Healio
Healio
April 25, 2008
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Looking to the Future

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In the coming years, breast cancer will increasingly be seen and treated as a heterogeneous disease. This will spell the end of large, global neoadjuvant and adjuvant breast cancer treatment studies that approach breast cancer as a homogenous disease entity in favor of smaller studies that focus on treatment of disease subtypes. It is important to realize that to conduct these studies will continue to require screening a large number of patients in order to find the subset that is eligible for a particular study. The era of molecular predictors has already begun. Genomic technologies such as Oncotype DX and other gene signatures help identify subtypes of breast cancers and treatment strategies will increasingly be selected based on these markers. ER-positive highly endocrine sensitive cancers, triple negative disease, and HER2-positive tumors are already considered different disease entities requiring different treatment strategies and clinical trials.

The current first-generation genomic predictors including MammaPrint, Oncotype DX, and several others derive their value from being able to identify a particularly favorable prognostic group among the ER-positive patients and also define another ER-positive group that gains the most benefit from adjuvant chemotherapy. The current proposed chemotherapy response predictors predict chemoresponsiveness in a broad sense and their regimen specificity, if any, is unproven. Unfortunately almost all ER-negative patients are called high risk by MammaPrint or Oncotype DX despite their variable clinical course. Nevertheless, these assays represent a small but important improvement over older clinical variable–based risk prediction methods. When the clinical variable–based and genomic risk predictions are discordant (approximately 30% of all cases), the genomic predictors seem to be more accurate. This is probably due to their ability to better characterize patients with intermediate clinical risk features, in particular those with intermediate histological grade. Equally importantly, they provide an easily interpretable risk score that represents the combined information from multiple variables. This is an important advance over simply listing quantitative ER, PR, HER2, Ki67, and other marker results as it used to be presented in traditional pathology reports.

The available tests already provide us with the opportunity to start to individualize treatment strategies. In the near future, clinical trials may routinely select patients according to molecular phenotype. Different research hypotheses and different therapeutic questions may be appropriate for different genomic groups. This will allow us to apply the currently available and the emerging new therapies more judiciously.

For the next generation of genomic tests, it will be important to try to risk stratify ER- and HER2-negative breast cancers. Combining multiple different genomic predictors including determination of ER and HER-2 status into a single assay could greatly enhance the cost-effectiveness of these tests. There is also a lot of interest to test the hypothesis in the clinic that in vitro cell-line derived, drug-specific response predictors can be developed and can predict response in patients.

In addition, as we understand more about the molecular targets that characterize certain subtypes of breast cancer, we will begin to explore the use biologic treatments in concert with chemotherapy to individualize therapy for these breast cancer subtypes.

At the close of the panel session, Dr. Burstein asked each participant to predict how the recent advances in targeted therapy for breast cancer will influence approaches to treatment in the next 5 years. The faculty provided the following insight:

Dr. Pusztai
Dr. Pusztai

Dr. Pusztai on molecular prognostic tools: I think that breast cancer will not be treated as a homogeneous disease. It will resemble more the current approach to lymphomas where physicians would not think of doing a general lymphoma study but rather design separate studies for Hodgkin’s lymphoma versus various subtypes of non-Hodgkin’s lymphomas. The current large global adjuvant and neoadjuvant studies may be the last generation of this simplistic approach to breast cancer. Molecular risk and treatment stratification will be more commonly used; several rivals for Oncotype DX will probably appear. Distinct treatment strategies will be adopted for ER-positive endocrine sensitive cancers compared to ER-positive endocrine-insensitive tumors or for triple receptor negative cancers

Dr. Budd
Dr. Budd

Dr. Budd on chemotherapy: By 2012, in terms of routine practice, physicians will be routinely doing genomic signatures, perhaps pharmacogenomic signatures, in selecting patients who are candidates for chemotherapy. At some point, I hope physicians will be able to use this to choose the type of chemotherapy. The clinical trials will routinely stratify patients or select patients from some genomic predictor and then try to derive a signature that is predictive of the question at hand. So, there will be a hypothesis presented in a specific genomic group that is tested, but we will be using this to select patients who are candidates for treatment routinely in 5 years. I do not think physicians will be picking particular drugs in 5 years. Although physicians will still be limited in the number of regimens, there will be more judicious application. The question will primarily be integration of biologic treatments with chemotherapy and some of these newer agents that have been discussed, both with chemotherapy and hormonal therapy.

Dr. Munster
Dr. Munster

Dr. Munster on endocrine therapy: I hope the future will hold more answers on how long to treat with endocrine therapy and who will benefit. Additionally, it will be important to differentiate the women with ER-positive who will benefit from or need endocrine therapy from those who will not, as has been proposed for chemotherapy. The patients who will benefit from chemotherapy may not benefit from hormonal therapy and vice versa, hence we may need to subdivide the treatment approach further. As we learn to more optimally use hormonal therapy, physicians may in fact better select the population likely to benefit, as physicians did with other targeted therapy. Furthermore, physicians may need to add other targeted therapy to the currently used hormonal manipulations. At present, physicians only use therapy targeting the estrogen receptor. Physicians may need to further address methods to inhibit the progesterone receptor, as well as the down-stream and cross-signaling associated with both of these receptors.

Dr. Burstein
Dr. Burstein

Dr. Burstein: One of the curious things about the oncotype assay is actually that those high risk patients seem to get negligible benefit from Tamoxifen yet, we still, of course, give them endocrine treatment. Do you think we will have a molecular test that will be so good that it will tell us patients who have an excellent prognosis and do not need endocrine therapy, even though they are ER-positive, or conversely, where they are so resistant to endocrine therapy that you would not recommend it?

Dr. Munster: I think we will have a test to tell us who would not benefit from endocrine therapy. I do not think we will have a test to tell us who does not need endocrine therapy.

Dr. Arteaga
Dr. Arteaga

Dr. Arteaga on novel presurgical and neoadjuvant clinical trials: In breast cancer, there are many novel single-agent therapies and combinations in preclinical and clinical development. For the majority, if not all, of these therapies, there is not a clear biomarker profile in tumors that can allow for (1) the selection or exclusion of patients into phase 2 clinical trials with these new drugs or combinations, and (2) the prediction of longer term patient outcome. Data presented at the SABCS 2007 suggest that short presurgical or neoadjuvant, tissue-based pharmacodynamic trials may provide information that can later be used for patient selection and/or identifying the odds of treatment response or failure. For example, administration of antiestrogens for a short period of a few weeks to 4 months and assessment of the proliferative response in situ as measured by Ki67 in the resected cancer, may inform the prediction of the long-term outcome of that individual patient after adjuvant hormonal therapy. It is speculated that this approach, when applied to other agents, may expedite the drug development process and provide tumor material for the open-ended discovery of molecular biomarkers predictive of response or resistance. In this regard, breast cancer may well be at the forefront of tumors where these novel approaches can be tested.


References

  1. Harris L, Fritsche H, Mennel R, et al. American Society of Clinical Oncology 2007 Update of Recommendations for the Use of Tumor Markers in Breast Cancer. J Clin Oncol. November 20, 2007 2007;25(33):5287-5312.
  2. Baselga J, Tripathy D, Mendelsohn J, et al. Phase 2 study of weekly intravenous recombinant humanized anti-p185HER2 monoclonal antibody in patients with HER2/neu-overexpressing metastatic breast cancer. J Clin Oncol. Mar 1996;14(3):737-744.
  3. Lynch TJ, Bell DW, Sordella R, et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. N Engl J Med. May 20 2004;350(21):2129-2139.
  4. Brenton JD, Carey LA, Ahmed AA, Caldas C. Molecular Classification and Molecular Forecasting of Breast Cancer: Ready for Clinical Application? J Clin Oncol. October 10, 2005 2005;23(29):7350-7360.
  5. Hess KR, Anderson K, Symmans WF, et al. Pharmacogenomic Predictor of Sensitivity to Preoperative Chemotherapy With Paclitaxel and Fluorouracil, Doxorubicin, and Cyclophosphamide in Breast Cancer. J Clin Oncol. September 10, 2006 2006;24(26):4236-4244.
  6. Iwao-Koizumi K, Matoba R, Ueno N, et al. Prediction of Docetaxel Response in Human Breast Cancer by Gene Expression Profiling. J Clin Oncol. January 20, 2005 2005;23(3):422-431.
  7. van ‘t Veer LJ, Dai H, van de Vijver MJ, et al. Gene expression profiling predicts clinical outcome of breast cancer. Nature. 2002;415(6871):530-536.
  8. Wang Y, Klijn JG, Zhang Y, et al. Gene-expression profiles to predict distant metastasis of lymph-node-negative primary breast cancer. Lancet. Feb 19-25 2005;365(9460):671-679.
  9. Desmedt C, Piette F, Loi S, et al. Strong Time Dependence of the 76-Gene Prognostic Signature for Node-Negative Breast Cancer Patients in the TRANSBIG Multicenter Independent Validation Series. Clin Cancer Res. June 1, 2007 2007;13(11):3207-3214.
  10. Durbecq V, Toussaint J, Haibe-Kains B, et al. Transforming genomic grade index (GGI) into a user-friendly qRT-PCR tool which will assist clinicians and patients in optimizing treatment of early breast cancer (BC). J Clin Oncol (Meeting Abstracts). June 20, 2007 2007;25(18_suppl):21058-.
  11. Kaklamani V. A genetic signature can predict prognosis and response to therapy in breast cancer: Oncotype DX. Expert Rev Mol Diagn. Nov 2006;6(6):803-809.
  12. Gong Y, Yan K, Lin F, et al. Determination of oestrogen-receptor status and ERBB2 status of breast carcinoma: a gene-expression profiling study. Lancet Oncol. Mar 2007;8(3):203-211.
  13. Pusztai L, Anderson K, Hess KR. Pharmacogenomic Predictor Discovery in Phase 2 Clinical Trials for Breast Cancer. Clin Cancer Res. October 15, 2007;13(20):6080-6086.
  14. Gruvberger S, Ringner M, Chen Y, et al. Estrogen receptor status in breast cancer is associated with remarkably distinct gene expression patterns. Cancer Res. Aug 15 2001;61(16):5979-5984.
  15. Pusztai L, Ayers M, Stec J, et al. Gene expression profiles obtained from fine-needle aspirations of breast cancer reliably identify routine prognostic markers and reveal large-scale molecular differences between estrogen-negative and estrogen-positive tumors. Clin Cancer Res. Jul 2003;9(7):2406-2415.
  16. Sotiriou C, Lacroix M, Lespagnard L, Larsimont D, Paesmans M, Body JJ. Interleukins-6 and -11 expression in primary breast cancer and subsequent development of bone metastases. Cancer Lett. Aug 10 2001;169(1):87-95.
  17. Peintinger F, Anderson K, Mazouni C, et al. Thirty-Gene Pharmacogenomic Test Correlates with Residual Cancer Burden after Preoperative Chemotherapy for Breast Cancer. Clin Cancer Res. July 15, 2007 2007;13(14):4078-4082.
  18. Pusztai L, Hatzis C, Sotiriou C, et al. Combined use of genomic prognostic and treatment response predictors in lymph node-negative breast cancer. Presented at: American Society of Clinical Oncology 2007 Breast Cancer Symposium. San Antonio, Texas; December 16, 2007; Abstract 53.
  19. Bogaerts J, Cardoso F, Buyse M, et al. Gene signature evaluation as a prognostic tool: challenges in the design of the MINDACT trial. Nat Clin Pract Oncol. Oct 2006;3(10):540-551.
  20. Sparano JA. TAILORx: trial assigning individualized options for treatment (Rx). Clin Breast Cancer. Oct 2006;7(4):347-350.
  21. Deininger MW, Goldman JM, Melo JV. The molecular biology of chronic myeloid leukemia. Blood. Nov 15 2000;96(10):3343-3356.
  22. Nowell PC, Hungerford DA. Chromosome studies on normal and leukemic human leukocytes. J Natl Cancer Inst. Jul 1960;25:85-109.
  23. Capdeville R, Buchdunger E, Zimmermann J, Matter A. Glivec (STI571, imatinib), a rationally developed, targeted anticancer drug. Nat Rev Drug Discov. Jul 2002;1(7):493-502.
  24. Resources. FDA Approves Tykerb for Advanced Breast Cancer Patients. Available at: http://www.fda.gov/bbs/topics/NEWS/2007/NEW01586.html. Accessed 01/30/08.
  25. Resources. National Cancer Institute. FDA Approval for Erlotinib Hydrochloride. Available at: http://www.cancer.gov/cancertopics/druginfo/fda-erlotinib-hydrochloride/print?page=&keyword=#Anchor-No-35312. Accessed 01/30/08.
  26. Resources. FDA Approves First Angiogenesis Inhibitor to Treat Colorectal Cancer. Available at: http://www.fda.gov/bbs/topics/NEWS/2004/NEW01027.html. Accessed 01/30/08.
  27. Resources. National Cancer Institute. Available at : http://www.cancer.gov/cancertopics/druginfo/fda-temsirolimus. Accessed 01/30/08.
  28. Resources. National Cancer Institute. Available at : Resources. National Cancer Institute. Available at : http://www.cancer.gov/cancertopics/druginfo/fda-sorafenib-tosylate. Accessed 01/30/08.
  29. Resources. FDA Approves New Treatment for Gastrointestinal and Kidney Cancer. http://www.fda.gov/bbs/topics/news/2006/NEW01302.html. Accessed 01/30/08.
  30. Resources. Centerwatch Clinical Trials Listing Service. Available at: http://www.centerwatch.com/patient/drugs/dru850.html. Accessed 01/30/08.
  31. Resources. FDA Approves ERBITUX(R) (Cetuximab) For Treatment Of Head And Neck Cancer. Available at: http://www.medicalnewstoday.com/articles/38678.php. Accessed 013108.
  32. Resources. FDA Approves a New Drug for Colorectal Cancer, Vectibix. Availabe at: http://www.fda.gov/bbs/topics/NEWS/2006/NEW01468.html. Accessed 013108.
  33. Kim TY, Han SW, Bang YJ. Chasing targets for EGFR tyrosine kinase inhibitors in non-small-cell lung cancer: Asian perspectives. Expert Rev Mol Diagn. Nov 2007;7(6):821-836.
  34. Mulloy R, Ferrand A, Kim Y, et al. Epidermal growth factor receptor mutants from human lung cancers exhibit enhanced catalytic activity and increased sensitivity to gefitinib. Cancer Res. Mar 1 2007;67(5):2325-2330.
  35. George DJ, Kaelin WG, Jr. The von Hippel-Lindau Protein, Vascular Endothelial Growth Factor, and Kidney Cancer. N Engl J Med. July 31, 2003 2003;349(5):419-421.
  36. Blackwell KL, Kaplan EH, Franco SX, et al. A phase 2, open-label, multicenter study of GW572016 in patients with trastuzumab-refractory metastatic breast cancer. J Clin Oncol (Meeting Abstracts). July 15, 2004 2004;22(14_suppl):3006-.
  37. Storniolo AM, Burris III HA, Overmoyer B, et al. A phase 1, open-label study of the safety, tolerability and pharmacokinetics of lapatinib (GW572016) in combination with trastuzumab. Breast Cancer Res Treat. 2005;94(Suppl 1):S64 (Abstract 1073).
  38. Cameron D, Casey M, Press M, et al. A phase 2I randomized comparison of lapatinib plus capecitabine versus capecitabine alone in women with advanced breast cancer that has progressed on trastuzumab: updated efficacy and biomarker analyses. Breast Cancer Res Treat. Jan 11 2008.
  39. Geyer CE, Forster J, Lindquist D, et al. Lapatinib plus Capecitabine for HER2-Positive Advanced Breast Cancer. N Engl J Med. December 28, 2006 2006;355(26):2733-2743.
  40. Lin NU, Paul D, Dieras V, al. e. Lapatinib and capecitabine for the treatment of brain metastases in patients with HER2+ breast cancer an updated analysis from EGF105084. Presented at the 30th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 13-16, 2007. Abstract 6076.
  41. Berns K, Horlings HM, Hennessy BT, et al. A Functional Genetic Approach Identifies the PI3K Pathway as a Major Determinant of Trastuzumab Resistance in Breast Cancer. Cancer Cell. 2007;12(4):395-402.
  42. Krop IE, Beeram M, Modi S, et al. A phase I study of trastuzumab-DM1, a first-in-class HER2 antibody-drug conjugate, in patients with advanced HER2+ breast cancer. Presented at the 30th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 13-16, 2007. Abstract 310.
  43. von Minckwitz G, Vogel P, Schmidt M, et al. Trastuzumab treatment beyond progression in patients with HER2 positive metastatic breast cancer – the TBP study (GBG 26/BIG 3-05). Presented at: American Society of Clinical Oncology 2007 Breast Cancer Symposium. San Antonio, Texas; December 16, 2007; Abstract 4056.
  44. Wong KK, Fracasso PM, Bukowski RM, et al. HKI-272, an irreversible pan erbB receptor tyrosine kinase inhibitor: Preliminary phase 1 results in patients with solid tumors. J Clin Oncol (Meeting Abstracts). June 20, 2006 2006;24(18_suppl):3018-.
  45. Burstein H, Awada A, Badwe R, et al. HKI-272, an irreversible pan erbB receptor tyrosine kinase inhibitor: preliminary phase 2 results in patients with advanced breast cancer. Presented at the 30th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 13-16, 2007. Abstract 6061.
  46. Modi S, Stopeck A, Kinden H, et al. Tanespimycin (an Hsp90 inhibitor) and trastuzumab is an active combination in patients (pts) with Her2-positive trastuzumab-refractory metastatic breast cancer (MBC): phase 2 trial. Presented at the 30th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 13-16, 2007. Abstract 6066.
  47. deGraffenried LA, Friedrichs WE, Russell DH, et al. Inhibition of mTOR Activity Restores Tamoxifen Response in Breast Cancer Cells with Aberrant Akt Activity. Clin Cancer Res. December 1, 2004 2004;10(23):8059-8067.
  48. Fridman JS, Caulder E, Hansbury M, et al. Selective Inhibition of ADAM Metalloproteases as a Novel Approach for Modulating ErbB Pathways in Cancer. Clin Cancer Res. March 15, 2007 2007;13(6):1892-1902.
  49. Gonzalez-Angulo AM, Hennessy BT, Meric-Bernstam F, et al. Activation of the PI3K/AKT signal transduction pathway is inversely associated with estrogen receptor levels and correlates with survival in hormone receptor-positive Her2/neu-negative breast cancer. J Clin Oncol (Meeting Abstracts). June 20, 2007 2007;25(18_suppl):10588-.
  50. Young O, Jones RJ, Clack G, et al. Src kinase activity in early breast cancer (EBC): A quantitative luminometric and immunohistochemical (IHC) approach. J Clin Oncol (Meeting Abstracts). June 20, 2006 2006;24(18_suppl):13010-.
  51. Kreike B, van Kouwenhove M, Horlings H, et al. Gene expression profiling and histopathological characterization of triple-negative/basal-like breast carcinomas. Breast Cancer Res. 2007;9(5):R65.
  52. Carey LA, Mayer E, Marcom PK, et al. TBCRC 001: EGFR inhibition with cetuximab in metastatic triple negative (basal-like) breast cancer. Presented at the 30th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 13-16, 2007. Abstract 307.
  53. O’Shaughnessy J, Weckstein DJ, Vukelja SJ, et al. Preliminary results of a randomized phase 2 study of weekly irinotecan/carboplatin with or without cetuximab in patients with metastatic breast cancer. Presented at the 30th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 13-16, 2007. Abstract 308.
  54. Finn RS, Dering J, Ginther C, et al. Dasatinib, an orally active small molecule inhibitor of both the src and abl kinases, selectively inhibits growth of basal-type/”triple-negative” breast cancer cell lines growing in vitro. Breast Cancer Res Treat. Nov 2007;105(3):319-326.
  55. Huang F, Reeves K, Han X, et al. Identification of Candidate Molecular Markers Predicting Sensitivity in Solid Tumors to Dasatinib: Rationale for Patient Selection. Cancer Res. March 1, 2007 2007;67(5):2226-2238.
  56. Berry DA, Cronin KA, Plevritis SK, et al. Effect of Screening and Adjuvant Therapy on Mortality from Breast Cancer. N Engl J Med. October 27, 2005 2005;353(17):1784-1792.
  57. Effects of chemotherapy and hormonal therapy for early breast cancer on recurrence and 15-year survival: an overview of the randomised trials. Lancet. May 14-20 2005;365(9472):1687-1717.
  58. Pritchard KI, Shepherd LE, O’Malley FP, et al. HER2 and Responsiveness of Breast Cancer to Adjuvant Chemotherapy. N Engl J Med. May 18, 2006 2006;354(20):2103-2111.
  59. O’Malley FP, Chia S, Tu D, et al. Prognostic and predictive value of topoisomerase II alpha in a randomized trial comparing CMF to CEF in premenopausal women with node positive breast cancer (NCIC CTG MA.5). J Clin Oncol (Meeting Abstracts). June 20, 2006 2006;24(18_suppl):533-.
  60. Ejlertsen B, Nielsen KV, Rasmussen BB, et al. Relationship between ESR1 copy number and ER expression in the DBCG 89D trial. Presented at the 30th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 13-16, 2007. Abstract 403.
  61. Bria E, Nistico C, Cuppone F, et al. Benefit of taxanes as adjuvant chemotherapy for early breast cancer: pooled analysis of 15,500 patients. Cancer. Jun 1 2006;106(11):2337-2344.
  62. Estevez LG, Munoz M, Alvarez I, et al. Evidence-based use of taxanes in the adjuvant setting of breast cancer. A review of randomized phase 2 trials. Cancer Treat Rev. Aug 2007;33(5):474-483.
  63. Hayes DF, Thor AD, Dressler LG, et al. HER2 and Response to Paclitaxel in Node-Positive Breast Cancer. N Engl J Med. October 11, 2007 2007;357(15):1496-1506.
  64. Citron M, Berry D, Cirrincione C, et al. Superiority of dose-dense (DD) over conventional scheduling (CS) and equivalence of sequential (SC) vs. combination adjuvant chemotherapy (CC) for nodepositive breast cancer (CALGB 9741, INT C9741). Presented at the 25th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 11-14, 2002. Abstract 15.
  65. Citron ML, Berry DA, Cirrincione C, et al. Randomized trial of dose-dense versus conventionally scheduled and sequential versus concurrent combination chemotherapy as postoperative adjuvant treatment of node-positive primary breast cancer: first report of Intergroup Trial C9741/Cancer and Leukemia Group B Trial 9741. J Clin Oncol. Apr 15 2003;21(8):1431-1439.
  66. Berry DA, Ueno NT, Johnson MM, et al. High-dose chemotherapy with autologous stem-cell support versus standard-dose chemotherapy: meta-analysis of individual patient data from 15 randomized adjuvant breast cancer trials. Presented at the 30th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 13-16, 2007. Abstract 11.
  67. Paik S, Shak S, Tang G, et al. Expression of the 21 genes in the Recurrence Score assay and prediction of clinical benefit from tamoxifen in NSABP study B-14 and chemotherapy in NSABP study B-20. Presented at the 27th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 14-17, 2004. Abstract 24.
  68. Paik S, Tang G, Shak S, et al. Gene expression and benefit of chemotherapy in women with node-negative, estrogen receptor-positive breast cancer. J Clin Oncol. Aug 10 2006;24(23):3726-3734.
  69. Albain K, Barlow W, O’Malley F. Prognostic and predictive value of the 21-gene recurrence score assay in postmenopausal, node-positive (N+), ER-positive (ER+) breast cancer. SWOG 8814, TBCI 0100. Presented at the 30th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 13-16, 2007. Abstract X.
  70. Albain K, Barlow W, O’Malley F. Concurrent (CAFT) versus sequential (CAF-T) chemohormonal therapy (cyclophosphamide, doxorubicin, 5-fluorouracil, tamoxifen) versus T alone for postmenopausal, node-positive, estrogen (ER) and/or progesterone (PgR) receptor-positive breast cancer: mature outcomes and new biologic correlates on phase 2I intergroup trial 0100 (SWOG-8814). [Abstract] Breast Cancer Res Treat 88 (Suppl 1): A-37, 2004.
  71. Goldstein L, Ravdin P, Gray R, et al. Prognostic utility of the 21-gene assay compared with Adjuvant! in hormone receptor (HR) positive operable breast cancer with 0-3 positive axillary nodes treated with adjuvant chemohormonal therapy (CHT): an analysis of intergroup trial E2197. Presented at: American Society of Clinical Oncology 2007 Breast Cancer Symposium. San Antonio, Texas; December 16, 2007; Abstract 63.
  72. Peto R. Updated results from ATLAS. Presented at the 30th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 13-16, 2007. Abstract 48.
  73. Fisher B, Dignam J, Bryant J, et al. Five Versus More Than Five Years of Tamoxifen Therapy for Breast Cancer Patients With Negative Lymph Nodes and Estrogen Receptor-Positive Tumors. J. Natl. Cancer Inst. November 6, 1996 1996;88(21):1529-1542.
  74. Dodwell D, Williamson D. Beyond tamoxifen: Extended and late extended endocrine therapy in postmenopausal early breast cancer. Cancer Treat Rev. Nov 12 2007.
  75. Cuzick J. Hot flushes and the risk of recurrence – retrospective, exploratory results from the ATAC trial. Presented at the 30th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 13-16, 2007. Abstract 2069.
  76. Forbes JF, Cuzick J, Buzdar A, Howell A, Baum M. ATAC: 100 month median follow-up (FU) shows continued superior efficacy and no excess fracture risk for anastrozole (A) compared with tamoxifen (T) after treatment completion. Presented at the 30th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 13-16, 2007. Abstract 41.
  77. Results of the ATAC (Arimidex, Tamoxifen, Alone or in Combination) trial after completion of 5 years’ adjuvant treatment for breast cancer. The Lancet. 2005;365(9453):60-62.
  78. Sestak I, Group oBotAT. Risk factors for joint symptoms in the ATAC trial. Presented at the 30th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 13-16, 2007. Abstract 2071.
  79. Eisner A, Falardeau J, Toomey MD, JT V. Increased prevalence of retinal hemorrhages among anastrozole users. Presented at the 30th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 13-16, 2007. Abstract 2080.
  80. Gnant M, Mlineritsch B, Luschin-Ebengreuth G, et al. Bone mineral density (BMD) at 5 years after diagnosis in premenopausal patients with endocrine-responsive breast cancer, after 3 years of adjuvant endocrine treatment with goserelin and tamoxifen or anastrozole or both treatments in combination with zoledronic acid – new results from ABCSG-12. Presented at the 30th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 13-16, 2007. Abstract 26.
  81. Brufsky A, Bosserman L, Caradonna R, et al. The effect of zoledronic acid on aromatase inhibitorassociated bone loss in postmenopausal women with early breast cancer receiving adjuvant letrozole: the Z-FAST study 36-month follow-up. Presented at the 30th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 13-16, 2007. Abstract 27.
  82. Ellis MJ, Tao Y, Luo J, et al. Outcome prediction for clinical stage II and III ER+ breast cancer based on treatment response, pathological stage, tumor grade, Ki67 proliferation index, and estrogen receptor status after neoadjuvant endocrine therapy. Presented at the 30th Annual San Antonio Breast Cancer Symposium. San Antonio, TX, December 13-16, 2007. Abstract 62.

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