P.O. Box 16
Milford, Michigan 48381
1-866-944-4223
Milford, Michigan 48381
1-866-944-4223
Common IBC Symptoms:
Things You need to know:
Mammograms usually don't pick up IBC because so often there is no lump.
Why - Reason #1
Doctors misdiagnose Inflammatory Breast
Cancer as a breast infection or mastitis.
Why - Reason #2
We need to push this message across the country.
Who..
Our group of dedicated advocates are, and a brief message about
each one of us.
Tips:
These are TIPS that doctors and patients have given
to people dealing with first symptoms of Inflammatory Breast
Cancer, plus TIPS from patients who have gone through chemotherapy.
The information contained on the 'eraseibc.com' web site is presented for the purpose of educating people on Inflammatory Breast Cancer. Nothing contained on this web site should be construed nor is intended to be used for medical diagnosis or treatment. It should not be used in place of the advice of your physician or other qualified health care provider. Should you have any health care related questions, please call or see your physician or other qualified health care provider promptly.
Education is the MOST powerful tool in the fight against misdiagnosis and improper treatment of Inflammatory Breast Cancer.
Our Foundation's mission is to educate the public and the medical community when needed, that this form of breast cancer is different and is rarely picked up by mammograms.
Towards this mission, the third
Wednesday of the month our
radio show, called
IBC FACT & FALLACIES,
will dispel the myths and help educate our listeners.
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"Life isn't about waiting for the storm to pass....It's about learning to dance in the rain"
Andy Rooney
Click here to take a look at current IBC research.
Click on the links below to find more information on these wonderful facilities
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Fox Chase Cancer Center |
| Morgen Welch Inflammatory Breast Cancer Program and Clinic | |
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MD Anderson IBC Clinic |
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The Seattle Cancer Care Alliance (SCCA) |
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Tumor Vaccine Group |
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Dana Farber Cancer Institute |
Researchers Develop Novel 3-D Culture System for Inflammatory Breast Cancer
Inflammatory breast cancer (IBC) is a very rare and aggressive disease that progresses rapidly and is associated with a very low survival rate. To understand how this type of cancer spreads, it's crucial to characterize the interactions between cancer cells and their 3D environment. Researchers at Fox Chase Cancer Center have developed a novel, 3D culture system that mimics the environment surrounding these cancer cells. This model could be used to test new anticancer drugs capable of inhibiting the spread of IBC tumors.
"The tumor microenvironment plays a pivotal role in tumor development and progression, and it also plays a big role in restricting tumorigenesis," says senior study co-investigator Edna Cukierman, PhD, Associate Professor of Cancer Biology at Fox Chase. "So understanding the interactions between the tumor and the environment will help us to come up with new ways to target the tumor." K Alpaugh, a co-author in this collaborative work, will present the study findings at the 2012 CTRC-AACR San Antonio Breast Cancer Symposium on December 8, 2012.
For the study, Cukierman, a tumor microenvironment expert, and her colleagues in the lab of Massimo Cristofanilli, MD, Professor at Fox Chase and a leading expert in inflammatory breast cancer, used tumor-associated stromal cells from patients with advanced IBC to build a 3D structure consisting of cell-derived extracellular matrix -- scaffold that provides structural and biochemical support to cells.
After culturing a plethora of established and patient-derived cancer cells in the stromal 3D system, the researchers categorized them into two groups. While some cells showed a significant increase in proliferation and resembled those seen in aggressive tumors, others were more similar to cells in less-aggressive tumors. These two types of cells modified the extracellular matrix in distinct ways, indicating that there is a dynamic interplay between cancer cells and the microenvironment.
Moreover, exposure to the matrix caused all of the cancer cells to increase their expression of the protein epithelial cadherin (i.e., E-Cadherin), whose levels are often elevated in IBC tumors. These findings suggest that the microenvironment may promote the proliferation, growth and invasion of IBC tumors.
"Our system could be used to predict the in vivo behavior of cells and to study the signaling mechanisms that are responsible for tumor-microenvironment interactions in IBC cancer," Cukierman says. "We have some gene candidates that we believe are responsible for the degree of aggressiveness we observe in the 3D model, so we would like to manipulate these genetically using mutants or pharmacologically using inhibitors to block the proteins that we believe are responsible. If that reverses the aggressiveness, it could give us a good hint of what types of targets we could perhaps try to develop and bring to the clinic in the future."
Co-investigators on this study include Xiaoshen Dong, Janusz Franco-Barraza, Zhaomei Mu, R. Katherine Alpaugh and Massimo Cristofanilli from Fox Chase.
8q24 cancer risk allele associated with major metastatic risk in inflammatory breast cancer
Bertucci F, Lagarde A, Ferrari A, Finetti P, Charafe-Jauffret E, Van Laere S, Adelaide J, Viens P, Thomas G, Birnbaum D, Olschwang S.
Source
Centre de Recherche en Cancérologie de Marseille, Department of Molecular Oncology, Institut Paoli-Calmettes, Marseille, France.
ABSTRACT
BACKGROUND:
Association studies have identified low penetrance alleles that participate to the risk of cancer development. The 8q24 chromosomal region contains several such loci involved in various cancers that have been recently studied for their propensity to influence the clinical outcome of prostate cancer. We investigated here two 8q24 breast and colon cancer risk alleles in the close vicinity of the MYC gene for their role in the occurrence of distant metastases.
METHODOLOGY/PRINCIPAL FINDINGS:
A retrospective series of 449 patients affected with breast or colon adenocarcinoma was genotyped for the rs13281615 and/or rs6983267 SNPs. Statistical analyses were done using the survival package v2.30 in the R software v2.9.1. The two SNPs did not influence the development of distant metastases of colon cancer; rs6983267 showed a mild effect on breast cancer. However, this effect was greatly emphasized when considering inflammatory breast cancer (IBC) solely. Replicated on a larger and independent series of IBC the contribution of the genotype to the metastatic risk of IBC was found an independent predictor of outcome.
CONCLUSIONS/SIGNIFICANCE:
Our study shows first that the monitoring of this specific germline variation may add a substantial tool for IBC prognostication, an aggressive disease that evolves towards distant metastases much more frequently than non-IBC and for which no reliable prognostic factor is available in medical practice. Second, it more generally suggests that risk alleles, while associated with low susceptibility, could correlate with a high risk of metastasis.
Received from: http://www.ncbi.nlm.nih.gov/pubmed/22666420
Researchers Develop a New Cell and Animal Model of Inflammatory Breast Cancer
Genomic and Proteomic Pathway Mapping Reveals Signatures of Mesenchymal-Epithelial Plasticity in Inflammatory Breast Cancer
Circulating tumor cells not linked to survival in newly diagnosed inflammatory breast cancer
Results also suggest patients who have stray tumor cells in the blood should receive aggressive treatment, even if imaging shows no metastases
SAN ANTONIO, TX -- The presence of circulating tumor cells in the blood appears to have no relationship to survival in women who have just been diagnosed with inflammatory breast cancer, according to new research from Fox Chase Cancer Center. However, the research shows that these stray tumor cells may signal that the disease has spread to other parts of the body, even before imaging reveals any metastases. The results will be presented on Friday, December 9 at the 2011 CTRC-AACR San Antonio Breast Cancer Symposium.
If a woman is diagnosed with inflammatory breast cancer, a particularly fast-growing form of the disease, doctors should consider close imaging to monitor and possibly continue aggressive treatment if she also has circulating tumor cells (CTCs), regardless of what imaging shows, recommends study author Massimo Cristofanilli, M.D., F.A.C.P., chair of the department of medical oncology at Fox Chase. "You should be carful before stopping treatment in someone who has evidence of circulating cells, particularly when dealing with a disease like inflammatory breast cancer, which can progress rapidly."
Previous research by Cristofanilli and his colleagues found that the number of stray cancer cells circulating in the blood is the best predictor of both how long a woman with metastatic breast cancer will live and the amount of time until her cancer progresses. But the researchers have also found that the presence or lack of CTCs has little to say about prognosis in women with metastatic inflammatory breast cancer, an aggressive disease with extremely poor outcomes in spite of multidisciplinary modality treatment.
During the current study, Cristofanilli and his team reviewed the records of 84 women who had just learned they have inflammatory breast cancer, either in stage III or stage IV. A total of 64 (76.2%) women had at least 1 CTC and 29 (34.5%) had at least 5. The researchers found that women with no CTCs had comparable survival and spent the same amount of time progression-free as women with one or more CTCs. The results suggest that there is little prognostic value in measuring CTCs in women newly diagnosed with inflammatory breast cancer.
It's not clear why CTCs appear to be linked to prognosis in some forms of cancer but not others, says Cristofanilli. Inflammatory breast cancer is already an aggressive disease, he says, so compared to other forms of breast cancer whether or not cells have broken off and entered the blood may say little more about an otherwise already aggressive disease.
Inflammatory breast tumors are typically fast-growing, and travel quickly to lymph nodes and the brain. During follow-up in the current study, which lasted more than 22 months for half of patients, more than 30% of the entire group had died.
Perhaps "the most important finding from the study," says Cristofanilli, is that more than three-quarters of women who just learned they have inflammatory breast cancer had CTCs that can be detected in the blood. In comparison, he adds, only 15% of women with non-inflammatory breast cancer typically have CTCs. "So there is a huge difference in inflammatory breast cancer and other forms of breast cancer." These stray tumor cells, therefore, may indicate something about inflammatory breast cancer, he reasons, perhaps serving as an early sign that it has already spread. Indeed, only approximately one-third of women with inflammatory breast cancer have detectable metastases at diagnosis, but 60% will eventually develop them.
Currently, says Cristofanilli, doctors primarily measure CTCs in women with metastatic disease, since a decrease in CTCs can signal that treatment is working. But given that most women with inflammatory breast cancer are likely metastatic at the time of diagnosis, this test could serve another purpose ? to guide doctors towards more aggressive and prolonged forms of treatment, says Cristofanilli. "If women with inflammatory breast cancer have CTCs, perhaps we should continue to treat them as if they have already established metastatic breast cancer, even if imaging does not show metastases."
Source: Fox Chase Cancer Center
AACR Press Releases
Signaling Pathway Linked to Inflammatory Breast Cancer
May Drive Disease Metastasis
Findings represent first evidence of ALK activity in inflammatory breast cancer.
Data emphasize importance of proteins and enzymes to define molecular biology.
Identification of ALK pathway activation could allow for more targeted treatment.
SAN FRANCISCO - Amplification of anaplastic lymphoma kinase, which has been reported in other cancers such as non-small cell lung cancers, may be a primary driver of the rapid metastasis that patients with inflammatory breast cancer experience.
If validated, the use of anaplastic lymphoma kinase (ALK) inhibitors may be a new treatment approach for patients with this lethal form of breast cancer.
These data were presented at the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics, held Nov. 12-16, 2011.
"A diagnosis of inflammatory breast cancer carries with it a very low five-year survival rate of about 40 percent, clearly indicating the critical need for an understanding of the molecular basis of the disease," said Fredika M. Robertson, Ph.D., professor in the department of experimental therapeutics at The University of Texas M.D. Anderson Cancer Center and a member of the Morgan Welch Inflammatory Breast Cancer Research Program. "However, there are few molecules that have been identified that are matched with available targeted therapies of clinical benefit in patients with inflammatory breast cancer."
Robertson and colleagues used patient-derived tumors, tumor cell lines and animal models to evaluate protein-signaling pathways and genetic abnormalities with the goal of identifying molecules that may be associated with the increased metastases of inflammatory breast cancer. They discovered ALK amplification in 13 of 15 tumor samples taken from patients with this lethal variant of breast cancer. They then validated the presence of this abnormality in tumor cell lines and newly developed xenograft models.
Gene amplification of ALK is only found in about 2 percent of the overall breast cancer population, according to Robertson. However, results from this analysis indicate that in inflammatory breast cancer, it could be occurring in up to 86 percent of patients.
"The observation that ALK is amplified may be comparable to the observation of HER2 oncogene amplification in some cases of breast cancer, which revolutionized how the disease was treated," Robertson said. "Our observation that ALK is amplified in inflammatory breast cancer suggests that ALK may serve as a good target for treatment."
To test this, the researchers evaluated the effects of a drug that inhibits ALK using tumor cells isolated from patients with metastatic inflammatory breast cancer and in two animal models that recapitulate the disease. Results indicated that the use of this drug resulted in tumor cell death.
"Patients with inflammatory breast cancer are now being evaluated for ALK genetic abnormalities, and if found and eligible, may be enrolled in a phase 1, dose-escalation clinical trial of a small-molecule ALK/cMet inhibitor," Robertson said. She added that Massimo Cristofanilli, M.D., chair of medical oncology at Fox Chase Cancer Center in Philadelphia has implemented this trial at the center's Inflammatory Breast Cancer Clinic.
Moving forward, Robertson emphasized the importance of collaborating with a research team with expertise in using both proteomic and genomic approaches to define molecular biology of tumors, to identify therapeutic targets and, once validated, to rapidly translate these findings to the clinic.
"Our results demonstrate that, had we only been using genomic platforms, the likelihood of identifying ALK as a therapeutic target would have been significantly diminished," she said.
The funding for these studies came from an American Airlines/Komen Race for the Cure Promise Grant KGO81287 entitled, "Novel Targets for Treatment and Detection of Inflammatory Breast Cancer." Robertson and Cristofanilli are co-principal investigators on this grant. The proteomics studies were performed in collaboration with Emanuel F. Petricoin III, Ph.D., and Lance Liotta, M.D., Ph.D., at the George Mason Center for Applied Proteomics and Molecular Medicine in Manassas, Va.
Understanding inflammatory breast cancer:
An interview with Dr. Fredika Robertson
Dr. Fredika Robertson shares the story of her current research focused on the most aggressive form of breast cancer, called inflammatory breast cancer (IBC). She discusses her laboratory's contribution to understanding the molecular basis for this aggressive breast cancer phenotype and the role that cancer stem cells play in the metastasis that often occurs in patients exhibiting this disease.
Dr. Robertson's story focuses on the development of useful 3D in vitro models for breast cancer. These models impact our ability to understand how cancer stem cells are responsible for highly metastatic breast cancer phenotypes such as those exhibited in IBC. In this interview, she discusses the effort in her laboratory to identify therapeutics that target inflammatory breast cancer. Her research has implications for potential clinical approaches to effectively increase the survival from this type of breast cancer that is responsible for a very high percentage of the >40,000 breast cancer–related deaths that occur annually.
Dr. Robertson is currently Professor in the Department of Experimental Therapeutics and Laboratory of Translational Therapeutics, Morgan Welch Inflammatory Breast Cancer Research Program at the University of Texas MD Anderson Cancer Center in Houston, Texas.
Can you provide an overview of
your research?
We're studying the most aggressive form of breast cancer, called inflammatory breast cancer or IBC. This disease is different from other breast cancers. The tumors associated with this highly metastatic phenotype contain subpopulations of cells that are called tumor-initiating cells (TICs) or cancer stem cells (CSCs). Most solid tumors have a specific gene signature that includes the loss of specific genes that maintain an epithelial phenotype. This includes loss of E-cadherin, which maintains tight cell–cell adhesion. There is also a gain of genes that regulate motility and invasion of single tumor cells, leading to a stem cell phenotype. The gain and loss of genes occurs during the process associated with metastasis defined as the epithelial-mesenchymal transition (EMT). We find that in IBC, this doesn't hold true. IBC cells actually overexpress the E-cadherin gene, and in fact this plays a very important role in the ability of tumor cells to tightly adhere to each other. These tumor cells form nests of cells defined as tumor emboli. These rapidly colonize tissue and establish micrometastases. In addition, tumor emboli isolated from patients with IBC form cell lines that generate emboli when grown in mice. These emboli are enriched for CSCs, and this may in part be responsible for their resistance to chemotherapeutic agents and radiation.
We are very excited about our progress toward our goal of making a significant impact on improving diagnosis and treatment of this very lethal disease. In order to drive the development of therapeutic strategies that can be used against this disease, we have focused recent efforts to generate 3D tumor spheroid models. The models we've developed provide more information and are better models of tumor progression in IBC than the existing models, which have more commonly used adherent cells grown in 2D on plastic culture plates. In addition, we are developing approaches to image and characterize the gene, protein, and microRNA signatures of CSCs in these models of inflammatory breast cancer, using confocal microscopy. We will soon be using multiphoton microscopy that will allow us to perform in vivo imaging as well. Information about these gene and protein signatures is necessary for identifying biomarkers and therapeutic targets that will allow us to move to clinical trials.
You say that inflammatory breast cancer is a highly aggressive cancer. Can you explain more about why this breast cancer is different from other forms of breast cancer?
Unlike other breast cancers, the tumors in IBC invade the skin and chest wall and are more resistant to chemotherapy that other breast tumors are sensitive to. Also, unlike other breast cancers that typically appear to invade as single cells, this cancer forms tight aggregates of cells defined as tumor emboli, which invade by crawling into the lymphovascular endothelium. This very distinct involvement of the lymphatic system leads to common lymph node metastasis at the time of first diagnosis of IBC, and is associated with its high rate of metastasis to distant organ sites, including lung, liver, bone, and brain. Patients with inflammatory breast cancer have a very low survival rate at 2 years and 5 years after diagnosis, compared to other variants of breast cancer. It is this aggressiveness combined with misdiagnosis and delays in treatment that in part contributes to the rapid disease progression and very poor prognosis of IBC.
Why is inflammatory breast cancer more difficult to diagnose than other breast cancers?
Inflammatory breast cancer was named because the tumor emboli that lodge within the lymphatic system of the skin cause the breast to swell,
so that the signs and symptoms of inflammatory breast cancer are very different. Inflammatory breast cancers do not typically present as a lump as other breast cancers do. Because of this, inflammatory breast cancer is commonly dismissed or misdiagnosed as mastitis or swollen breast, for which antibiotics are prescribed. If this happens, then during the time the woman is on antibiotic treatment, the disease progresses very quickly, and patients with inflammatory breast cancer often have metastasis at the time of first accurate diagnosis. So, by the time the woman returns, say a month later, the disease has already invaded the lymph nodes and often has moved to sites distant from the primary tumor nests in the breast. It is imperative that treatment is initiated as soon as possible, and without that the chances for effective treatment are greatly diminished.
What proportion of breast cancer diagnosis does this represent?
While IBC represents only about 2–5% of all breast cancers, between misdiagnosis and the extreme aggressiveness of inflammatory breast cancer, about 15% of all breast cancer deaths are caused by this disease. It's also unfortunate that this particular type of breast cancer tends to hit women at a younger age than other breast cancers.
How has funding been?
Historically, IBC has been an understudied and underfunded area of research. Although the disease was first described in 1924, it has only recently received more attention, primarily because of the active involvement of patients and their families in advocacy for IBC. For instance, a recent Promise Grant award from American Airlines–Susan G. Komen Race for the Cure Organization, which funds very specific projects, was awarded to our program to support our research focused on identifying novel targets and biomarkers for inflammatory breast cancer.
What are some ways that your recent work has impacted cancer research?
We've developed new models of IBC and have primarily been working in vitro with 3D models that we've used to help drive cancer discovery in its purest form. In addition to an original 3D model, we've now developed three other models of IBC that have been made available. This was particularly important because the 2D models didn't mimic the cancer well enough to serve as the best models. Now we can use these 3D tumor spheroid models of IBC, which are enriched for these tumor-initiating cells, and gain much clearer insights into the role CSCs play in metastasis and how this unfolds in real time.
Are there particular research tools that have helped you reach this point?
I've been using Molecular Probes® products for years, starting with when I was Director of the Analytical Cytometry Core Laboratory at the Ohio State University Comprehensive Cancer Center. Today we are more focused on using confocal imaging of live tumor spheroids, which enrich for cells with a CSC phenotype. In our research we had used BrdU in the past and became interested in the Click-iT® EdU assay primarily because it didn't denature the DNA. Using live-cell imaging, this approach has really accelerated our understanding of how IBC cells stay together and how they undergo apoptosis in response to newly developed drugs that we are testing for potential clinical trials. In our research we also use a lot of Molecular Probes® products, including TO-PRO® dye (as a nuclear counterstain), MitoSOX™ indicator (as an indicator of superoxide anion production in live cells), and many different Alexa Fluor® dye compounds for tags. We routinely use Gibco® B-27® media supplement and growth factors as well.
Tell me about your long-term goals.
We are very focused on identifying biomarkers and therapeutic targets to improve the rate of accurate diagnosis and to identify more effective treatments for IBC patients. It's very important that we accelerate clinical trials for these patients who often have very few therapeutic options. These IBC patients are treated very differently than other variants of breast cancer. Because the tumor invades the skin and chest wall, patients receive chemotherapy before surgery. If they do not respond to chemotherapy, then they are not candidates for surgery because it is not possible to obtain a clean margin. Developing more effective IBC-specific therapeutics that target the tumor emboli and specifically hit these tumor nests that have characteristics of CSCs is very important to increase the survival rate of these women. We're also working with patient advocate groups to make this disease more understood. Education and outreach efforts are critically important for a disease that is this misunderstood.
What are the current efforts around education and outreach?
There are grassroots advocacy movements with patients, their families, and friends. These groups have been instrumental in pushing states, such as Texas and New Mexico, for funds to be set aside to develop more clinics for diagnosis and treatment of inflammatory breast cancer. There are two foundations, the Inflammatory Breast Cancer Foundation that supports a radio program each month and has a support website, and the Inflammatory Breast Cancer Research Foundation, whose members pushed for development of tissue repositories for banking of tumor tissue and serum from patients with inflammatory breast cancer. Other outreach efforts have focused on reaching out to particular groups of underserved women who don't have adequate access to health care. In this case, because the cancer is so aggressive, by the time the women are seen the first time, the cancer is already so far along that their lifespan is significantly shortened. It is critical to make sure that we educate everyone about the signs and symptoms of inflammatory breast cancer since women as young as 14 have been diagnosed with it. Unfortunately, these young women often have the most aggressive types of breast cancer. Making sure that primary physicians are aware of this disease and how it presents itself is important, too, since it looks like an infection but it is commonly metastatic at the time of first diagnosis. You never know who you will reach and whose life you can impact by spending the time to share this information, so I talk about this at every opportunity.
What's next for you?
We are very excited about our recent efforts to identify markers specific for IBC, and about clinical trials that are on the horizon. Working together, our research team here at MD Anderson, at Fox Chase Cancer Center in Philadelphia, and at the Institute of Advanced Proteomics and Molecular Medicine at George Mason University have identified a molecular pathway that we believe drives the aggressive metastasis of inflammatory breast cancer. We are working to complete this work, and while I can't talk too much about this today, we will be presenting this information for publication and presentation in the very near future.
What thought do you want to leave us with?
Inflammatory breast cancer is so misunderstood, and it's critical that this disease be recognized and discussed. We need to be sure that we don't lose sight of the fact that the simple action of discussing the signs and symptoms of this type of breast cancer can impact someone's life and you never know who that could be or when that could happen. I am blessed to have the support of the IBC patients who willingly participate in all aspects of our research and clinical programs. I am also very fortunate to have wonderful colleagues and a terrific laboratory research team who are just as dedicated to this mission as I am. I am also very privileged to have the grant support for our research from the American Airlines–Susan G. Komen Race for the Cure Organization Promise Grant and The State of Texas Fund for Rare and Aggressive Breast Cancers. I believe that the work that we are engaged in will significantly impact patients with inflammatory breast cancer, and the hope is that collectively, our work will ultimately change the standards of diagnosis and care of these patients as well as increase their survival.
Nanoshells appear to kill cancer at the root, including IBC, click on the link below to read the fascinating article.
Nanoshells appear to kill cancer at root...
Our President Patti Bradfield recently met with part of the research team working on this research at MD Anderson
Pictured below is: left to right...
David Weksberg, MD (resident/trainee in radiation oncology); Dr. Wendy Woodward
Wendy Woodward, M.D, Ph.D., (an Assistant Professor and the Director of Clinical
Breast Radiation Research in Department of Radiation Oncology), Afsaneh Keyhani,
(MDA IBC lab manager), Dr. Jim Rueben (Professor, Department of Hematopathology,
Division of Pathology)
By TODD ACKERMAN HOUSTON CHRONICLE
Proceedings of the First International Inflammatory Breast Cancer Conference
Novel detection method unmasks circulating breast cancer cells
Click image for story
"One of the lead authors, Dr. Massimo Cristofanilli*, associate professor in the Department of Breast Medical Oncology at The University of Texas M. D. Anderson Cancer Center. "The CellSearch(R) CTC test provides an early indication about patients' disease progression and overall survival."
New York University Langone Medical Center
Researchers Identify Key Gene in Deadly Inflammatory Breast Cancer
This study was co-authored by Dr. Silvia Formenti, chair of the department of radiation oncology at NYU Langone Medical Center and the Sandra and Edward H. Meyer Professor of Radiation Oncology at NYU School of Medicine, and Dr. Paul Levine of George Washington University, who contributed tissues.
(Re-printed with permission from Thomas A. Buchholz, M.D.)
Locoregional Treatment Outcomes After Multimodality Management of Inflammatory Breast Cancer
Ian J. Bristol, M.D., Wendy A. Woodward, M.D., Ph.D., Eric A. Strom, M.D., Massimo Cristofanilli, M.D., Delora Domain, B.S., S. Eva Singletary, M.D., George H. Perkins, M.D., Julia L. Oh, M.D., Tse-Kuan Yu, M.D., Ph.D., Welela Terrefe, M.D., Aysegul A. Sahin, M.D., Kelly K. Hunt, M.D., Gabriel N. Hortobagyi, M.D., Thomas A. Buchholz, M.D.
Purpose
The aims of this study were to determine outcomes for patients with inflammatory breast cancer (IBC) treated with multimodality therapy, to identify factors associated with locoregional recurrence, and to determine which patients may benefit from radiation dose escalation.
Methods and Materials
We retrospectively reviewed 256 consecutive patients with nonmetastatic IBC treated at our institution between 1977 and 2004.
Results
The 192 patients who were able to complete the planned course of chemotherapy, mastectomy, and postmastectomy radiation had significantly better outcomes than the 64 patients who did not. The respective 5-year outcome rates were: locoregional control (84% vs. 51%), distant metastasis–free survival (47% vs. 20%), and overall survival (51% vs. 24%) (p < 0.0001 for all comparisons). Univariate factors significantly associated with locoregional control in the patients who completed plan treatment were response to neoadjuvant chemotherapy, surgical margin status, number of involved lymph nodes, and use of taxanes. Increasing the total chest-wall dose of postmastectomy radiation from 60 Gy to 66 Gy significantly improved locoregional control for patients who experienced less than a partial response to chemotherapy, patients with positive, close, or unknown margins, and patients < 45 years of age.
Conclusions
Patients with IBC who are able to complete treatment with chemotherapy, mastectomy, and postmastectomy radiation have a high probability of locoregional control. Escalation of postmastectomy radiation dose to 66 Gy appears to benefit patients with disease that responds poorly to chemotherapy, those with positive, close, or unknown margin status, and those < 45 years of age.
Breast cancer more aggressive among obese women, states a new study. Dr. Massimo Cristofanilli, Co-director of the Inflammatory Breast Cancer Clinic at M.D. Anderson Cancer Center, Houston Texas, and his colleagues observed 606 women in this study, which was published in the March 15 issue of Clinical Cancer Research, a journal of the American Association for Cancer Research.
Presented at NCCN Separate Treatment Algorithm Created for Inflammatory Breast Cancer
