More Good News About the Declining Use of HRT

Impact of Hormone Replacement Therapy

On Premalignant Changes in the Breast

 

 

Approximately 85% of breast cancers arise from cells that line the milk ducts of the breast.  But most of these cancers do not arise “overnight;” instead, they tend to develop over time in a progression from “normal” through various stages of increasing abnormality until, finally, they acquire the three characteristics of cancer cells:  immortality, invasiveness, metastasis.

 

One of the steps along the path from normal to cancer is a distinct phase known as atypical ductal hyperplasia.  Such cells appear abnormal when viewed under the microscope, (which is how the diagnosis is made), but they are also abnormal in terms of their DNA:  their genes are altered and headed in the direction of malignant transformation.

 

Women who are diagnosed with atypical ductal hyperplasia have a 3-5 times increased risk for breast cancer.  Thus, the finding of atypical ductal hyperplasia is considered a trigger for increased surveillance in women who are diagnosed with it.

 

In recent years the declining use of hormone replacement therapy has been associated with a decline in the number of new cases of breast cancer.  It now appears that the declining use of hormone replacement therapy is also associated with a decline in the incidence of atypical ductal hyperplasia.

 

In a recent review of patients and 2.4 million mammograms performed between 1999-2005, researchers reported that the use of hormone replacement therapy fell from 35% in 1999 to 11% in 2005, while at the same time the incidence of atypical ductal hyperplasia fell from 5.5 to 2.4 (per 10,000 cases.)  It is therefore reasonable to expect that the reduction, by half, of the incidence of atypical ductal hyperplasia (from 5.5 to 2.4) will similarly reduce the number of new cases of breast cancer that arise by this path.

 

Whatever else can be made of the data reported in this study, one fact takes obvious and overwhelming precedence:  the declining use of hormone replacement therapy is a good thing.

 

It is now abundantly clear that avoiding hormone replacement therapy is one of the simplest ways to reduce both the incidence and the propensity for breast cancer.  In these days when the most livid conversations are over healthcare reform, when political leaders can only dream of finding ways to bend the cost curve of medicine, here is an intervention – avoid hormone replacement therapy – that bends it quite nicely and, in so doing, yields longer, healthier lives.

 

Reference:  Menes, T. New Key to Puzzle of Hormone Therapy and Breast Cancer. Cancer Epidemiology Biomarkers & Prevention, November 11, 2009

Two New Powerpoint Presentations: The History of Research on the Pink Virus, and What is a Virus? What is Cancer? Is There A Virus Thought to Cause Breast Cancer?

The first presentation is a summary of the history of research on the mammary tumor virus.  It is pretty clear but packed with references, and it includes a pretty extensive bibliography at the end.

The second presentation, which the scientifically-challenged might find easier to digest, is a simple explanation for how viruses work, the nature of cancer cells, and the relation between the two.

Enjoy, and please leave comments and suggestions so that we can improve the slide show for others.

The Pink Virus

What is a Virus

Antiviral Therapy for Cancer Patients: Hope for a New Direction

Given that between 15-20% of all cancers are thought to be related to a virus (H. zur Hausen, Viruses in human cancers, Curr.Sci. 81, 2001, 523-527; D.M.Parkin, The global health burden of infection-associated cancers in the year 2002, Int. J. Cancer 118, 2006, 3030-3-044), and given that there is compelling and converging evidence that a mammary tumor virus may be involved in a significant portion of human breast cancer (V. Brower, Mouse mammary tumor virus:  new tumor virus of just a rumor virus? JNCI News, Vol. 101, Issue 5, March 4, 2009), the following article reporting positive results from a Canadian study that used the antiviral medication, ribavirin, in patients with a variety of cancers points the way, especially as regards the mammary tumor virus, for a new way of thinking and funding research.

Antiviral Therapy for Cancer Patients- Canadian Study

The Pink Virus: Does a Virus Cause Breast Cancer in Women?

This is a power point presentation I created today to help tell the story of the mammary tumor virus, aka the Pink Virus.  I hope it helps women understand why it is so important to get this question answered . . . without waiting another seventy years for the answer!

The Pink Virus

Women With Breast Cancer, Please Write on SHE WRITES.COM

I’ve just created a women’s writing group on a web site I discovered a few days ago and that I just love:  SHEWRITES.COM

Women with breast cancer, please write.

http://www.shewrites.com/group/womenwithbreastcancerwrite

 

Very Interesting Development re: Viruses/Cancer/Targeted Therapy

This just crossed my radar screen.  It is well worth sharing.  Feel free to ask questions; I will do my best to answer therm.

It is taken from Science Daily today, November 3:

(Nov. 2, 2009) — Targeted immunotherapy has been an attractive new therapeutic area for a number of cancers because it has the potential to destroy tumor cells without damaging surrounding normal tissue. New study results demonstrate high success rates using specialized white blood cells to prevent or treat lymphoma associated with the Epstein-Barr virus (EBV-lymphoma) in patients who have received a hematopoietic stem cell transplant (HSCT). This study was recently published online in Blood, the official journal of the American Society of Hematology.

 

Lymphoma is a cancer of white blood cells called lymphocytes that are largely responsible for maintaining the body’s immunity, and EBV is one of the most common human viruses that can have a long-lasting impact on the body’s immune system. Immune-compromised patients who receive HSCT, especially from mismatched donors or matched but unrelated donors, may be at higher risk of developing EBV-lymphoma than other patients. Previous studies have suggested that EBV-lymphoma occurs most often in the first few months post-transplant.

The researchers hypothesized that aggressive EBV-lymphomas may be responsive to control or eradication with EBV-specific cytotoxic T lymphocyte (CTL) treatment. (CTLs are highly specialized white blood cells that build the body’s defenses against disease.) To test their theory, the team infused EBV-specific CTL lines into two groups of patients: those who were undergoing HSCT and were at high risk of developing EBV-lymphoma, and patients who had already developed lymphoma. The study reported that CTL treatment successfully prevented the development of EBV-lymphoma in all 101 patients in the at-risk group who received the therapy prophylactically and achieved sustained complete remission in 11 of the 13 patients (85 percent) treated therapeutically (those who already had the disease).

“Therapy with EBV-specific CTLs was effective for these severely immunocompromised patients. The CTLs successfully reached tumors, multiplied, and were able to kill the tumor cells,” said lead study author Helen Heslop, MD, of the Center for Cell and Gene Therapy at Baylor College of Medicine, The Methodist Hospital, and Texas Children’s Hospital.

While the successful outcomes result from a number of factors in the study, the researchers attribute some of the success of the trial to the time of treatment. The CTL lines were infused soon after stem cell transplantation, when the existing white blood cell count was still low and was not quickly regenerating, allowing the infused cells to more quickly multiply and mediate anti-viral and anti-tumor effects. In addition, by marking and tracking the CTL genes, the team was able to demonstrate that the cells could survive for up to nine years in the body, conferring long-term protection.

With strong clinical outcomes, the study team is working to determine the most appropriate role and timing for CTL infusions. Some newer therapies (such as monoclonal antibodies) offer prophylactic and therapeutic options but cannot offer long-term protection. Therefore, treatment with CTLs may be reserved for the highest risk patients — those with a diagnosis of immune deficiency or a history of EBV-lymphoma, or those who develop elevated EBV levels after therapy with monoclonal antibodies.

Importantly, the study found that this type of therapy is not only effective, but economically advantageous. A preliminary analysis showed that a patient-specific CTL line can be manufactured, tested, and infused for approximately $6,000, a cost that compares well with other modalities used in the treatment of EBV-lymphoma. Moreover, the team determined that it is possible to manufacture cells in one location and ship them to another center for infusion, with reproducible and consistent results and clinical outcomes.

“It’s important to note that this promising therapy is not only effective, but it is also a cost-effective option for high-risk patients,” said Dr. Heslop.

 

Bibliography for the Mammary Tumor Virus

Many have asked for a reference list for the mouse and human mammary tumor virus.  Given below is an abbreviated, though not short, list.  For those who enjoy a good old-fashioned hunt, have fun!

 

Bibliography

 

Andersson A, Expression of human endogenous retrovirus ERV3 (HERV-R) mRNA in normal and neoplastic tissues, Int J Onc, 1998, 12: 309-313

 

Axel R, Presence in Human Breast Cancer of RNA homologous to Mouse Mammary Tumour Virus RNA, Nature, 1972, 235:32-36

 

Benit L, Identification, Phylogeny, and Evolution of Retroviral Elements Based on Their Envelope Genes, J Virology, 2001, 75: 23, 11709-11719

 

Bera T, Defective Retrovirus Insertion Activates c-Ha-ras Proto-oncogene in an MNU-Induced Rat Mammary Carcinoma, Biochem Biophy Res Comm, 1998, 248: 835-840

 

Berkhout B, Identification of an Active Reverse Transcriptase Enzyme Encoded by a Human Endogenous HERV-K Retrovirus, J Virology, 1999, 73: 3, 2365-2375

 

Bittner J, Science, August 14, 1936, 84: 2171, p 162

 

Bittner J, The Milk-Influence of Breast Tumors in Mice, Science, 1 May 1942, 95:462-463

 

Bock M, Endogenous retroviruses and the human germline, Current Opinions in Genetics & Development, 2000, 10: 651-655

 

Chopra H, Cancer Research, 1970, 30: 8, 2081-2086

 

Callahan R, Detection and cloning of human DNA sequences related to the mouse mammary tumor virus genome, Proc Natl Acad Sci USA, 1982, 79:5503-5507

 

Dalton A, Some Ultrastructural Characteristics of a Series of Primary and Transplanted Plasma-Cell Tumors of the Mouse, JNCI, 1961, 26: 5, 1221-1266

 

Day N, Antibodies reactive with murine mammary tumor virus in sera of patients with breast cancer:  Geographic and family studies, Proc Natl Acad Sci USA, 1981, 78:2483-2487

 

Dion A, Retrovirus association with breast cancer: a critical appraisal, Breast Cancer Research and Treatment, 1987, 9:155-156

 

Fennelly J, Co-amplification of tail-to-tail copies of MuRVY and APE retroviral genomes on the Mus musculus Y Chromosome, Mammalian Genome, 1996, 7: 31-36

 

Franklin G, Expression of Human Sequences Related to Those of Mouse Mammary Tumor Virus, Journal of Virology, 1988, 62:1203-1210

 

Gay F, Morphogenesis of Bittner Virus, Journal of Virology, June 1970, 5:801-816

 

Golovkina T, Coexpression of Exogenous and Endogenous Mouse Mammary Tumor Virus RNA In Vivo Results in Viral Recombination and Broadens the Virus Host Range, Journal of Virology, 1994, 68:5019-5026

 

Gray D, Activation of int-1 and int-2 Loci in GRf  Mammary Tumors, Virology, 1986, 154: 271-278

 

Griffiths D, Endogenous retroviruses in the human genome sequence, Genome Biology, 2001, 2: 6, 1017.1-1017.5

 

Held W, Reverse Transcriptase-dependent and –independent Phases of Infection with Mouse Mammary Tumor Virus: Implications for Superantigen Function, J Exp Med, 1994, 180:2347-2351

 

Holland J, Breast Cancer Res Treat, 2006, 100:Absract 6

 

Hughes J, Evidence for genomic rearrangements mediated by human endogenous retroviruses during primate evolution, Nature Genetics, 2001, 29: 487-489

 

Imai S, Distribution of Mouse Mammary Tumor Virus in Asian Wild Mice, Journal of Virology, 1994, 68:3437-3442

 

Karlsson H Retroviral RNA identified in the cerebrospinal fluids of brains of individuals with schizophrenia, PNAS, 2001, 98: 8, 4634-4639

 

Larson E, Human Endogenous Proviruses, Current Topics in Microbiology and Immunology, 1989, 148:115-132

 

Lawson J, From Bittner to Barr:  a viral, diet and hormone breast cancer aetiology hypothesis, Breast Cancer Res, 2001, 3:81-85

 

Leib C, Endogenous Retroviral Elements in Human DNA, Cancer research (Supp), 1990, 50:5636-5642

 

Links J, The Growth Accelerating Effect of Bittner Virus in Monolayers of Baby Mouse Kidney Cells, J. Gen Virol, 1969, 5:547-550

 

Lower R, A General Method for the Identification of Transcribed Retrovirus Sequences (R-U5 PCR) Reveals the Expression of the Human Endogenous Retrovirus Loci HERV-H and HERV-K in teratocarcinoma Cells, Virology, 1992, Virology, 192: 501-511

 

Lower R, The pathogenic potential of endogenous retroviruses:  facts and fantasies, Trends in Microbiology, 1999, 7: 9, 350-356

 

Mager D, HERV-H Endogenous Retroviruses:  Presence in the New World Branch but Amplification in the Old World Primate Lineage, Virology, 1995, 213: 395-404

 

Mager D, Novel Mouse Type D Endogenous Proviruses and ETn Elements Share Long Terminal Repeat and Internal Sequences, J Virology, 2000, 74: 16, 7221-7229

 

Marchetti A, Host Genetic Background Effect o the Frequency of Mouse Mammary Tumor Virus-Induced Rearrangements of the int-1 and int-2 Loci in Mouse Mammary Tumors, J Virology, 1991, 65: 8, 4550-4554

 

Marrack P, A maternally inherited superantigen encoded by a mammary tumour virus, Nature, 1991, 349:524-525

 

McGrath C, J Virology, 1972, 9: 2, 367-376

 

Melana S, Characterization of viral particles isolated from primary cultures of human breast cancer cells, Cancer Res, 2007, 67:8960-8965

 

Mesa-Tehada R, Detection in human breast carcinomas of an antigen immunologically related to a group-specific antigen of mouse mammary tumor virus, Proc Natl Acad Sci USA, 1978,75:1529-1533

 

Mueller-Lantzsch N, Human Endogenous Retroviral Element K10 (KERV-K10) Encodes a Full-Length Gag Homologous 73-kDa Protein and a Functional Protease, AIDS Research and Human Retroviruses, 1993, 9: 4, 343-350

 

Nusse R, The int genes in mammary tumorigenesis and in normal development, TIG, 1988, 4: 10, 291-295

 

Nusse R, Insertional Mutagenesis in Mouse Mammary Tumorigenesis, Current Topics in Microbiology and Immunology, 1991, 171:43-65

 

Ono M, Stimulation of Expression of the Human Endogenous Retrovirus Genome by Female Steroid Hormones in Human Breast Cancer Cell Line T47D, Journal of Virology, 1987, 61:2059-2062

 

Paces J, HERVd:  database of human endogenous retroviruses, Nucleic Acids Research, 2002, 30: 1, 205-206

 

Palmarini M, The Exogenous Form of Jaagsiekte Retrovirus Is Specifically Associated with a Contagious Lung Cancer of Sheep, J of Virology, 1996, 70: 3, 1618-1623

 

Peters G, Tumorigenesis by Mouse Mammary Tumor Virus: Evidence for a Common Region for Provirus Integration in Mammary Tumors, Cell, 1983, 33:36-377

 

Pogo B, Possibilities of a Viral Etiology for Human Breast Cancer, A Review, Biological Trace Element Research, 1997, 56:131-142

 

Prak E, Mobile Elements and the Human Genome, Nature Reviews Genetics, 2000, 1: 134-144

 

Reus K, HERV-K (OLD):  Ancestor Sequences of the Human Endogenous Retrovirus Family HERV-K (HNL-2), J Virology, 2001, 75: 19, 8917-8926

 

Reuss F, cDNA Sequence and Genomic Characterization of Intracisternal A-Particle-Related Retroviral Elements Containing an Envelope Gene, J Virology, 1991, 65: 11, 5702-5709

 

Shackleford G, Mouse mammary tumor virus infection accelerates mammary carcinogenesis in Wnt-1 transgenic mice by insertional activation of int-1/Fgf-3 and hst/Fgf-4, Proc Natl Acad Sci USA, 1993, 90:740-744

 

Smit A, Interspersed repeats and other mementos of transposable elements in mammalian genomes, Current Opinion in Genetics & Development, 1999, 9: 657-663

 

Stewart A, Identification of Human Homologues of the Mouse Mammary Tumor Virus Receptor, Archives of Virology, 147:577-581

 

Stewart T, Breast Cancer Incidence Highest in the Range of One Species of House Mouse, Mus Domesticus, British Journal of Cancer, 2000, 82:446-451

 

Sumidaie A, Particles with Properties of Retroviruses in Monocytes from Patients with Breast Cancer, The Lancet, 1988, 5-9

 

Szabo S, Of Mice, Cats and Men:  Is human breast cancer a zoonosis? Microsc Res Tech, 2005, 68:197-208

 

Tchenio T, Defective Retroviruses Can Disperse in the Human Genome by Intracellular Transposition, Journal of Virology, 1991, 65:2113-2118

 

Time, Cancer Virus, March 18, 1946

 

Tonjes R, Characterization of Human Endogenous Retrovirus Type K Virus-like Particles Generated from Recombinant Baculoviruses, Virology, 1997, 233: 280-291

 

Tristem M, Identification and Characterization of Novel Human Endogenous Retrovirus Families by Pylogenetic Screening of the Human Genome Mapping Project Database, J Virology, 2000, 74: 8, 3715-3730

 

Turner G, Insertional polymorphisms of full-length endogenous retroviruses in human, Current Biology, 2001, 11: 1531-1535

 

 

Wang Y, Detection of MMTVlike LTR and LTR-env gene sequences in human breast cancer, Int J Oncology, 2001, 18: 1041-1044

 

Westley B, The human genome contains multiple sequences of varying homology to mouse mammary tumour virus DNA, Gene, 1984, 28:221-227

 

Witkin A, antigens and Antibodies Cross-Reactive to the Murine Mammary Tumor Virus in Human Breast Cyst Fluids, J Clin Invest, 1981, 67:216-222

 

Zotter S, Mouse Mammary Tumour Virus-related Antigens in Core-like Density Fractions from Large Samples of Women’s Milk, Euro J Cancer, 1980, 16:455-467

Postponing Your Demise

6 Things to Do Everyday to Slow Or Reverse Aging

How would you like to slow or reverse the aging process six times a day by taking only three steps?  Here’s the plan:

 

1. Begin each day with 15 minutes of yoga.  I highly recommend “A.M. Yoga with Rodney Yee.  I have been doing it myself for over three years.  I cannot start my day without it.  Think about it:  after a good night’s rest, you start your day with yoga, limber up and stretch those muscles, and then you’re centered and ready for the wild blue yonder.
2. Eat 3 meals and one snack, all composed of plant-based foods.  Fruits, vegetables, beans, whole grain products.  That’s it.  Pure, clean fuel.  The kind of pure fuel you’d put in the gas tank of a Ferrari if you were lucky enough to own one.  You probably don’t, but you do own a machine that is world’s better – your adaptive, restoring, evolving body.  Put only clean fuel in your body.  This means:  no meat, no dairy, no poultry, no fish, no eggs, no oil, and no fats.  The good news is that you can have a glass of wine occasionally.  Enjoy.  (Your wallet is going to love this diet, too.)
3. Exercise aerobically for thirty minutes.  You can just walk (briskly)!  A pair of tennis shoes and appropriate dress and out the door you go – or, to the treadmill or bicycle you go.  But go!  If you are ambitious, and have disposable income, find the perfect personal trainer to guide you through aerobic exercises and weight training.  Take dance classes.  Learn fencing.  Play golf, but carry your clubs.  I find that walking for 30 minutes a day, at a brisk pace, is the easiest way to get this task done.  It allows me to think, and think more clearly because I am moving more oxygen to my brain where it is used for clarity and insight.

That’s it.  That’s my recipe for postponing one’s demise and improving your health for the time you have on earth.

Enjoy.

 

Reference:  Prevent and Reverse Heart Disease by Caldwell Esselstyn

The Pink Virus

SUMMARY OF RESEARCH ON THE MOUSE MAMMARY TUMOR VIRUS

Scientists have proven that the human papilloma virus (“HPV”) causes cervical cancer.  In fact, Dr. Van Hausen, the scientist who first made this discovery, won the Nobel Prize for medicine in 2008 for his groundbreaking research..

But HPV is not the only virus known to cause cancer.  At least six other viruses are proven cancer agents and scientists now believe that as much as 15-20% of all human cancers are of viral origin.  Of all of the potential tumor viruses presently under investigation the one with the greatest potential impact on women is  the mouse mammary tumor virus (“MMTV”) a virus found in mice that causes breast cancer in 95% of the animals it infects.

Although MMTV was first discovered in 1936, research proceeded slowly at first, primarily because scientists lacked the technology to study it well. But as technology improved, and as other viruses were shown to cause other cancers, there was renewed interest in MMTV and its relation to human breast cancer.

In the 19990’s Dr. Beatriz Pogo of Mt. Sinai University found a DNA “fingerprint” that was 98% similar to MMTV in 38% of the breast cancer tissues she examined.  She also discovered that the DNA fingerprint contained elements that responded to hormonal stimulation, as does MMTV..

During this same time, another researcher, Dr. Polly Etkind, found viral sequences similar to MMTV in patients who had both breast cancer and lymphoma.  Interestingly, these sequences were not found in the normal breast tissue of these patients.

To date, at least seven groups of researchers have found viral gene sequences in human breast cancer tissue and have reported their findings in ten separate studies.  One group has reported that the virus, that they now refer to as human mammary tumor virus, HMTV, can infect and rapidly spread to normal human breast cells.

Dr. Paul Levine of George Washington University discovered that 74% of Tunisian women with breast cancer had evidence of MMTV compared to only 36% of women in the United States. But, interestingly, 75% of women in the United States who have inflammatory breast cancer show evidence of MMTV.

To prove that MMTV/HMTV causes human breast cancer we must know exactly where and how the virus infects humans and we must determine exactly how the virus alters the DNA of normal breast cells and transforms them into cancer cells.

The question remains open:  Does a virus cause breast cancer in women?  The lines of inquiry have not yet converged to answer that question, but Pogo, Levine, Holland, Etkind and others, here in the United States and around the world, continue their quest to answer the question and solve the puzzle.

If researchers can confirm a causal connection between MMTV and human breast cancer, then the implications for the treatment and prevention of breast cancer would be dramatic.  Another 1.3 million new cases of breast cancer will be diagnosed around the world by the end of 2009, and hundreds of thousands more women will die this year of the disease.   Millions of lives and billions of dollars are at stake:   it is a question that needs to be answered…as soon as possible.

Tracking Down Breast Cancer, One Cell at a Time

 

“We’re making progress!”  You’ve heard that before, and it’s true.  Progress is being made seemingly everywhere in the field of breast cancer research:  in understanding causes, developing strategies for prevention, diagnosing the disease earlier, and treating patients more effectively.

As always, the biggest strides are made in the direction of more effective treatments. One breakthrough called lab-on-chip technology promises to allow doctors to adjust chemotherapy based on analysis of a patient’s individual breast cancer cells.

Before I explain how lab-on-chip technology works, it would be helpful to review some of the ways that breast cancer cells differ from normal breast cells.

1. Cancer cells live forever.  Now there’s a survival advantage.
2. Cancer cells invade normal tissues.  They do not respect borders or tissue planes; they wantonly grow in any direction they please.
3. Cancer cells metastasize.  That is, they relocate and create new terrorist colonies in other organs, like the liver or lung.  Metastasis, not the original tumor, is what usually kills the patient.

In addition to the sinister characteristics listed above, breast cancer cells in a given patient are not all the same.  Breast cancer cells comprise a mixed bag of different sub-types of cells, like different colored candies in a bag of M&M’s.  Because breast cancer cells are a mixed bag, it is sometimes difficult to kill them all with one, or even several drugs.  If you find a way to kill all the red ones, the blue ones escape unscathed.  If you use combination chemotherapy, or add radiation therapy to the treatment regimen, you can increase the likelihood that you kill different sub-types of cancer cells, but some may survive the assault nevertheless… and live forever, and invade, and metastasize.  You can see that leaving just a few breast cancer cells behind might mean recurrence further down the road.  Finding better ways to track down cancer cells, and getting rid of them, would be very helpful indeed.

It is not uncommon to find some breast cancer cells circulating in the bloodstream.   For years doctors have tried to capture them and analyze them as a guide to tailoring chemotherapy for their patients.  But until recently, this tracking down of circulating cancer cells has been tedious and fraught with error. That is where lab-on-chip technology (LOCT) comes in, making the process easier, faster and cheaper.

LOCT uses magnetic beads to find, grab and isolate a single breast cancer cell as it circulates in the bloodstream.   It then breaks down the wall of the breast cancer cell, gets inside and obtains specific genetic material, genetic material that is used as a blueprint to make specific breast cancer proteins.  LOCT captures these blueprints, called messenger RNAs, and amplifies the proteins they make to better reveal their presence.   This then allows doctors to target these proteins with specific treatments that block their function.

The preliminary work with lab-on-chip technology was carried out as a collaborative project among European researchers, and is also being replicated here in the United States.  Scientists will now begin to test this new technology at the bedside to see how well it works in clinical practice.  The hope is that LOCT will allow clinicians to isolate and analyze specific breast cancer cells and use this information to tailor treatment that produces a better chance for cure.