Edith Perez

JACKSONVILLE, Flórida, 21 de outubro de 2014 — Depois de acompanhar pacientes de câncer de mama por mais de oito anos, em média, pesquisadores dizem que o acréscimo do trastuzumabe (Herceptin) à quimioterapia melhorou significativamente a sobrevida das pacientes, sem a doença, de mulheres com câncer de mama HER2-positivo em estágio inicial. Os pesquisadores descobriram que o trastuzumabe melhorou em 37% a sobrevida e 40% em redução de risco de reincidência do câncer, em comparação com as pacientes tratadas apenas com a quimioterapia.

JACKSONVILLE, Florida — Después de hacer seguimiento a las pacientes con cáncer de mama durante un promedio de más de ocho años, los investigadores dicen que la adición de trastuzumab (Herceptin) a la quimioterapia mejoró significativamente la sobrevivencia global y libre de enfermedad de las mujeres con cáncer de mama HER2-positivo en etapa temprana. Los expertos encontraron que el uso de trastuzumab produjo una mejoría del 37 por ciento en la sobrevivencia y una reducción del 40 por ciento en el riesgo de ocurrencia de cáncer, en comparación con las pacientes tratadas con quimioterapia sola. Estos hallazgos, publicados en la revista, Journal of Clinical Oncology, demuestran cuán importante ha sido el trastuzumab en el tratamiento de esta forma de cáncer de mama, expresa la doctora Edith A. Perez, M.D., autora principal del estudio, directora adjunta en general del Centro Oncológico de la  Clínica Mayo y directora del Programa Traslacional de Genómica del Cáncer de Mama de la Clínica Mayo da Florida.

JACKSONVILLE, Flórida 30 de setembro de 2014 — Análises em mais de 8 mil mulheres, que participaram do maior estudo mundial de dois medicamentos para o câncer de mama HER2-positivo, reforçam outras descobertas de estudos clínicos mostrando que o trastuzumabe (Herceptin) deve permanecer como o padrão de tratamento desse tipo de câncer, diz uma pesquisadora da Clínica Mayo.

JACKSONVILLE, Florida, 30 de septiembre 2014 — Investigaciones en más de 8.000 mujeres, que participaron en el estudio más grande del mundo de dos tratamientos para el cáncer de mama HER2-positivo, refuerzan otros hallazgos de este ensayo clínico que demuestran que el fármaco trastuzumab (Herceptin) debiera seguir siendo el tratamiento estándar en este tipo de cáncer, expresa una investigadora de la Clínica Mayo.

JACKSONVILLE, Fla., Sept. 29, 2014 — Analysis of more than 8,000 women who participated in the world’s largest study of two treatments for HER2-positive breast cancer reinforces other findings from the clinical trial showing that trastuzumab (Herceptin) should remain the standard of care for this cancer, says a Mayo Clinic researcher. http://youtu.be/BcFszcq4CJo

SAN ANTONIO, Texas — Adding the drug trastuzumab to chemotherapy prevents cancer recurrence and improves survival in a large number of women with early stage HER2-positive breast cancer. But trastuzumab does not stop tumors from returning in about 25 percent of patients — and oncologists haven't been able to identify these women before treatment. This situation may soon change, according to a Mayo Clinic study being presented at the 2012 CTRC-AACR San Antonio Breast Cancer Symposium.

VIDEO ALERT: Video of Dr. Perez is available on the Mayo Clinic News Network.

A team of U.S. researchers, led by oncologists at Mayo Clinic's campus in Florida, have discovered 27 genes that are significantly associated with a good outcome with concurrent use of trastuzumab and chemotherapy, as well as five other genes linked to a poor outcome using the same treatment regimen. Results of their study — believed to be the first to use gene expression profiling to predict outcome to trastuzumab as part of adjuvant breast cancer therapy — offer a number of future potential benefits, says Edith Perez, M.D., deputy director at large of the Mayo Clinic Comprehensive Cancer Center and director of the Breast Cancer Translational Genomics Program at Mayo Clinic. "These findings also are getting us closer to unraveling the biological factors that are relevant to patient outcome, which will help us improve clinical care," Dr. Perez says. For example, the discovery may help scientists devise a genetic test that can help oncologists select the best treatment for their HER2-positive patients, she says. Further analysis will illuminate the inner biological workings of individual HER2-positive tumors, which could provide clues for novel treatments, Dr. Perez adds. The researchers have already found that the genes linked to outcome can be grouped into different categories that affect tumor functioning, such as cell cycle, cell death, cell receptor signaling, and gene transcription. Dr. Perez and her team plan to validate their findings through collaborations with researchers in the United States and Europe who have led other trastuzumab clinical studies.

JACKSONVILLE, Fla. — July 31, 2012.  A potentially powerful new approach to treating two lethal metastatic cancers — triple negative breast cancer and clear cell renal cell carcinoma, the most common form of kidney cancer — has been discovered by researchers at Mayo Clinic in Florida. In the online issue of Molecular Cancer Therapeutics, they report that two drugs, romidepsin and decitabine, work cooperatively to activate a potent tumor suppressor gene that is silenced in these cancers. Once the gene, secreted frizzled related protein one or sFRP1, went to work after the drugs were used, the laboratory tumor cells stopped growing and died. Both drugs are approved by the Food and Drug Administration to treat blood cancer and are being tested individually in numerous solid cancers in which sFRP1 is disabled. This study was the first to test the use of both in these metastatic cancers linked to sFRP1, and the results are very encouraging, says senior investigator John Copland, Ph.D., a Mayo Clinic molecular biologist. "We now have the basis for a clinical trial aimed at providing effective therapy for two drug-resistant cancers and perhaps many more tumor types in the future," Dr. Copland says. In addition to breast and kidney cancer, sFRP1 is disabled in colon, ovarian, lung, liver and other tumor types. Dr. Copland and his colleagues earlier discovered that sFRP1 was silenced in certain cancers. This new work demonstrates that its expression can be restored by romidepsin, which is a histone deacetylase inhibitor, and decitabine, a methyltranferase inhibitor. Both are epigenetic drugs, modifying genes in a way that affects whether they are turned on or off. "Individually, each drug did not induce any form of cell death but, together, they killed all of the different cell lines of kidney and triple negative breast cancer that we tested in the laboratory," says lead investigator Simon Cooper, Ph.D., a Mayo Clinic molecular biologist who specializes in renal cancer. The two cancers affect up to 80,000 Americans each year and therapies to treat both, especially when they are advanced, have been very limited, says co-author Edith Perez, M.D., deputy director of Mayo Clinic Cancer Center. "But now, not only do we have a very promising lead on future therapy, but if this combination treatment works as we hope it does, we will have a biomarker to be able to test which patients might benefit the most," she says. "In other words, a biopsy test could identify patients whose tumors had lost sFRP1 function." The approach to finding this potential new treatment strategy is novel, adds oncologist Michael Menefee, M.D., who is also a study co-author.

JACKSONVILLE, Fla. — April 10, 2012.   Mayo Clinic researchers have discovered a new class of molecular mutation in various forms of breast cancer, a finding that may shed new light on development and growth of different types of breast tumors. Called fusion transcripts, the mutated forms of RNA may also provide a way to identify tumor subtypes and offer new strategies to treat them, investigators say. Their study, published in the April 15 issue of Cancer Research, is the first to systematically search for fusion genes and fusion transcripts linked to different types of breast tumors. Oncologists currently recognize three basic types of breast tumors — estrogen-receptor (ER)-positive, HER2-positive, and triple negative. "But breast cancer is much more complex than indicated by these three subtypes, and one of the challenges of treating the disease is to identify gene markers that predict how a tumor will respond to a specific treatment," says senior investigator Edith Perez, M.D., deputy director of the Mayo Clinic Comprehensive Cancer Center in Florida and director of the Breast Cancer Translational Genomics Program, which involves researchers at all three Mayo Clinic campuses. "The discovery of subtype-specific fusion transcripts in breast cancer represents a step in this direction," she says. "Our findings indicate that fusion transcripts are much more common in breast cancer than had been realized. They represent a new class of mutation whose role in breast cancer is not understood at all." "Fusion transcripts have the power to produce proteins that are relevant to tumor development, growth, and sensitivity to treatment, so we may have a brand new set of genomic changes that may help us understand, and treat, breast cancer in a new way," says E. Aubrey Thompson, Ph.D., professor of Biology at Mayo Clinic's Comprehensive Cancer Center, and co-director of the Breast Cancer Translational Genomics Program. "This is a novel discovery that will now require additional investigation," he says. "We need to understand what these fusion transcripts and proteins are doing." Fusion transcripts are created when chromosomes break apart and recombine, an event that commonly occurs in cancer cells. During this process, fusion genes are created when two halves of normal genes become linked. Fusion genes (DNA) create fusion transcripts (RNA), which then produce fusion proteins. "Mistakes are made," Dr. Thompson says. "That is one of the salient properties of tumor cells, because they are defective in repairing damage to their genes." "These mutated proteins may have an entirely new, cancer-promoting function, or they may interfere with normal cellular functions." Fusion transcripts are common in blood cancers, such as leukemia and lymphoma. Before this discovery, however, few were found in solid cancers such as breast tumors. Because fusion genes, transcript, and protein are generally found only in tumors, they make ideal biomarkers to identify tumor cells, Dr. Perez says.