, the scientists examined a large group of blood samples from women with a certain cancer-causing BRCA-1 mutation. Among the women who went on to develop breast cancer, they found that a certain gene cluster was methylated.
The genes in question are involved in helping stem cells to differentiate. Stem cells can divide endlessly and become any type of cell the body might need. If this process goes awry and these super-cells start working against the body instead of for it, the result is cancer. Although the exact process is unknown, methylation of these genes is linked to higher rates of cancer.
But the real question was, do women without a BRCA-1 mutation who go on to develop cancer also have these same methylated genes? The researchers were surprised and pleased to discover that they do.
Widschwendter’s team isn’t yet sure whether the methylated DNA is one of the factors that directly causes breast cancer, or if the methyl signature is just a handy biomarker. Still, his team's research could be part of a new wave of early breast cancer detection.
Barron’s Medical Journal concludes, data is encouraging since it shows the potential of a blood based epigenetic test to identify breast cancer risk in women without known predisposing genetic mutations.
Friday, June 13, 2014
The Business of Breast Cancer And Apple HealthKit Announcement Will Create Two Million USA Jobs
Stop Look And Listen: The Business of Breast Cancer And Apple HealthKit Announcement Will Create Two Million USA Jobs
Rio de Janeiro --- ( AP ) : Apple Corporation has laid out the blue print to join the Health Care Revolution. Apple along with the success of President Obama Health Care Reform ( Obama Care ) And Genomics Science 
has created a platform to create over two million United States Jobs. At its WWDC 2014 developer’s conference, Apple (AAPL) new initiative that’s generating real buzz is HealthKit, the new Apple health functionality being baked into iOS 8.
However, arch-rival Samsung (SSNLF) SAMI (Samsung Architecture Multimodal Interactions) also in San Francisco A week before Apple unveiled its own health technology ambitions with its cloud-based SAMI health platform, Simband hardware and $50 million for “accelerating digital health innovation.”
This is great news says Rose Conrad of Sam Houston Biotech as Dr. Conrad points to the Canadian National Breast Screening showing no decline in breast cancer mortality rates even from regular mammograms. Apple see’s the emergence of predictive genomics to anticipate health issues is a winner.
Source: Apple
Six months ago, health technology with smartphones was largely a question of whether to choose a Fitbit sensor or a Nike (NKE) Fuel Band. Most of us were just holding our breath for Apple’s long-anticipated iWatch. Would it pack sensors that could put those fitness trackers out of business?
The easiest way to improve the health of any given population would be to give everyone in it access to Obama care, but this is a perennial impossibility since fighting illness and death are axiomatically unprofitable. At a certain point the cost of care for an individual eclipses their earning potential and 
accrued savings, leaving providers, patients, and family members in the paradoxical position of paying increasingly costly prices for postponement of a universal end. This industry can operate at a profit only in the medium term, but Apple and its healthcare app developers are attempting to triangulate the differing currencies driving the healthcare industry, convincing its users that increased data monitoring in their lives is a healthy thing to do, while providing a new generation of data-hungry entrepreneurs raw material to build their emerging products, while further securing Apple’s centrality to every aspect of a person’s life.
The iWatch was a no-show at WWDC 2014, but AAPL actually unveiled something far more ambitious (at least in terms of health technology): Apple health products will be integrated into iOS 8, able to communicate with and store data from third-party sensors and apps and able to share that data with your doctor. Brought To You By 2014 Cadillac ELR
Conrad also points to a study presented at the 50th annual meeting of the American Society of Clinical Oncology in Chicago.
“This study may change our ability to treat triple negative breast cancer patients,” says Barbara Pockaj, M.D., lead investigator of the study and Mayo Clinic surgeon. “We may have signs that these patients can be treated with immunotherapy. We don’t have a lot of options for these patients and this would really expand our options.”
Triple negative breast cancer is an aggressive form of breast cancer that evades the immune system because it lacks expression of genes for estrogen receptor, progesterone receptor and HER2. This limits treatment options. The study examined biomarkers involved in immune evasion including the gene PD-L1 and its 
association with other biological pathways as potential treatment options. In other cancers, patients who have the PD-L1 gene have been treated with immunotherapy – enhancing the body’s immune system – and some of the results have been dramatic, Dr. Pockaj says.
“This is important because immunotherapy is evolving as an effective treatment for patients with cancer,” she says. “We’ve seen remarkable results with patients with melanoma, renal cell carcinoma and even lung cancer. The question is, ‘Can we expand this type of treatment to patients with breast cancer?’”
The study analyzed 511 triple negative breast cancer samples using a multiplatform approach, including whole genome mRNA expression, protein expression, gene copy number changes and gene sequencing. The study found that 25 to 30 percent had the PD-L1 gene, which means those patients may be candidates for immunotherapy. There is a suggestion that the percentage may be even higher for patients who carry the BRCA1 gene, which produces tumor suppressor proteins. While the results need further investigation, they illustrate how molecular profiling can be used to identify potential treatment targets in triple negative breast cancer and other difficult-to-treat cancers.
“We now want to do validation studies in which we would hope to determine whether those patients who overexpress PD-L1 also have changes in their DNA repair genes,” Dr. Pockaj says. “And if they have both, it suggests the combination immunotherapy and chemotherapy may work.”
“Healthkit,” it will pull together data such as blood pressure and weight, collected by a growing plethora of healthcare apps on the iPhone or iPad, Apple executives told developers. The company will work in tandem with Nike Inc., a major player in fitness tracking, and the Mayo Clinic on the new feature, which will be included with the latest versions of Apple’s mobile software.
“That information lives in silos,” said Craig Federighi, Apple’s senior vice president of software engineering. “You can’t get a single comprehensive picture.”
Apple, which will discuss new software features with the thousands of developers gathered in San Francisco this week, did not elaborate on Healthkit’s features and capabilities.
Apple’s new HealthKit platform, according to Federighi, is a “single place that applications can contribute to a composite profile of your activity and health.” A related app, called simply Health, displays user-selected metrics in dashboard form. Both come standard with the just-unveiled iOS 8.
That’s great for the fitness nuts and quantified selfers out there, but that’s a limited market. It’s been done before. Remember Google Health? Microsoft’s HealthVault? Any of a number of untethered personal health records that have floundered on the market, in some cases for two decades, because direct-to-consumer simply doesn’t work in an industry where people expect third parties—insurance companies—to pick up the tab?
There might be a difference, however. That’s because Apple,
traditionally a consumer company, has partnered with Mayo Clinic and major electronic health records vendor Epic Systems to ensure that HealthKit can connect with organizational EHRs, and institutions will be able to intervene with patients whose readings fall out of normal range. But there’s no guarantee it will be different.
American Cancer Society and Susan G. Komen organization plus other breast cancer association investments and research funding now has the mussels to reach every American Breast Cancer Patients