All cancer cells are not created equal: Some cell types control continued tumor growth, others prepare the way for …

ScienceDaily (May 15, 2012) A study from Massachusetts General Hospital (MGH) researchers suggests that specific populations of tumor cells have different roles in the process by which tumors make new copies of themselves and grow. In their report in the May 15 issue of Cancer Cell, researchers identify a tumor-propagating cell required for the growth of a pediatric muscle tumor in a zebrafish model and also show that another, more-differentiated tumor cell must first travel to sites of new tumor growth to prepare an environment that supports metastatic growth.

“Most investigators have thought that tumor-propagating cells — what are sometimes called cancer stem cells — must be the first colonizing cells that travel from the primary tumor to start the process of local invasion and metastasis, but in this model, this is simply not the case,” says David Langenau, PhD, of the MGH Department of Pathology and Center for Cancer Research, who led the study. “Instead, the colonizing cells lack the ability to divide and instead prime newly infiltrated regions for the eventual recruitment of slow-moving cancer stem cells. It will be important to test how broadly this phenomenon is found in a diversity of animal and human cancers.”

Langenau’s team has long been using zebrafish to study rhabdomyosarcoma (RMS), an aggressive pediatric cancer. In embryonic zebrafish, RMS can develop within 10 days, and since the tiny fish are transparent at that stage, fluorescent markers attached to particular cellular proteins can easily be imaged. The current study used these properties to monitor how specific populations of tumor cells develop and their role in initiating new tumor growth.

Previous research from the MGH team had discovered that RMS cells expressing marker proteins also seen on muscle progenitor cells had significantly more tumor-propagating potential than did other tumor cells. Fluorescently labeling proteins associated with different stages of cellular differentiation revealed distinct populations of RMS cells in the zebrafish model. Cells expressing the progenitor cell marker myf5, were labeled green, and those expressing myogenin, a marker of mature muscle cells, were labeled red.

In a series of experiments, the research team confirmed that myf5-expressing RMS cells had powerful tumor-propagating potential, but the ability to visualize how tumor cells move in living fish produced a surprising observation. While myf5-expressing cells largely remained within the primary tumor itself, myogenin-expressing RMS cells easily moved out from the tumor, entering the vascular system and passing through usually impenetrable layers of collagen. Only after the more-differentiated but non-proliferative myogenin-expressing cells had colonized an area did the myf5-expressing tumor-propagating cells appear and start the growth a new tumor. Imaging the labeled tumor cells also revealed that different cellular populations tended to cluster in different areas of later-stage tumors.

“Our direct in-vivo imaging studies are the first to suggest such diverse cellular functions in solid tumors, based on differentiation and the propensity for self-renewal,” says Myron Ignatius, PhD, of MGH Pathology and Center for Cancer Research, the study’s first author. “I think we will find that this kind of division of labor is a common theme in cancer, especially given that the vast majority of cells within a tumor are not tumor-propagating cells. We suspect there will be molecularly defined populations that make niches for tumor-propagating cells, secrete factors to recruit vasculature and create boundaries to suppress immune cell invasion.”

Langenau adds, “Division of labor is a new and emerging concept in cancer research that we hope will lead to new targets for rationally designed therapies. In rhabdomyosarcoma it will be important to target both the tumor-propagating cells and the highly migratory colonizing cells for destruction — a major focus of ongoing studies in our group.” Langenau is an assistant professor of Genetics at Harvard Medical School and a principal faculty member at the Harvard Stem Cell Institute.

Additional co-authors author of the Cancer Cell article are Eleanor Chen, Adam Fuller, Ines Tenente Rayn Clagg, Sali Liu, Jessica Blackburn, MGH Pathology and Center for Cancer Research; Andrew Rosenberg, and Petur Neilsen, MGH Pathology; Natalie Elpek and Thorsten Mempel, MGH Center for Immunology and Inflammatory Diseases; and Corinne Linardic, Duke University Medical Center. The study was supported by grants from the National Institute of Health, the Alex’s Lemonade Stand Foundation, the Sarcoma Foundation of America, the American Cancer Society and the Harvard Stem Cell Institute.

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Stem cell debate could flare in Neb. regents race

A long-standing dispute over embryonic stem cell research is likely to resurface during the general election race for candidates of the University of Nebraska Board of Regents.

Regent hopefuls in at least one district differ on the use of research, which has divided the board in past years and caught the attention of an influential Nebraska anti-abortion group.

The primary vote will eliminate candidates from three of four seats that are up for re-election. The nonpartisan, unpaid board has eight members plus one nonvoting student regent for each of the four University of Nebraska campuses. The top two vote-getters in the primary advance to the November general election, where they will compete for a six-year term in office.

The Board of Regents voted 4-4 in 2008 on a proposition to limit the stem cell research at the university to types allowed under President George W. Bush. The board needed a majority of its eight members to approve the measure, and many backers thought they had the necessary votes.

Outgoing state Sen. Lavon Heidemann, a Republican primary winner vying for a seat on the board, said he expected embryonic stem cell research to surface as an issue in the general election. Heidemann’s general election opponent, Mike Jones, has said he supports embryonic stem cell research.

Both candidates are seeking to replace Regent Jim McClurg of Lincoln, who did not seek re-election after his vote to allow expanded stem cell research.

“It’s not the only issue but is important,” Heidemann said, pointing to his endorsement by the group Nebraska Right to Life. “I think that’s going to pop up throughout the campaign.”

The primary winners of another district _ Norfolk attorney David Copple and Columbus veterinarian Jim Pillen _ have both voiced opposition to stem cell research. One of the two will replace Regent Chuck Hassebrook, who has voted to allow the expanded research.

About $88 million in federal funding went to embryonic stem cell research in 2008, according to the National Institutes of Health, but the University of Nebraska saw none of that funding at the time because of tight federal guidelines. When the guidelines were lifted, university scholars applied for millions of dollars in research grants.

The race for the University of Nebraska Board of Regents attracted a number of well-known politicians and business executives for Tuesday’s primary who have promised to keep college affordable and use the university as an engine for economic growth.

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Boston scientists grow lung tissue from cystic fibrosis patients’ skin cells

By Carolyn Y. Johnson, Globe Staff

Two teams of Boston scientists have developed new ways to turn stem cells into different types of lung tissue, surmounting a major hurdle for scientists trying to harness the power of stem cell biology to study and develop treatments for major lung diseases.

One team then used skin cells from cystic fibrosis patients to create embryonic-like stem cells, then working in lab dishes used those cells to grow tissue that lines the airways and contains a defect responsible for the rare, fatal disease. The technique — essentially a recipe for growing such lung tissue — could provide a powerful platform to screen drugs and study the biology of the disease.

Growing lung tissue in the laboratory has long been a goal of stem cell scientists, but has been more technically difficult than growing other types of tissues, such as brain cells or heart cells. Such lung tissue is valuable because it could be used to screen potential drugs and more closely probe the problems that underlie diseases such as asthma, emphysema, and rare genetic diseases. Such techniques may also one day help researchers grow replacement tissues and devise ways to restore or repair injured lung tissue.

A team led by Massachusetts General Hospital researchers created lung tissue from a patient with the genetic mutation that most commonly underlies cystic fibrosis and researchers hope the technique will also be a powerful tool to study other diseases that affect the airway tissue, such as asthma and lung cancer. The other team, led by Boston University School of Medicine scientists, was able to derive cells that form the delicate air sacs of the lung from mouse embryonic stem cells. The team is hoping to refine the recipe for making the cells so that they can be used to derive lung tissue from a bank of 100 stem cell lines of patients with lung disease. Both papers were published Thursday in the journal Cell Stem Cell.

Vertex Pharmaceuticals, a Cambridge biotechnology company, earlier this year received approval for Kalydeco — the first drug to directly target the underlying cause of cystic fibrosis. That compound was discovered by screening massive numbers of potential drugs against cells engineered to carry the same defect that underlies cystic fibrosis.

We had to use engineered cells, and certainly using more native human cells … would be potentially beneficial, said Dr. Frederick Van Goor, head of biology for Vertexs cystic fibrosis research program. We had to rely on donor tissue obtained from patients with cystic fibrosis, and its a bit more challenging, because the number of donor lungs you can get and the number of cells you can derive from there are more limited.

Van Goor said it was too soon to say whether the company would use the new technology in screening, but noted that the tests the company had used to determine whether a drug was likely to work against the disease had, in some cases, given scientists false leads. Some molecules that worked on the engineered cells did not work in the complicated biology of the lung.

Its a significant event for the lung field, said Dr. Thiennu Vu, associate professor of medicine at the University of California San Francisco, who was not involved in the research. She added that much work remains before such cells could be used to repair or replace damaged tissue, and even before such cells would necessarily be useful for drug screening. It will be important, she said, to refine the recipe to ensure that the technique yields pure populations of the specific types of functional lung cells.

In the competitive world of science, where credit for being the first to do something is crucially important, the two research teams accomplishments are an unusual example of competitors turning into collaborators — forging a relationship that both teams felt helped speed up progress.

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Lenalidomide prolongs disease control for multiple myeloma patients after stem cell transplant

Public release date: 15-May-2012 [ | E-mail | Share ]

Contact: Elisa Williams willieli@ohsu.edu 503-494-4530 Oregon Health & Science University

PORTLAND, Ore. Multiple myeloma patients are better equipped to halt progression of this blood cancer if treated with lenalidomide, or Revlimid, following a stem cell transplant, according to a study co-authored by a physician with the Oregon Health & Science University Knight Cancer Institute.

The study, published in the New England Journal of Medicine, found a 63 percent reduction in the risk of progressive myeloma or death for the stem cell transplant patients that were treated with lenalidomide maintenance therapy.

“These results add to the evidence that the combination of standard therapies such as stem cell transplantation with the emerging biologic therapies, like lenalidomide, have extended the lives of multiple myeloma patients,” said Richard Maziarz, M.D., of the OHSU Knight Cancer Institute who was one of the study’s co-authors. Maziarz serves as medical director of the Adult Stem Cell Transplantation Program & Center for Hematologic Malignancies at the OHSU Knight Cancer Institute. “We know that for at least three years following a transplant that maintenance therapy with this drug vastly improves the chances that the cancer won’t come back and worsen.”

These data were supported by similar Phase III studies reported from France and Italy in the same issue of the New England Jounal of Medicine demonstrating that maintenance therapy after stem cell transplantation was associated with improved disease control.

Multiple myeloma is a cancer that affects plasma cells, a type of white blood cell normally responsible for producing antibodies. In patients impacted by multiple myeloma, collections of abnormal plasma cells accumulate in the bone marrow, interfering with the production of normal blood cells. The study focused on patients who received an autologous hematopoietic cell transplant (AHCT). AHCT procedures use patients’ own blood stem cells.

While lenalidomide increased a patient’s ability to stave off progression of the disease, questions remain regarding future approaches recognizing that quality of life measurements were not incorporated within these studies, that long-term safety issues remain unclear as there was a small but discernable risk of second cancers observed in the treated patients. In addition to the need for that cost-benefit analysis, a comparison remains to be performed with other emerging myeloma maintenance therapies.

This Phase III study of lenalidomide was conducted at 47 medical centers and involved 568 patients. It was sponsored by the National Cancer Institute (NCI). Revlimid’s manufacturer, Celgene Corp., provided the NCI with lenalidomide for this research.

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Scientists Discover Marker to Identify, Attack Breast Cancer Stem Cells

Cell surface protein blows potent cells cover; targeted drug works in preclinical tests

Newswise HOUSTON Breast cancer stem cells wear a cell surface protein that is part nametag and part bulls eye, identifying them as potent tumor-generating cells and flagging their vulnerability to a drug, researchers at The University of Texas MD Anderson Cancer Center report online in Journal of Clinical Investigation.

Weve discovered a single marker for breast cancer stem cells and also found that its targetable with a small molecule drug that inhibits an enzyme crucial to its synthesis, said co-senior author Michael Andreeff, M.D., Ph.D., professor in MD Andersons Departments of Leukemia and Stem Cell Transplantation and Cellular Therapy.

Andreeff and colleagues are refining the drug as a potential targeted therapy for breast cancer stem cells, which are thought to be crucial to therapy resistance, disease progression and spread to other organs.

Its been difficult to identify cancer stem cells in solid tumors, Andreeff said. And nobody has managed to target these cells very well.

The marker is the cell surface protein ganglioside GD2. The drug is triptolide, an experimental drug that Andreeff has used in preclinical leukemia research. The team found triptolide blocks expression of GD3 synthase, which is essential to GD2production.

Triptolide stymied cancer growth in cell line experiments and resulted in smaller tumors and prolonged survival in mouse experiments. Drug development for human trials probably will take several years.

Cancer stem cells are similar to normal stem cells

Research in several types of cancer has shown cancer stem cells are a small subpopulation of cancer cells that are capable of long-term self-renewal and generation of new tumors. More recent research shows they resist treatment and promote metastasis.

Cancer stem cells are similar to normal stem cells that renew specialized tissues. The breast cancer findings grew out of Andreeffs long-term research in mesenchymal stem cells, which can divide into one copy of themselves and one differentiated copy of a bone, muscle, fat or cartilage cell.

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In Venezuela, top diplomat steps into the void while cancer forces lower profile for Chavez

CARACAS, Venezuela After nearly a year of cancer treatment that has forced President Hugo Chavez to step back from the spotlight, a burly former bus driver with a dark mustache and affable smile is emerging more than ever as the president’s stand-in.

In recent weeks, Foreign Minister Nicolas Maduro has led news conferences, touted a new labor law and criticized the U.S. government with gusto. He even rallied a crowd of supporters while wearing a track suit emblazoned with the yellow, blue and red of Venezuela’s flag, just like one Chavez sometimes wears.

Maduro’s prominence is generating speculation that he could be a leading candidate to succeed the president, or at least represent him during grueling campaign events, if Chavez’s health fails ahead of Venezuela’s Oct. 7 presidential election.

Chavez has built his 13-year-old presidency around his own larger-than-life persona and hasn’t anointed a successor, instead pledging to recover from cancer treatment and once again return to the front line of his campaign. Nonetheless, Maduro’s role as government spokesman has grown in the past month, and his regular appearances at Chavez’s side have many thinking he has received the presidential nod.

“I think the best-trained politician Chavez has is Nicolas Maduro,” said former diplomat Vladimir Villegas, a journalist who hosts a Venezuelan radio program.

Villegas said Maduro seems to outshine Vice President Elias Jaua with his experience on the international stage, his ties to labor groups and his close relationship with Cuba’s government. Maduro has been the country’s top diplomat since 2006.

Speaking with confidence, Maduro took to championing a newly approved labor law before government supporters earlier this month, while the president was receiving cancer treatment in Cuba.

“With our commander Chavez, today Venezuela is at the vanguard, ahead in the fight for a new humankind, for another humankind, for a new world,” Maduro said. “That world is being built here, and that world has one single name: socialism of the 21st century.”

While heaping praise on Maduro, the president likes to note that critics once derided his foreign minister as a simpleton because of his working-class roots, which included a stint as a union leader for workers in the Caracas Metro subway system.

Chavez’s close friendship with Maduro goes back to the 1980s, when the leftist president was an army officer and formed a clandestine movement that eventually carried out a failed coup attempt in 1992.

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Exclusive: Hampton man celebrates 5-year survival of cancer

When Floyd Walker, now 62, was diagnosed with prostate cancer five years ago, his treatment choices were limited, both by his health history and available therapies in the area. After checking out local options, he took matters into his own hands and self-referred to Cancer Treatment Centers of America in Philadelphia.

On Friday, he’ll return there to participate in “Celebrate Life,” an annual event honoring 5-year cancer survivors. “As far as I know now, I’m cancer-free,” Walker says.

It all happened quickly in June 2007, when a VA doctor told him his PSA reading was high. Walker then went to a primary care doctor followed by a urologist, whose tests confirmed the diagnosis. Initially, his doctor encouraged the Hampton resident to go to Norfolk for surgery where doctors were using the DaVinci robot. But Walker’s hernia surgery a decade earlier, which involved having mesh inserted, made the operation inadvisable.

Back then, the Vietnam veteran and retired Army reservist was working as a nuclear pipe welder at the shipyard in Newport News he retired last fall after 43 years service. One night after work, he flipped on the TV and saw an ad for Cancer Treatment Centers of America, a group of four regional hospitals that specialize in integrative cancer care for advanced and complex cases. (A fifth hospital is slated to open in Atlanta, Ga., in August 2012.) He called out the toll-free number to his wife, Leslie, to write down. They called and talked to a representative who encouraged Walker to make a 3-day visit to Philadelphia to get a second opinion.

CTCA sent him the plane tickets. The centers’ rep picked him up at the airport. It provided an inexpensive 2-bedroom apartment for him and his wife to stay. The Walkers also ate free at the hospital’s cafeteria. Its standard services include verifying insurance, gathering medical records, booking travel and scheduling evaluations, anything effectively to reduce stress.

“It’s different from other cancer hospitals. It’s patient-empowered care. You have a whole team that stays with you,” says spokeswoman Mamie Cargile. “It’s very stressful for patients to have to bounce around. You stay in your room and people come to you.”

Kane Dawson, an administrator in Philadelphia before becoming CEO, CTCA of the Southeast, expands on the patient empowerment theme. “Even the physical design helps patients to feel comfortable and less overwhelmed,” he says. “Two-thirds of the patients are traveling great distances. It helps to have everything under one roof.” Its employee-providers include oncologists, radiologists, hospitalists, nurses, massage therapists, naturopaths, dietitians and more.

A team ran a series of tests on Walker and decided on the use of HDR brachytherapy (pronounced “breaky-therapy”). Walker explains that it involves high dosage radiation delivered internally through six-inch needles, or catheters, inserted through the scrotum into the prostate. The actual sessions take minutes but are conducted over two days. After the treatment he returned home and went back to work.

Two weeks later, he headed back to the 58-bed Philadelphia hospital to receive a course of TomoTherapy external radiation daily for five weeks. “I did naturopathic medicine and herbal medicine too fish oil, green tea extract. I’m still taking it. I can put in an order and it’s delivered to my door by FedEx the next day,” he says. Between his insurance and the CTCA helping out, Walker’s out-of-pocket costs have been manageable.

Until last year, Walker checked back in with the treatment center three times a year. “I really enjoyed them. They do a lot of things that others don’t do. They flew me and my wife back and forth a few times. The staff is excellent, the nicest I’ve been around. They tell you straight up.”

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Mind, Body and Cancer

PHOENIX, May 16, 2012 (GLOBE NEWSWIRE) — When it comes to cancer, there are obvious mind-body links. Stress, pessimism and other emotional factors have been proven to play a role, increasing the risk of cancer, metastasis and early mortality. This is a double-whammy for cancer patients, who must overcome anxiety from the moment they are diagnosed. In particular, stress has been shown to depress the immune system, increase inflammation and affect our bodies on the molecular level, even damaging DNA.

In a recent lecture in Phoenix, AZ at the American Academy of Anti-Aging Medicine (A4M) Fellowship, integrative medicine pioneer Isaac Eliaz, M.D., L.Ac. discussed how negative emotions hinder immune response and fuel cancer formation and metastasis. He followed by sharing research on mind-body therapies such as meditation, yoga and Qigong which work to counteract the negative effects of stress and boost health in numerous ways. Highlighting an array of published studies, Dr. Eliaz showed how chronic stress can be deadly to lymphocytes and DNA integrity, and conversely, how mind body therapies and emotional support can ramp up immunity and provide numerous health benefits.

“The contrasts are amazing,” says Dr. Eliaz. “Chronic stress significantly reduces the immune response, while something as simple as family support or mindful meditation can boost it just as dramatically.”

The negative effects of stress have been studied in a variety of cancers including breast, ovarian, and digestive tract. In one study cited by Dr. Eliaz, breast cancer risk doubled for women after a divorce, separation or the death of their spouse.

In addition to reducing our body’s resistance to cancer, stress, depression and isolation also increase metastasis and tumor vascularization. While these facts may be daunting, there are solutions that can make a substantial difference.

In his presentation, Dr. Eliaz discussed a variety of mind-body techniques, including meditation, yoga and Qigong — an ancient Chinese system of mindful exercises — that can calm stress and restore the body’s healthy balance. In particular, meditation reduces cortisol levels, pro-inflammatory cytokines, systolic blood pressure, anxiety, depression and stress. It also has been proven to increase multiple areas of cognitive function, including information processing, memory and decision making.

“Study after study shows that reducing stress, and its associated negative effects, boosts the immune system and enhances brain function,” says Dr. Eliaz.

Yoga fares equally well, helping post-operative breast cancer patients by accelerating healing, reducing hospital stays and enhancing quality of life. The practice has also been shown to reduce the nausea associated with chemotherapy. Qigong has similar benefits.

As a meditation practitioner with over 25 years of experience, Dr. Eliaz has cultivated a deep understanding of the philosophies and application of mindful meditation for healing and personal growth. To integrate practice with theory and research, Dr. Eliaz shared important meditation exercises and take home tools for beginners, to enable participants to experience the benefits of meditation first hand.

“Through all this research, we see one common thread–the calming, healing power of our brains when harnessed through meditation and mind body practice,” says Dr. Eliaz. “Simple acts, like breathing mindfully, can have a dramatic effect on all aspects of our being, right down to the molecular level. When practiced regularly, mind body therapies can be powerful tools to help us maintain optimal mental, emotional and physical health.”

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Breast cancer study reveals 'substantial genetic diversity'

A new study of the protein-coding genes in 100 breast cancer tumors revealed vast differences among the cancers and highlights how complicated the disease really is, researchers said Wednesday.

A sobering perspective on the complexity and diversity of the disease is emerging, they wrote in the online edition of the journal Nature (subscription required), which is publishing a series of studies of the genetic changes in breast cancer.

The scientists, led by Michael Stratton at the Wellcome Trust Sanger Institute in Hinxton, England, found 73 different combinations of disease-causing mutations in the tumors, each involving up to six different genes from a set of 40 driver genes.

Seven of the 40 individual driver genes were mutated in more than 10% of cases, but 33 others that were less common also contributed to the development of the cancers, the team reported. In 28 cases, a single mutation was enough to cause disease.

The researchers identified nine new genes that caused the cancers, and also found mutations in genes that were already known to cause breast and other cancers.

Discovering that a single disease breast cancer can appear in so many different guises means that developing targeted therapies tailored to a patients tumor type will remain a tall order in the near future.

The situation is more complex than anyone would like to see, said Christina Curtis, an assistant professor of preventive medicine at the Keck School of Medicine at USC and first author of another paper in Nature, released in April, that detailed several new breast cancer subcategories.

But it seems were getting closer, Curtis added. With each study were getting a new vantage point.

Curtis said that finding new driver genes and new combinations of driver genes could still eventually pave the way to new treatment options, once researchers dig further and figure out exactly how the different combinations of mutations change cellular function, causing cancer.

Her team at USC is working on techniques to examine mutations in single cells, which will let scientists study genetic variation within tumors as well as between then.

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Why we need a good screening test for ovarian cancer

STORY HIGHLIGHTS

Editor’s note: CNN conditions expert Dr. Otis Webb Brawley is the chief medical officer of the American Cancer Society, a world-renowned cancer expert and a practicing oncologist. He is also the author of the book, “How We Do Harm: A Doctor Breaks Ranks About Being Sick in America.”

(CNN) — Q: This week the U.S. Preventive Services Task Force issued preliminary guidelines for ovarian cancer screening. It recommends against routine screening saying that the risk of false positive diagnoses outweighs the benefits. How can this be and why is it so hard to find a good screening test for ovarian cancer?

A: The U,S. Preventive Services Task Force is a group of medical experts who assess the scientific literature on an issue, such as ovarian cancer screening, before making a recommendation. They do influence how doctors practice medicine.

The statement recommends against routine ovarian cancer screening because they find the evidence of harm associated with screening is greater than the evidence of benefit.

Unfortunately we do not have a good screening test for ovarian cancer, the fifth leading cause of cancer death in women. We need something as effective for ovarian cancer screening as pap smears are for cervix cancer screening.

It is a surprise to many that a screening test could be considered more harmful than helpful. The problem is routine ovarian cancer screening starts a cavalcade of medical procedures associated with harms that are greater than the ultimate benefits. Importantly, it is not that there is no benefit to ovarian cancer screening. The problem is there is not a “net benefit.”

The blood test CA 125 is elevated in about half of women who are known to have ovarian cancer. If effectively treated by surgery or chemotherapy, the CA 125 level in the blood goes down. It has been used for nearly three decades to follow progress in treatment.

This test was suggested for screening in the late 1980s. Screening is doing a test in asymptomatic patients who are not suspected of having the disease but are at risk because of age and gender. Very early on, many thought CA 125 would not work well as a screening test.

A teacher gave me this example more than 20 years ago and it still holds. It is dense in numbers, but I think it is followable. It illustrates how a public health physician thinks of a screening test and the trouble with CA 125.

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