Randomized Clinical Trial Results on Preoperative Chemotherapy in Early Breast Cancer

Eight cycles of preoperative chemotherapy was no better than six cycles in women with early breast cancer who had responded to two initial cycles, according to data from a randomized controlled trial. Additionally, women who failed to respond to the first two cycles of one drug combination did not benefit from switching to a different drug combination for four additional cycles, compared with those who continued receiving the original combination for four more cycles.

Preoperative chemotherapy, also known as neoadjuvant chemotherapy, is used to shrink the tumor to improve surgical options and provide early information about a patient’s response to treatment.

In a randomized controlled trial, Gunter von Minckwitz, M.D., of the Universit盲ts-Frauenklinik in Frankfurt and colleagues in the German Breast Group treated 2,090 women with two cycles of preoperative docetaxel, doxorubicin, and cyclophosphamide (TAC). The researchers then randomly assigned the 1,390 women whose tumors responded to therapy to either four or six additional cycles of TAC. The proportion of women who had a complete pathological response was similar in the two arms鈥”21 percent and 23.5 percent, respectively.

The 622 women who failed to respond to the initial two cycles of TAC were randomly assigned to either four additional cycles of TAC or four cycles of capecitabine plus vinorelbine (NX). Increasing the number of TAC cycles or switching regimens did not appear to improve outcomes. Only 5.3 percent of women on TAC achieved a complete pathological response and 6.0 percent of the women on NX.

In an accompanying editorial, Francisco J. Esteva, M.D., Ph.D., and Gabriel N. Hortobagyi, M.D., of the University of Texas M. D. Anderson Cancer Center in Houston review the results of the German trial and other trials that tested neoadjuvant therapy. The data indicate that neoadjuvant therapy is effective and that the full benefit can be achieved with a limited number of treatment cycles. Not all women benefit equally though, and therefore new treatment approaches are needed.
“Patients who do not respond to the initial chemotherapy should be considered for alternative treatment approaches, if possible as part of a clinical trial,” the editorialists write.

Contact:

* Articles: Stefanie Hildebrandt, Stefanie.Hildebrandt@germanbreastgroup.de

* Editorial: Laura Sussman, lsussman@mdanderson.org

Frequent Blood Donation Unrelated to Donors’ Risk of Cancers

Frequent blood donation does not change an individual’s risk of developing cancer.

While iron is a vital trace element for essentially all living organisms, too much iron has been implicated as a possible risk factor for certain cancers. If true, blood letting might be protective. On the other hand, blood cell proliferation after donation might increase the risk of malignancy. The interpretation of previous studies has been complicated by the fact that blood donors have a healthier lifestyle than most comparison groups. Therefore, blood donors should ideally be compared with other blood donors.

Gustaf Edgren, Ph.D., of the Karolinska Institute in Stockholm and colleagues performed a case-control study within a larger group of Swedish and Danish blood donors. They compared the frequency of donations among 10,866 regular blood donors who developed malignancies with the frequency of donations among 107,104 regular donors who did not.

They found no clear trend for an increased or decreased risk of cancer with increased donations. “In conclusion, we found that repeated blood donation was not associated with risk of cancer overall,” the authors write.

Contact: Gustaf Edgren, gustaf.edgren@ki.se

Novel Mechanism to Overcome Resistance to Targeted Therapy Identified

Combining ABT-737, a molecularly targeted drug that promotes programmed cell death, with a second agent that induces metabolic stress increases acute lymphoblastic leukemia (ALL) cell death in vitro and overcomes resistance to single-agent ABT-737 treatment.

ABT-737 inhibits Bcl-2, a pro-survival protein that is overexpressed in many tumor types. Drugs that increase the production of reactive oxygen species, such as 4-HPR [N-(4-hydroxyphenyl)retinamide], increase metabolic stress and promote programmed cell death.

To find out if combining ABT-737 and 4-HPR would improve the anti-cancer activity of ABT-737, Min H. Kang, Pharm.D., of the University of Southern California Children’s Hospital Los Angeles tested the drugs in seven human ALL cell lines. Two of the lines tested were resistant to single-agent ABT-737 therapy.

The addition of 4-HPR increased cell death in all lines tested, compared with treatment with either single agent alone. Treating cells with 4-HPR reduced expression of a cellular protein, Mcl-1, and decreased cell signaling activity, which helped overcome resistance to ABT-737 treatment.

“The inhibition of Mcl-1 expression by 4-HPR is a novel observation, and the inhibition of Mcl-1 expression is likely to underlie, at least in part, the synergistic cytotoxicity between ABT-737 and 4-HPR in ALL cell lines,” the authors write.

Contact: Min Kang, mkang@chla.usc.edu

Also in April 8 JNCI:

* High-Intensity Chemotherapy Does Not Improve Survival In Small Cell Lung Cancer

* Estrogen Therapy Increases Benign Breast Disease Risk

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Notes:

The Journal of the National Cancer Institute is published by Oxford University Press and is not affiliated with the National Cancer Institute. Attribution to the Journal of the National Cancer Institute is requested in all news coverage. Visit the Journal online at http://jnci.oxfordjournals.org/.

Source:
Liz Savage
Journal of the National Cancer Institute

Women who took conjugated equine estrogen, a commonly prescribed form of estrogen, had more than twice the risk of developing specific types of benign breast disease as women who took a placebo, according to a randomized controlled trial published online April 8 in the Journal of the National Cancer Institute.

The impact of conjugated equine estrogen on the risk of developing benign proliferative breast disease, a condition that is associated with increased risk of breast cancer, has been unclear. Some studies have reported an association while others have not. In the Women’s Health Initiative study, 10,739 postmenopausal women with hysterectomy were assigned to either conjugated equine estrogen or a placebo. Previous analyses did not show an increase in breast cancer incidence in the women who took estrogen alone after a median follow-up of seven years.

To determine whether the hormone increases the risk of benign proliferative breast disease, Tom Rohan, M.D., Ph.D., of the Albert Einstein College of Medicine in New York and colleagues identified and examined non-cancerous breast biopsies in each of the Women’s Health Initiative trial arms.

A total of 232 cases of benign proliferative breast disease were identified, with 155 cases among the women who took estrogen supplements and 77 in the placebo group. The risk of developing benign disease increased by more than two-fold for women taking conjugated equine estrogen, compared with those taking a placebo.

“The prevailing hypothesis concerning the natural history of breast cancer is that benign proliferative breast disease without atypia, proliferative disease with atypia, and in situ cancer represent successive steps preceding the development of invasive breast [cancer]. In keeping with this hypothesis, women with benign proliferative breast disease have an increased risk of subsequent breast cancer,” the authors write.

Although the women taking conjugated equine estrogen have not yet shown a significant increased risk of breast cancer in the Women’s Health Initiative study, if this hypothesis holds true, they might show increased risk later. Ongoing follow up of the study participants may help to resolve this issue.

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The Journal of the National Cancer Institute is published by Oxford University Press and is not affiliated with the National Cancer Institute. Attribution to the Journal of the National Cancer Institute is requested in all news coverage. Visit the Journal online at http://jnci.oxfordjournals.org/.

Source:
Liz Savage
Journal of the National Cancer Institute

Another piece of the puzzle that is breast cancer has been found by University of Queensland researchers.

Dr Melissa Brown, from UQ’s School of Molecular and Microbial Sciences, and her team have discovered how a particular gene associated with breast cancer behaves, which may lead to better testing for the debilitating disease.

Dr Brown and Dr Juliet French at UQ, together with their colleagues at The University of Oxford, studied the BRCA1 gene and found that it exists in a looped formation.

“Our studies suggest that BRCA1 looks a bit like a bow when the gene is switched off, and that part of this ‘bow’ disappears when the gene is switched on,” Dr Brown said.

“Interestingly, the shape of the bow changes in different breast cancer cells, raising the possibility that this gene looping may contribute to the cancer process.”

She said ongoing studies would identify the specific DNA sequences and DNA binding molecules involved in BRCA1 gene looping.

“The status of these sequences in a larger cohort of breast cancer patients will also be determined,” she said.

“This information may lead to more sensitive pre-symptomatic testing for breast cancer and the identification of new therapeutic targets.”

The research was recently published in the scientific journal Proceedings of the National Academy of Sciences.

The University of Queensland, Brisbane Australia

National Breast and Ovarian Cancer Centre welcomes the listing of the breast cancer drug lapatinib (Tykerb®) on the Pharmaceutical Benefits Scheme (PBS) for the treatment of people with HER-2 positive metastatic or advanced breast cancer.

Lapatinib is taken once daily in tablet form. Clinical trials have shown that when given in combination with chemotherapy, lapatinib slows the development of advanced breast cancer, nearly doubling the length of time it takes for the disease to progress (8.4 months) compared to treatment with chemotherapy alone (4.4 months).

The new PBS listing will take effect from 1 May 2008 providing an additional treatment option for women with HER-2 positive advanced or metastatic breast cancer for whom other treatments, including Herceptin®, have stopped working.

“The Australian Government’s decision to subsidise lapatinib is a commitment not only to improving life expectancy but also quality of life for women with advanced breast cancer,” said Dr Karen Luxford, General Manager National Breast and Ovarian Cancer Centre.

“The listing of lapatinib on the PBS will provide hope to women with advanced breast cancer across Australia.

“People undergoing treatment for advanced or metastatic breast cancer should discuss with their oncologist or surgeon whether lapatinib is a suitable treatment option for them,” said Dr Luxford.

Notes:

- Lapatinib is only used in the treatment of people with HER-2 positive advanced breast cancer. ‘HER-2 positive’ means these people have a particular protein called ‘HER-2′ on their cancer cells. Approximately 20-25 per cent of people diagnosed with breast cancer each year have HER-2 positive breast cancer - a more aggressive form of the disease.

- Advanced or metastatic breast cancer means the cancer cells have spread from the breast to other areas of the body, such as the bones or lungs. About 15 per cent of women with breast cancer in Australia have advanced or metastatic disease at diagnosis.

- Herceptin® is a targeted breast cancer therapy currently approved for use in Australia in the treatment of women with HER-2 positive advanced breast cancer.

National Breast and Ovarian Cancer Centre is funded by the Australian Government and works with consumers, health professionals, cancer organisations, researchers and governments to improve care and cancer control in breast and ovarian cancer.

National Breast and Ovarian Cancer Centre

Green tea is high in the antioxidant EGCG (epigallocatechin-3- gallate) which helps prevent the body’s cells from becoming damaged and prematurely aged. Studies have suggested that the combination of green tea and EGCG may also be beneficial by providing protection against certain types of cancers, including breast cancer. A new study conducted by researchers at the University of Mississippi researchers now finds that consuming EGCG significantly inhibits breast tumor growth in female mice. These results bring us one step closer to better understanding the disease and potentially new and naturally occurring therapies.

The study was conducted by Jian-Wei Gu, Emily Young, Jordan Covington, James Wes Johnson, and Wei Tan, all of the Department of Physiology & Biophysics, University of Mississippi Medical Center, Jackson, MS. Dr. Gu will present his team’s findings, entitled, Oral Administration of EGCG, an Antioxidant Found in Green Tea, Inhibits Tumor Angiogenesis and Growth of Breast Cancer in Female Mice, at the 121st Annual Meeting of the American Physiological Society, part of the Experimental Biology 2008 scientific conference.

The Study

Epidemiological studies suggest that green tea and its major constituent, EGCG, can provide some protection against cancer. Because these studies were very limited, the anti-cancer mechanism of green tea and EGCG was not clear. As a result, the researchers examined whether drinking EGCG (just the antioxidant infused in water) inhibited the following: expression of VEGF (vascular endothelial growth factor, which is found in a variety of breast cancer types); tumor angiogenesis (thought to help tumors expand by supplying them with nutrients); and the growth of breast cancer in female mice.

Seven week old female mice were given EGCG (25 mg/50 ml) in drinking water for five weeks (approximately 50-100 mg/kg/day.) The control mice received regular drinking water. In the second week of the study mouse breast cancer cells were injected in the left fourth mammary glands of the mice. Tumor size was monitored by measuring the tumor cross section area (TCSA). Tumors were eventually isolated and measured for tumor weight, intratumoral microvessel (IM) density (using staining), and VEGF protein levels (using ELISA).

At the end of the five week period the researchers found that oral consumption of EGCG caused significant decreases in TCSA (66%), tumor weight (68%), IM density 155±6 vs.111±20 IM#mm^2) and VEGF protein levels (59.0±3.7 vs. 45.7±1.4 pg/mg) in the breast tumors vs. the control mice, respectively (N=8; P
Dr. Gu, the senior researcher for the study, hypothesized that the reason for the link between EGCG and the reductions in the cancer data was because EGCG directly targets both tumor blood vessels and tumor cells of breast cancer for suppressing the new blood vessels formation in breast tumor, the proliferation and migration of breast cancer cells.

Gu concluded by saying, “In this study we have demonstrated that the frequent ingestion of EGCG significantly inhibits breast tumor growth, VEGF expression and tumor angiogenesis in mice. We believe our findings will help lead to new therapies for the prevention and treatment of breast cancer in women.”

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Physiology is the study of how molecules, cells, tissues and organs function to create health or disease. The American Physiological Society has been an integral part of this discovery process since it was established in 1887.

The APS annual meeting is part of the Experimental Biology 2008 (EB ‘08) gathering and runs April 5-9, 2008 at the San Diego, CA Convention Center.

Source: Donna Krupa
American Physiological Society

Democratic presidential candidate Sen. Hillary Rodham Clinton (N.Y.) recently told talk show host Ellen DeGeneres that if elected president, she would increase breast cancer research and treatment funding by $300 million annually and set a goal of finding a cure for the disease within 10 years, the AP/Google.com reports. On DeGeneres’ show, which is scheduled to air on Monday, Clinton also said she would eliminate Medicare copayments for mammograms and introduce other initiatives to help more low-income women access mammograms and other screenings.

Clinton said she would increase funding for breast cancer programs at NIH, the National Cancer Institute and the Defense Department’s Congressionally Directed Medical Research Programs. According to Clinton’s plan, the research would focus on finding treatments and examining genetic and environmental causes of the disease. In addition, she plans to propose a new program looking at racial disparities in breast cancer diagnoses and treatment (AP/Google.com, 4/7).

Reprinted with kind permission from http://www.nationalpartnership.org. You can view the entire Daily Women’s Health Policy Report, search the archives, or sign up for email delivery here. The Daily Women’s Health Policy Report is a free service of the National Partnership for Women & Families, published by The Advisory Board Company.

© 2007 The Advisory Board Company. All rights reserved.

Democratic presidential candidate Sen. Hillary Rodham Clinton (N.Y.) on an episode of the “The Ellen DeGeneres Show” scheduled to air on Monday announced a proposal that would provide an additional $300 million in annual federal funds for breast cancer research, the AP/Contra Costa Times reports.

Under the proposal, NIH, the National Cancer Institute and the Congressionally Directed Medical Research Program at the Department of Defense would use the funds to find treatments for breast cancer and study potential genetic and environmental causes of the disease. As president, Clinton told DeGeneres, she would set a goal of finding a cure for the disease within 10 years. In addition, the proposal also would seek to make breast cancer screenings more affordable for low-income women through the elimination of Medicare copayments for such tests and other measures.

Clinton also announced a proposal to study racial disparities in diagnosis and treatment of breast cancer (AP/Contra Costa Times, 4/7).

Opinion Pieces
Summaries of several opinion pieces and a letter to the editor related to health care issues in the presidential election appear below.

• Marie Cocco, Albany Times-Union: A recent survey conducted by Indiana University School of Medicine indicates that physicians are “way ahead of politicians in daring to go where the rest of the industrialized world has already gone: to a national health insurance system,” syndicated columnist Cocco writes in the Times-Union. The presidential campaign has “offered a bumper crop of politicians and a thicket of platitudes about the American health insurance system,” but only former Democratic candidate Rep. Dennis Kucinich (Ohio) proposed a single-payer system, Cocco writes. According to Cocco, an “increasing proportion of the public” is “warming to national health insurance,” despite the “caveat that taxes might have to be raised to pay for it.” She adds, “It’s the politicians who are lacking in courage, too cautious to confront the fear tactics that the insurance industry, the drug industry and other big players roll out every time” (Cocco, Albany Times-Union, 4/5).
  
  
• Gregory D’Angelo, Salt Lake Tribune: The health care proposal announced by Democratic candidate Sen. Barack Obama (Ill.) “would only push health care costs higher,” D’Angelo, a policy analyst with the Center for Health Policy Studies at the Heritage Foundation, writes in a Tribune opinion piece. Among other provisions, the proposal would establish the National Health Insurance Exchange, a “regulatory agency empowered to set benefits and determine the terms” under which U.S. residents could obtain health insurance, D’Angelo writes. According to D’Angelo, under the proposal, “Washington bureaucrats would run the health insurance markets in every state.” He adds that Obama could “change the federal tax code, offer health care tax credits or direct assistance to the needy, and allow Americans to purchase insurance across state lines” to “create a real national market characterized by personal choice, private competition and portability of coverage” without “creating a new federal bureaucracy” (D’Angelo, Salt Lake Tribune, 4/4).
  
  
• Wayne Madsen, Raleigh News & Observer: The “bold and progressive” health care proposal announced by Obama “should be able” to expand health insurance to the “47 million Americans not now covered” and improve coverage for “tens of millions” of underinsured U.S. residents without “breaking a national treasury already depleted by six years of costly and unnecessary war,” Madsen, a contributing writer to Online Journal, writes in a News & Observer opinion piece. According to Madsen, the proposal, which would allow all residents to participate in the Federal Employees Health Benefits Program, is a “model of fairness” that would “send shockwaves through a health insurance, hospital and pharmaceutical troika that has drained our wallets and preyed on our physical and mental well-being for decades” (Madsen, Raleigh News & Observer, 4/4).
  
  
• Mendel Zilberberg, Washington Times: “Health care in America is in crisis,” but the presidential candidates have announced “at best one-dimensional” proposals to address the issue, Zilberberg, president and CEO of One World United, writes in a Washington Times letter to the editor. According to Zilberberg, each candidate has “mapped out their own particular approach,” but none of their proposals “discuss how we will begin to pay for the resulting benefits.” He adds, “We must seek meaningful and tangible ways to diminish the actual cost of health care.” In the event that “we fail to keep an open mind and neglect to recognize that, as a complex problem, the answer must be multidimensional, we will not be able to adequately address our needs” Zilberberg concludes (Zilberberg, Washington Times, 4/6).

Reprinted with kind permission from http://www.kaisernetwork.org. You can view the entire Kaiser Daily Health Policy Report, search the archives, or sign up for email delivery at http://www.kaisernetwork.org/dailyreports/healthpolicy. The Kaiser Daily Health Policy Report is published for kaisernetwork.org, a free service of The Henry J. Kaiser Family Foundation© 2007 Advisory Board Company and Kaiser Family Foundation. All rights reserved.

Cancer drug developer Antisoma plc (LSE: ASM; USOTC:ATSMY) announces the publication of data on the selective killing of breast cancer cells by Antisoma’s nucleolin-targeting aptamer AS1411. The work was carried out by Professor Daniel Fernandes and colleagues at the Medical University of South Carolina (MUSC) and is published in the April issue of the journal Cancer Research.

Professor Fernandes and his team compared the effects of AS1411 on a breast cancer cell line and on a normal breast cell line. A 5 umol/l dose clearly inhibited the growth of breast cancer cells. In contrast, a four-fold higher dose had no discernible effect on normal breast cells. The selective action of AS1411 on cancer cells correlated with two differences between cancer cells and normal cells. First, cancer cells expressed considerably more nucleolin in their cytoplasm. Second, cancer cells internalised more AS1411.

The authors investigated how AS1411 kills breast cancer cells once it is internalised. They showed that the drug down-regulates the messenger RNA encoding Bcl-2, a protein that allows cancer cells to avoid death by apoptosis. Previous work from Professor Fernandes’ group has shown that nucleolin plays an important role in maintaining Bcl-2 levels in certain cancer cells. It does this by binding to and stabilising Bcl-2 messenger RNA. AS1411 acts as a ‘molecular decoy,’ binding nucleolin and preventing its interaction with Bcl-2 messenger RNA. This leads to a fall in Bcl-2 messenger RNA levels, a consequent fall in the level of the Bcl-2 protein and, ultimately, apoptosis.

Professor Fernandes said: “We continue to gain new insights into how AS1411 acts though nucleolin to induce the death of tumour cells. Ability to avoid apoptosis is a fundamental property of cancer cells, and so the discovery that AS1411 interferes with the Bcl-2 pathway that protects cancer cells from apoptosis is an exciting observation.”

Dr Ursula Ney, Antisoma’s Chief Operating Officer, added: “These encouraging findings suggest that AS1411 could have potential in breast cancer, which is among the most common cancers worldwide.”

AS1411 is currently in a randomised phase II study in acute myeloid leukaemia, with further phase II studies planned in renal and other cancers.

Except for the historical information presented, certain matters discussed in this statement are forward looking statements that are subject to a number of risks and uncertainties that could cause actual results to differ materially from results, performance or achievements expressed or implied by such statements. These risks and uncertainties may be associated with product discovery and development, including statements regarding the company’s clinical development programmes, the expected timing of clinical trials and regulatory filings. Such statements are based on management’s current expectations, but actual results may differ materially.

Notes

Background on AS1411

Aptamers are short pieces of DNA or RNA that can fold into stable, three-dimensional structures capable of interacting with particular target proteins. AS1411 is the first aptamer to be tested as a treatment for cancer. It binds to the protein nucleolin, which is found on the surface of cancer cells. It is then internalised and has been shown to kill cancer cells from a variety of cell lines. The drug has also shown anti-cancer effects in animal models and promising signs of anti-cancer activity in the clinic. AS1411 was originally developed by Dr Paula Bates, Dr John Trent and Prof. Donald Miller at the University of Alabama and then at the University of Louisville. Antisoma added AS1411 to its pipeline when it acquired the Louisville-based company Aptamera Inc. in February 2007.

Background on Antisoma

Headquartered in London, UK, Antisoma is a biopharmaceutical company that develops novel products for the treatment of cancer. Antisoma fills its development pipeline by acquiring promising new product candidates from internationally recognised academic or cancer research institutions. Its core activity is the preclinical and clinical development of these drug candidates.

http://www.antisoma.com

The environment within primary breast tumors can “empower” cells that break free and enter the bloodstream to successfully invade other organs, researchers report in the April 4th Cell, a publication of Cell Press.

Specifically, through studies of hundreds of human breast tumors, the researchers found evidence that the cytokine TGF? in the tumor microenvironment primes breast cancer cells for metastasis to the lungs, one of the most common sites for the spread of breast and other cancers. TGF? signaling is often activated within tumors as a natural response to the oxygen starved and inflammatory conditions that come with tumor progression.

” The microenvironment of a tumor is not just cancer cells, but all other cell types that congregate there,” said Joan Massague of Memorial Sloan-Kettering Cancer Center in New York. In recent years, he said, increasing attention has been paid to the impact those other body cells can have on the tumor locally, through their affects on blood vessel growth, the ability of cancer cells to enter the circulation, and so on.

” Our study shows that it doesn’t end there,” he said. “The cancer cells can come out with instructions that serve them in the long run.”

The research team analyzed the expresssion of all 20,000 genes in the human genome within hundreds of primary breast tumors. Those tumors fell within two classical groups based on whether their estrogen receptor status was positive or negative (ER+ or ER-). In both tumor groups, the researchers found that about 40 percent of the tumors bore the genetic signature of TGF?’s influence.

They found that TGF? exposure didn’t seem to make any difference to the risk of cancer spread in ER+ tumors. In ER- tumors, however, TGF? correlated markedly with an increased risk for metastasis to the lung, but not to bone. In other words, Massague said, “context matters.”

The researchers continued to dig, ultimately uncovering the “fascinating biology” behind that correlation. They found that the TGF? exposure in ER- tumors leads to an increase in a second cytokine within the tumor cells, called angiopoietin-like 4 (ANGPTL4). Once those cells escape the tumor and lodge in the lungs, ANGPTL4 disrupts the connections between cells in the thin capillaries there. That separation of cell-cell contacts allows the cancer cells to cross the vessel wall and pass into the lung proper, Massague said.

The findings suggest that TGF?, or perhaps even better ANGPTL4, might serve as targets for drugs aimed at preventing the spread of breast cancer to the lungs. The TGF? signature could also offer a means of predicting those breast cancer patients at particularly high risk for developing metastatic lung cancer so that they might be monitored more closely and treated more aggressively with existing drugs.

Massague said he suspects the new findings are but one example of a more general cancer phenomenon.

“Entering and colonizing an organ requires of a tumor cell a number of special abilities,” he said. After all, “our bodies are not made up of cells that are allowed to go anywhere as tumor cells [sometimes] manage to do. We’ve shown that factors within primary tumors can act on cancer cells to enhance their ability” to selectively spread to other tissues.

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Researchers include David Padua, Memorial Sloan-Kettering Cancer Center, New York, New York; Xiang H-F. Zhang, Memorial Sloan-Kettering Cancer Center, New York, New York; Qiongqing Wang, Memorial Sloan-Kettering Cancer Center, New York, New York; Cristina Nadal, Institut de Malalties Hemato-Oncologiques, Hospital Clinic-IDIBAPS, Barcelona, Spain; William L. Gerald, Memorial Sloan-Kettering Cancer Center, New York, New York; Roger R. Gomis, Oncology Programme, Institute for Research in Biomedicine, Barcelona, Spain; and Joan Massague, Memorial Sloan-Kettering Cancer Center, New York, New York, Howard Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center, New York, New York.

Source: Cathleen Genova
Cell Press

In a new study examining disparities in postmastectomy breast reconstruction, researchers at Brigham and Women’s Hospital (BWH) and Dana-Farber Cancer Institute (DFCI) in Boston, Mass., concluded that lack of patient-provider discussion may contribute to socioeconomic, age and race-related inconsistencies in the use of breast reconstruction after mastectomy. However, the study also found that reconstruction was more likely to occur after the surgeon discussed options with the patient, suggesting that efforts are required to increase and improve these conversations. The full study appears in the April issue of the Journal of the American College of Surgeons.

Breast reconstructive surgery is an expensive elective procedure, but for many women it is a vital component of surgical care for breast cancer. The choice to have breast reconstruction is a complex decision that is influenced by access to care, patient preference and the provider’s interaction with the patient.

“Patient preferences should be respected, but an informative discussion of reconstruction is required to help patients understand and weigh the risks and benefits of this procedure,” said Caprice C. Greenberg, MD, Instructor of Surgery in the Center for Surgery and Public Health at BWH and the Center for Outcomes and Policy Research at DFCI. “We learned that physicians need to improve communications with patients and whenever possible, universally address the issue of reconstruction with all women undergoing a mastectomy, regardless of age, race or socioeconomic status.”

Using the National Initiative on Cancer Care Quality database, researchers evaluated 626 patients who underwent mastectomy for breast cancer. The data had been collected in a study commissioned by the American Society of Clinical Oncology (ASCO) and undertaken by researchers at the Rand Corporation and the Harvard School of Public Health. Researchers reviewed data collected via survey and chart review approximately four years after diagnosis of breast cancer. Of these patients, 253 (40.4 percent) received breast reconstruction, and 249 (39.8 percent) had medical records documenting the occurrence of a discussion about this option.

“The data from the NICCQ study are continuing to reveal important opportunities to improve cancer care,” said ASCO President Nancy Davidson, MD, professor of oncology and breast cancer research chair at the Sidney Kimmel Cancer Center at Johns Hopkins University in Baltimore. “As oncologists, we need to be sure that we are thoroughly communicating with patients about all of their options for care.”

Approximately 70 percent of patients who had a documented discussion about breast reconstruction with their provider underwent the procedure. However, researchers found that increasing age and lower levels of education were associated with lower rates of a documented discussion. Hispanic patients, patients born outside the United States and those whose primary language was not English were less likely to actually receive reconstruction once the procedure was discussed

Based on these results, the study authors suggest that physicians should systematically address the issue of reconstruction with all patients undergoing mastectomy, including why she is or is not a candidate. They also recommend optimizing physician-patient discussions by using interpreters and appropriate educational materials to ensure an informative conversation regardless of primary language, ethnicity, or education level.

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About the American College of Surgeons

The American College of Surgeons is a scientific and educational organization of surgeons that was founded in 1913 to raise the standards of surgical practice and to improve the care of the surgical patient. The College is dedicated to the ethical and competent practice of surgery. Its achievements have significantly influenced the course of scientific surgery in America and have established it as an important advocate for all surgical patients. The College has more than 72,000 members and is the largest organization of surgeons in the world. For more information, visit http://www.facs.org/.

Source: Sally Garneski
Weber Shandwick Worldwide