Logo of annoncLink to Publisher's site
Ann Oncol. 2011 Aug; 22(8): 1736–1747.
Published online 2011 Jun 27. doi:  10.1093/annonc/mdr304
PMCID: PMC3144634

Strategies for subtypes—dealing with the diversity of breast cancer: highlights of the St Gallen International Expert Consensus on the Primary Therapy of Early Breast Cancer 2011


The 12th St Gallen International Breast Cancer Conference (2011) Expert Panel adopted a new approach to the classification of patients for therapeutic purposes based on the recognition of intrinsic biological subtypes within the breast cancer spectrum. For practical purposes, these subtypes may be approximated using clinicopathological rather than gene expression array criteria. In general, systemic therapy recommendations follow the subtype classification. Thus, ‘Luminal A’ disease generally requires only endocrine therapy, which also forms part of the treatment of the ‘Luminal B’ subtype. Chemotherapy is considered indicated for most patients with ‘Luminal B', ‘Human Epidermal growth factor Receptor 2 (HER2) positive’, and ‘Triple negative (ductal)’ disease, with the addition of trastuzumab in ‘HER2 positive’ disease. Progress was also noted in defining better tolerated local therapies in selected cases without loss of efficacy, such as accelerated radiation therapy and the omission of axillary dissection under defined circumstances. Broad treatment recommendations are presented, recognizing that detailed treatment decisions need to consider disease extent, host factors, patient preferences, and social and economic constraints.

Keywords: adjuvant therapies, early breast cancer, St Gallen Consensus, subtypes


It is no longer tenable to consider breast cancer as a single disease. Subtypes can be defined by genetic array testing [13] or approximations to this classification using immunohistochemistry [47]. These subtypes have different epidemiological risk factors [8, 9], different natural histories [1012], and different responses to systemic and local therapies [1317]. These differences imply that clinicians managing breast cancer should consider cases within the various distinct subtypes in order to properly assess the relevant evidence and arrive at appropriate therapeutic advice.

St Gallen 2011: news and progress

The 12th International Breast Cancer Conference in March 2011 brought together some 4300 participants from 96 countries and a worldwide faculty representing all relevant disciplines. After presentation of recent research findings, a 51-member Expert Panel (see Appendix 1) considered a number of questions in order to arrive at treatment recommendations for the immediate future. As in previous St Gallen conferences [18], the Panel was charged with assessing the evidence, but also advising on the basis of expert opinion on those questions where the evidence was ambiguous or lacking. For the first time, this conference included an explicit approach to management of conflicts of interest (see Appendix 2).

Evidence was presented to support a less aggressive approach to axillary surgery in defined circumstances and the use of more convenient equally effective approaches to radiation therapy. For systemic therapy, the emphasis of this year’s consensus was to reach recommendations within each of the biological subtypes, since these already incorporate many of the risk factors and response predictors previously considered separately. Disease extent, host factors, patient preferences, and economic and social factors inevitably impact the choice and delivery of care. In general, the recommendations are intended to guide therapy considerations outside clinical trials in communities with reasonable levels of available resources, but noting where possible the availability of alternatives, which might be only marginally less effective but less expensive.

This report will first review the new findings presented at the meeting (Table 1) and then proceed to summarize the deliberations of the Panel, bringing these together to form broad therapy recommendations.

Table 1.
Recent research findings presented at the 12th International Conference on Primary Therapy of Early Breast Cancer and their implications for patient care

local therapies

New results from clinical trials supported the safety of omitting axillary dissection not only in patients with a negative sentinel node biopsy [19] but also in patients with a clinically node-negative axilla but pathological macrometastatic involvement of one or two sentinel nodes in the context of breast-conserving surgery with tangential field radiation therapy [20]. This continues a trend of reduced surgical extent without loss of efficacy, which dates back to the breast-conserving approaches pioneered by Veronesi [74] and Fisher [75].

Similarly, recent studies in radiation therapy have demonstrated the safety and efficacy of abbreviated schedules for improved patient convenience and the use of partial breast irradiation (PBI) under certain defined circumstances. These findings are summarized in Table 1.

breast cancer subtypes

Analysis of gene expression arrays has resulted in the recognition of several fundamentally different subtypes of breast cancer [1]. Because it is not always feasible to obtain gene expression array information, a simplified classification, closely following that proposed by Cheang et al. [7], has been adopted as a useful shorthand. Subtypes defined by clinicopathological criteria are similar to but not identical to intrinsic subtypes and represent a convenient approximation. As summarized in Table 2, this approach uses immunohistochemical definition of estrogen and progesterone receptor, the detection of overexpression and/or amplification of the human epidermal growth factor receptor 2 (HER2) oncogene, and Ki-67 labeling index, a marker of cell proliferation, as the means of identifying tumor subtypes.

Table 2.
Surrogate definitions of intrinsic subtypes of breast cancer (4, 7)

Clearly, this clinicopathological classification requires the availability of reliable measurements of its individual components. Guidelines have been published for estrogen and progesterone receptor determination [76] and for the detection of HER2 positivity [77]. For clinical decision making, the Panel supported using the US Food and Drug Administration definition of HER2 positivity based on the eligibility criteria for HER2 status determination from the pivotal clinical trials [80, 81]. It was noted that clarifications to the ASCO/CAP guidelines were in preparation, and these have subsequently been published [82]. Ki-67 labeling index presents more substantial challenges, but important guidelines for this test are under development [7, 8385]. In the proposed classification, Ki-67 labeling index is chiefly important in the distinction between ‘Luminal A’ and ‘Luminal B (HER2 negative)’ subtypes. If reliable Ki-67 labeling index assessment is not available, some alternative measure of proliferation such as a histological grade may be used in making this distinction.

panel deliberations

More than 100 questions were circulated and agreed among Panel members before the meeting. These were presented during the final session of the conference. Panel members had the opportunity to comment, and then voted electronically either yes or no on each question, with the option to abstain if they felt uninformed or conflicted. The detailed votes are not presented here: Rather, verbal descriptions of the extent of agreement or disagreement are given in the following sections.

axillary surgery

The Panel was clearly of the view that the routine use of immunohistochemistry to look for low-volume metastatic disease in sentinel nodes was not indicated, since metastases shown only by immunohistochemistry would not alter management. Furthermore, isolated tumor cells, and even metastases up to 2 mm (micrometastases) in a single sentinel node, were not considered to constitute an indication for axillary dissection regardless of the type of breast surgery carried out. The Panel accepted the option of omitting axillary dissection for macrometastases in the context of lumpectomy and radiation therapy for patients with clinically node-negative disease and 1–2 positive sentinel lymph nodes as reported from ACOSOG trial Z0011 with a median follow-up of 6.3 years [20]. The Panel, however, was very clear that this practice, based on a specific clinical trial setting, should not be extended more generally, such as to patients undergoing mastectomy, those who will not receive whole-breast tangential field radiation therapy, those with involvement of more than two sentinel nodes, and patients receiving neoadjuvant therapy.

radiation therapy

The Panel considered accelerated whole-breast radiotherapy to be an acceptable option in select patients: In particular, the Panel was divided about the use of this approach in the presence of extensive vascular invasion.

Partial breast irradiation (PBI) as definitive treatment in selected patients was supported by almost half of the Panel and by a strong majority for patients above the age of 70. There was considerable uncertainty about its use in lymphoma survivors who had previously undergone mantle field irradiation, where out-of-quadrant second cancers’ risks are considerable and for any patient groups different from the current eligible population in PBI trials. The Panel generally accepted PBI as an alternative to conventional external beam boost to the tumor bed.

Post-mastectomy radiation therapy was strongly supported for patients with four or more axillary lymph nodes involved. While not in general favoring irradiation for those with lesser nodal involvement, the Panel by a slim majority favored post-mastectomy radiation for patients younger than 45 years with 1–3 positive nodes and for patients at any age with extensive vascular invasion in two or more blocks in conjunction with 1–3 positive nodes.

A majority of the Panel supported radiation after complete excision of ductal carcinoma in situ (DCIS) but was prepared to countenance its omission for some elderly patients and those with low-grade low-risk DCIS.

definition of biological subtypes

The Panel strongly supported the clinicopathological determination of estrogen receptor, progesterone receptor, HER2, and Ki-67 as useful for defining subtypes, but did not support the incorporation of tests for cytokeratin 5/6 or epidermal growth factor receptor/HER1 for the determination of ‘basal-like’ tumors for clinical decision making. The endorsed clinicopathological criteria define a convenient alternative to formal subtyping and are likely to be refined in the future. The Panel did not require multigene array definition of tumor subtype, although there was acceptance of such assays for certain indications (see below). However, the Panel did recommend that the clinicopathological markers described above were generally sufficient to guide therapeutic choices.

selection of endocrine therapy in premenopausal women

The Panel accepted tamoxifen alone or ovarian function suppression plus tamoxifen as reasonable, though expressing a preference for tamoxifen alone. In patients with a contraindication to tamoxifen, ovarian function suppression alone was accepted as a treatment, while the combination of ovarian function suppression plus an aromatase inhibitor was also considered reasonable.

selection of endocrine therapy in postmenopausal women

The Panel was exactly equally divided about whether all postmenopausal patients should receive an aromatase inhibitor (if available and not contraindicated) at some point in treatment, but was more supportive of aromatase inhibitors in the presence of involved lymph nodes. A large majority felt that selected patients could be treated with tamoxifen alone, and that patients could be switched to tamoxifen if intolerant to aromatase inhibitors. The Panel stressed the need to ensure that patients receiving an aromatase inhibitor were indeed postmenopausal, whether by clinical or biochemical criteria.

The Panel considered that 5 years of an aromatase inhibitor was a sufficient duration and a majority opposed extension even in the presence of node-positive disease or among younger postmenopausal patients (<55 years of age). The Panel was almost unanimous in rejecting CYP2D6 testing to dictate choice of endocrine therapy type.


The Panel agreed that factors arguing for the inclusion of chemotherapy were high histological grade, high proliferation as measured by Ki-67, low hormone receptor status, positive HER2 status, and ‘Triple negative’ status in invasive ductal carcinoma of usual forms. These factors are largely captured in the tumor subtype definitions summarized in Table 2. There was a lack of complete consensus on the threshold indication for inclusion of chemotherapy for patients with ‘Luminal A’ or ‘Luminal B (HER2 negative)’ disease. In terms of disease extent, the Panel did not believe that node positivity per se was an indication for use of chemotherapy, though a strong majority would use it if more than three lymph nodes were involved.

Several tests are available which define prognosis [57, 58, 86]. These may indicate a prognosis so good that the doctor and patient decide that chemotherapy is not required. A strong majority of the Panel agreed that the 21-gene signature (Oncotype DX®) [57] may also be used where available to predict chemotherapy responsiveness in an endocrine-responsive cohort where uncertainty remains after consideration of other tests, but the majority agreed that the chemopredictive properties of the 70-gene signature (MammaPrint®) [58] were not yet sufficiently established. Trials are ongoing to clarify this role for both tests. The majority of the Panel did not support lymphovascular invasion as a sufficient indication for chemotherapy, and less than a quarter of the Panel supported uPA/PAI1 [86] as a predictive marker for the use of chemotherapy.

chemotherapy in subtypes

The Panel strongly agreed that the ‘Luminal A’ subtype was less responsive to chemotherapy; that chemotherapy was less useful in such patients; and that no preferred chemotherapy regimen could be defined for treatment of ‘Luminal A’ disease.

For ‘Luminal B’ disease, the Panel considered that both anthracyclines and taxanes should be included in the chemotherapy regimen. While the Panel could not define a single preferred chemotherapy regimen for ‘HER2 positive’ disease, the majority again favored the inclusion of both anthracyclines and taxanes. For ‘Triple negative’ disease of the usual ductal type, the Panel again supported the inclusion of anthracyclines and taxanes and an alkylating agent (typically cyclophosphamide), but did not support the routine use of cisplatin or carboplatin. A slim majority agreed that dose-dense chemotherapy [87] should be considered for such patients, and the Panel was strongly opposed to the inclusion of antiangiogenic therapies at this time, while noting that further trials are ongoing.


The Panel unanimously supported the use of 1 year of trastuzumab as standard adjuvant treatment for patients with ‘HER2 positive’ disease, and the majority were willing to extend this to patients with pT1b, but not pT1a pN0 disease. Trastuzumab administered for <1 year [88] was regarded as suboptimal if 1 year of therapy was feasible, but better than no trastuzumab if limited resources prevented its full duration use. While awaiting data from the ongoing HERA trial, the Panel did not support continuation of adjuvant trastuzumab beyond 1 year. While preferring that trastuzumab be initiated concurrently with chemotherapy, the Panel also accepted its sequential use. The Panel did not support the use of trastuzumab without chemotherapy if chemotherapy could be given, but was prepared to countenance such treatment in circumstances where chemotherapy could not be delivered.

neoadjuvant cytotoxic therapy

A majority of the Panel considered that neoadjuvant cytotoxic therapy was of value beyond its role in facilitating conservative surgery and noted the improved prognostic information associated with pathological complete response to such therapy, particularly in patients with ‘HER2 positive’ and ‘Triple negative (ductal)’ tumors [89], which may allow earlier change from an ineffective regimen.

The Panel considered that the choice of neoadjuvant chemotherapy should be made on the same basis as applied in the selection of postoperative adjuvant treatments. The Panel supported the incorporation of an anti-HER2 drug in the neoadjuvant therapy for patients with ‘HER2 positive’ disease, but did not support dual HER2 targeting at this point in time. The Panel did not support cytotoxic neoadjuvant therapy for tumors with low proliferation or high endocrine responsiveness.

neoadjuvant endocrine therapy

The Panel was almost unanimous in supporting the use of neoadjuvant endocrine therapy as an option for postmenopausal patients with highly endocrine-responsive disease. If given, the Panel considered that such treatment should be continued until maximal response or for a minimum of 4–8 months.


The Panel did not support the use of bisphosphonates for antitumor effect in either pre- [32] or postmenopausal [90] patients.

male breast cancer

Adjuvant tamoxifen was strongly supported, but only a slim majority would consider aromatase inhibitors in patients with contraindications to tamoxifen, such as thrombosis. The Panel did not support extended endocrine treatment beyond 5 years for male breast cancer. The lack of any evidence on these latter two points was acknowledged.

summary of systemic treatment recommendations

The approach to treatment within breast cancer subtypes greatly simplifies the definition of therapy indications, since the subtypes themselves incorporate many of the risk and predictive factors used in previous consensus recommendations. The broad recommendations are summarized in Table 3 and essentially indicate endocrine therapy alone for patients with clinicopathologically classified ‘Luminal A’ disease (except in defined high-risk cases), chemo-endocrine therapy for ‘Luminal B’, the addition of anti-HER2 therapy in the presence of ‘HER2 positivity’, and a reliance on chemotherapy for most patients with ‘Triple negative’ disease (e.g. those with invasive ductal carcinoma).

Table 3.
Systemic treatment recommendations for subtypes


Support for the conference was provided by SONK from registration fees paid by the conference attendees and by Grant No. CA75362 from the United States National Cancer Institute.


Aapro M., Roche (Speakers Bureau, Consultant), Novartis (Speakers Bureau, Consultant), Pfizer (Speakers Bureau, Consultant), Amgen (Speakers Bureau, Consultant), Genomic Health (Speakers Bureau, Consultant), GSK (Consultant, Research), Genomic Health (Speakers Bureau, Consultant); Albain K., Genomic Health (Speakers Bureau), Roche/Genentech (Speakers Bureau); Baselga J., Merck (Consultant); Bergh J., Onyx/Bayer (Consultant), AstraZeneca (Speakers Bureau), Roche (Speakers Bureau), Novartis (Speakers Bureau), Pfizer (Speakers Bureau), Amgen (Speakers Bureau), TRM (Speakers Bureau), Merck (Research), Tapestry Network (Consultant); Bertolini F., Pfizer (Research), Molmed (Research); Bonnefoi H., Sanofi-aventis (Speakers Bureau, Consultant), Roche (Consultant), Novartis (Speakers Bureau); Brisken C., None; Burstein H., None; Castiglione M.; None; Coates A., None; Coleman R., Novartis (Speakers Bureau), Amgen (Speakers Bureau, Consultant), Roche (Speakers Bureau, Consultant, Travel), Pfizer (Speakers Bureau); Colleoni M., None; Costa A., None; Curigliano G., None; Davidson N., None; DeCensi A., None; DiLeo A., AstraZeneca (Speakers Bureau), GSK (Speakers Bureau), Pfizer (Speakers Bureau), Roche (Speakers Bureau), Sanofi-aventis (Speakers Bureau), Cephalon (Speakers Bureau); Dowsett M., AstraZeneca (Speakers Bureau, Consultant, royalties), Roche (Speakers Bureau, Consultant), GSK (Consultant), Ipsen (Consultant), Cayar (Speakers Bureau, Consultant); Ejlertsen B., None; Forbes J., AstraZeneca (Speakers Bureau); Galimberti V., None; Garber J., Novartis (Spouse Consults); Gelber R., None; Glaus A., None; Glick J., None; Gnant M., AstraZeneca (Speakers Bureau, Consult, Travel), Novartis (Speakers Bureau, Consult, Travel), Roche (Consult, Research, Travel), Sanofi-aventis (Research), GSK (Speakers Bureau); Goldhirsch A., Pfizer (Travel), GSK (Speakers Bureau, Travel), Roche (Speakers Bureau, Travel), Ferring (Speakers Bureau); Gomis R., None; Goodwin P., Amgen (Speakers Bureau), Novartis (Employment), Pfizer (Travel); Goss P., Novartis (Speakers Bureau), GSK (Speakers Bureau), Novartis (Research); Harris J., None; Hayes D., DNAR (Speakers Bureau), Compendia (Speakers Bureau), Chugai (Speakers Bureau), GSK (Research), Pfizer (Research), Novartis (Research), Veridex/J&J (Research), OncImmune (Stock), Halcyon Diagnostics (Stock); Ingle J., Pfizer (Consultant uncompensated); Intra M., None; Iorio M., None; Jassem J., None; Jiang Z., None; Jordan V.C., None; Karlsson P., Sanofi-aventis (Travel), AstraZeneca (Travel), Amgen (Travel); Kaufmann M., AstraZeneca (Consultant, Travel), Pfizer (Consultant, Travel), Novartis (Consultant, Travel), Roche (Travel), GSK (Consultant, Travel), Amgen (Consultant, Travel), Sanofi-aventis (Consultant, Travel); Kerbel R., Taiho (Consultant), GSK (Consultant, Research), MetronomiX (Consultant), Pfizer (Research); Kuhl C., None; Lindemann G., Sanofi-aventis (Consultant); Mandelblatt J., None; Von Minckwitz G., Amgen (Consultant, Research, Travel), BSM (Research), Chugai (Speakers Bureau), GSK (Research), Mundipharma (Research), Novartis (Research), Pfizer (Research), Roche (Speakers Bureau, Consultant, Research), Sanofi-aventis (Consultant, Research), Wyeth (Research); Morrow M., None; Namer M., Sanofi-aventis (Speakers Bureau), Cephalon (Travel); Norton L., Biogen (Other); Orrecchia R., None.; Osborne C.K., None; Paik S., GSK (Research, Travel); Partridge A., None; Penault F., None; Perou C., University Genomics (Stock), Bioclassifier (Stock), Roche (Consultant, Research), AstraZeneca (Consultant), CancerGuides (Consultant); Piccart M., Roche (Consultant, Travel); Possinger K., AstraZeneca (Consultant, Travel); Pritchard K., Boehringer (Consultant), Roche (Travel), AstraZeneca (Consultant), Pfizer (Consultant), Abraxis (Consultant); Rutgers E., None; Semiglazov V., None; Senn H.J., Roche (Travel), Takeda (Travel); Smith I.E., Roche (Speakers Bureau, Consultant), Sanofi-aventis (Speakers Bureau), GSK (Speakers Bureau), Bayer (Consultant); Sotiriou C., Merck (Consultant), Novartis (Consultant), Ipsogen (Consultant); Stratton M., None; Thürlimann B., Roche (Consultant, Stock, Research, Travel), Novartis (Stock, Travel), Sanofi-aventis (Research), AstraZeneca (Consultant, Research), Janssen (Other), BMS (Consultant); Toi M., GSK (Speakers Bureau), Taiho (Research), Eli Lilly (Consultant); Tutt A., AstraZeneca (Travel), Sanofi-aventis (Consultant, Travel), Roche (Travel), Pfizer (Consultant, Travel), BMS (Consultant, Travel), Genentech (Research); Untch M., None; Urban C., None; Veronesi P., None; Veronesi U., None; Viale G., Roche (Consultant), GSK (Consultant), Novartis (Travel); Vicini F., None; Watanabe T., Pfizer (Speakers Bureau), AstraZeneca (Speakers Bureau), Asklep (Speakers Bureau), Novartis (Speakers Bureau), BMS (Speakers Bureau), McCann Health (Speakers Bureau), Chugai (Speakers Bureau), Taiho (Speakers Bureau), Janssen (Speakers Bureau), GSK (Speakers Bureau), Sanofi-aventis (Speakers Bureau), Takeda (Speakers Bureau); Wilcken N., GSK (Consultant, Travel), Roche (Consultant), Sanofi-aventis (Consultant), Novartis (Consultant), Specialize Thera/Abraxis (Consultant); Winer E., Genentech (Research); Wood W., OncImmune (Consultant).


The authors thank the participants in the 12th International Conference on Primary Therapy of Early Breast Cancer for many useful remarks and for substantial contributions to the process. We acknowledge the substantial contributions of Mrs. Shari Gelber and Mrs. Sabina Briner. We also thank Prof. Umberto Veronesi for his guidance and Dr Franco Nolè for his thoughtful remarks.

appendix 1. 

Members of the Panel are listed below. All had a significant input to the discussion and manuscript.

  • Matti Aapro, Clinique de Genolier, 3 Route du Muids, 1272 Genolier, Switzerland
  • Kathy S. Albain, Loyola University Medical Center, Cardinal Bernardin Cancer Center, Room 109, 2160 S First Ave, Maywood, IL 60153, USA
  • José Baselga, Massachusetts General Hospital Cancer Center, 55 Fruit Street, YAW 9, Boston, MA 02114, USA
  • Jonas Bergh, Radiumhemmet & Karolinska Oncology, Karolinska Institutet and University Hospital, 171 76 Stockholm, Sweden
  • Hervé Bonnefoi, Institut Bergonié Cancer Center, Université de Bordeaux, Bordeaux, France
  • Harold Burstein, Department of Medical Oncology/Solid Tumor Oncology, Dana-Farber Cancer Institute, 450 Brookline Avenue, Boston, MA 02215, USA
  • Monica Castiglione-Gertsch, Oncogynecology Unit, University Hospital, Bd. de la Cluse 30, 1211 Geneva, Switzerland
  • Alan S. Coates, International Breast Cancer Study Group and University of Sydney, Sydney, NSW 2006, Australia
  • Marco Colleoni, Research Unit Medical Senology, European Institute of Oncology, Via Ripamonti 435, 20141 Milan, Italy
  • Alberto Costa, ESO—European School of Oncology, Via del Bollo 4, 20123 Milan, Italy and Breast Unit of Southern Switzerland, Lugano, Switzerland
  • Giuseppe Curigliano, Division of Medical Oncology, European Insitute of Oncology, Via Ripamonti 435, 20141 Milan, Italy
  • Nancy E. Davidson, University of Pittsburgh Cancer Institute, 5150 Centre Avenue, UPMC Cancer Pavilion, 5th Floor, Suite 500, Pittsburgh, PA 15232, USA
  • Angelo Di Leo, ‘Sandro Pitigliani’ Medical Oncology Unit, Department of Oncology, Hospital of Prato, Piazza dell’Ospedale, 59100 Prato, Italy
  • Bent Ejlertsen, Department of Oncology, Bldg 4262 Rigshospitalet, 9 Blegdamsvej, 2100 Copenhagen, Denmark
  • John F. Forbes, Department of Surgical Oncology, University of Newcastle, Calvary Mater Hospital, ANZ BCTG, Edith Street Waratah, Newcastle 2298 NSW Australia
  • Richard D. Gelber, Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, 450 Brookline Avenue, Boston, MA 02215, USA
  • Agnes Glaus, ZeTuP, Center for Tumor Detection, Treatment and Prevention, Rorschacher Strasse 150, 9006 St Gallen, Switzerland
  • John H. Glick, University of Pennsylvania, Abramson Cancer Center, Perelman Center, 3400 Civic Center Blvd, Philadelphia, PA 19104, USA
  • Michael Gnant, Medical University of Vienna, Department of Surgery, Comprehensive Cancer Center Vienna, Währinger Gürtel 18-20, 1090 Wien, Austria
  • Aron Goldhirsch, International Breast Cancer Study Group, Department of Medicine, European Institute of Oncology, Via Ripamonti 435, 20141 Milan, Italy, and Swiss Center for Breast Health, Sant'Anna Clinics, 6924 Lugano-Sorengo, Switzerland (Chairman)
  • Pamela Goodwin, Department of Medicine, Division of Clinical Epidemiology, Samuel Lunenfeld Research Institute, Mount Sinai Hospital and Princess Margaret Hospital, University of Toronto, 1284-600 University Avenue, Toronto, ON M5G 1X4, Canada
  • Paul E. Goss, MGH Cancer Center, 55 Fruit Street, Boston, MA 02114, USA
  • Jay R. Harris, Department of Radiation Oncology, Dana-Farber Cancer Institute, Brigham and Women’s Hospital, Room 1622, 44 Binney Street, Boston, MA 02115, USA
  • Dan F. Hayes, Breast Care Center, University of Michigan, Comprehensive Cancer Center, 1500 East Medical Center Drive, Ann Arbor, MI 48109, USA
  • James N. Ingle, Mayo Clinic Cancer Center, Women’s Cancer Program, 200 First Street S.W., Rochester, MN 55905, USA
  • Jacek Jassem, Medical University of Gdansk, Deptartment of Oncology & Radiotherapy, Debinki Street 7, 80-211 Gdansk, Poland
  • Zefei Jiang, 307 Hospital, Academy of Military Medical Sciences, 8 Fengtai East Avenue, 100071 Beijing, China
  • Per Karlsson, Department of Oncology, Institute of Selected Clinical Sciences, Sahlgrenska Academy, Sahlgrenska University Hospital, 413 45 Göteborg, Sweden
  • Manfred Kaufmann, Department of Gynecology, Obstetrics, Breast Unit, J.W. Goethe University, Theodor Stern Kai 7, 60596 Frankfurt am Main, Germany
  • Gunter von Minckwitz, GBG Forschungs GmbH, Martin Behaim Strasse 12, 63263 Neu-Isenburg, Germany
  • Monica Morrow, Memorial Sloan-Kettering Cancer Center, Evelyn Lauder Breast Center, 300 East 66 Street, New York, NY 10065, USA
  • Moise Namer, Medical Oncology, Centre Antoine Lacassagne, 33 Av. de Valombrose, 06189 Nice Cedex 2, France
  • Larry Norton, Memorial Sloan-Kettering Cancer Center, Room H 901, 205 East 64th Street, Concourse Level, New York, NY 10021-6007, USA
  • C. Kent Osborne, Dan L. Duncan Cancer Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA
  • Frédérique Penault-Llorca, Service d’Anatomie Pathologie Moléculaire, Dépt. RIO, Centre Jean Perrin, 58 rue Montalembert, BP 392, 63011 Clermont-Ferrand Cedex 1, France
  • Charles M. Perou, Lineberger Comprehensive Cancer Center, Departments of Genetics and Pathology, The University of North Carolina, Chapel Hill, NC 27599, USA
  • Martine J. Piccart-Gebhart, Internal Medicine, Oncology, Institut Jules Bordet, Rue Héger-Bordet 1, 1000 Brussels, Belgium
  • Kurt Possinger, Universitätsklinikum Charité Campus Mitte, Centrum 14, M.S. Onkologie/Hämatologie, Charitéplatz 1, 10117 Berlin, Germany
  • Kathleen I. Pritchard, Sunnybrook Odette Cancer Centre, Ontario Clinical Oncology Group (OCOG), 2075 Bayview Avenue, Toronto, ON M4N 1H6, Canada
  • Emiel J.T. Rutgers, The Netherlands Cancer Institute, Department of Surgery, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands
  • Vladimir Semiglazov, N.N. Petrov Research Institute of Oncology, 68 Leningradskaya Street, Pesochny-2, 197758 St Petersburg, Russia
  • Ian Smith, Breast Unit, Royal Marsden Hospital and Institute of Cancer Research, Fulham Road, London, SW3 6JJ, UK
  • Beat Thürlimann, Breast Center, Kantonsspital St Gallen, 9007 St Gallen, Switzerland
  • Masakazu Toi, Department of Breast Surgery, Kyoto University Hospital, 54 Shogoin-Kawahara cho, Sakyo-ku, Kyoto 606-8507, Japan
  • Andrew Tutt, Breast Oncology Unit, Guy’s Hospital, King’s Health Partners AHSC, London, UK
  • Michael Untch, Department of Gynecology and Obstetrics, Multidisciplinary Breast Cancer Center, Helios Klinikum Berlin-Buch, Academic Hospital of the University of Göttingen, Schwanebecker Chaussee 50, 13125 Berlin, Germany
  • Giuseppe Viale, Department of Pathology, European Institute of Oncology and University of Milan, Via Ripamonti 435, 20141 Milan, Italy
  • Toru Watanabe, Department of Medicine, Hamamatsu Oncology Center, 3-6-13 Chuo Naka-Ku , 430-0929 Hamamatsu, Japan
  • Nicholas Wilcken, Department of Medical Oncology, University of Sydney, Westmead Hospital, Westmead 2145, NSW, Australia
  • Eric P. Winer, Breast Oncology Center, Dana-Farber Cancer Institute, 450 Brookline Avenue, Boston, MA, 02115, USA
  • William C. Wood, Department of Surgery, Winship Cancer Institute, 1365C Clifton Road, Atlanta, GA 30322, USA (Chairman)

appendix 2. 

Note: details of the declared conflicts of interest are available at http://www.oncoconferences.ch


1. Perou CM, Sorlie T, Eisen MB, et al. Molecular portraits of human breast tumours. Nature. 2000;406:747–752. [PubMed]
2. Prat A, Perou CM. Deconstructing the molecular portraits of breast cancer. Mol Oncol. 2011;5:5–23. [PubMed]
3. Parker JS, Mullins M, Cheang MCU, et al. Supervised risk predictor of breast cancer based on intrinsic subtypes. J Clin Oncol. 2009;27:1160–1167. [PMC free article] [PubMed]
4. Nielsen TO, Hsu FD, Jensen K, et al. Immunohistochemical and clinical characterization of the basal-like subtype of invasive breast carcinoma. Clin Cancer Res. 2004;10:5367–5374. [PubMed]
5. Blows FM, Driver KE, Schmidt MK, et al. Subtyping of breast cancer by immunohistochemistry to investigate a relationship between subtype and short and long term survival: a collaborative analysis of data for 10,159 cases from 12 studies. PLoS Med. 2010;7:e1000279. [PMC free article] [PubMed]
6. Hugh J, Hanson J, Cheang MC, et al. Breast cancer subtypes and response to docetaxel in node-positive breast cancer: use of an immunohistochemical definition in the BCIRG 001 Trial. J Clin Oncol. 2009;27:1168–1176. [PMC free article] [PubMed]
7. Cheang MCU, Chia SK, Voduc D, et al. Ki67 index, HER2 status, and prognosis of patients with luminal B breast cancer. J Natl Cancer Inst. 2009;101:736–750. [PMC free article] [PubMed]
8. Millikan RC, Newman B, Tse CK, et al. Epidemiology of basal-like breast cancer. Breast Cancer Res Treat. 2008;109:123–139. [PMC free article] [PubMed]
9. Phipps AI, Chlebowski RT, Prentice R, et al. Body size, physical activity, and risk of triple-negative and estrogen receptor-positive breast cancer. Cancer Epidemiol Biomarkers Prev. 2011;20:454–463. [PMC free article] [PubMed]
10. Phipps AI, Buist DS, Malone KE, et al. Reproductive history and risk of three breast cancer subtypes defined by three biomarkers. Cancer Causes Control. 2011;22:399–405. [PMC free article] [PubMed]
11. Liedtke C, Mazouni C, Hess KR, et al. Response to neoadjuvant therapy and long-term survival in patients with triple-negative breast cancer. J Clin Oncol. 2008;26:1275–1281. [PubMed]
12. Dignam JJ, Dukic V, Anderson SJ, et al. Hazard of recurrence and adjuvant treatment effects over time in lymph node-negative breast cancer. Breast Cancer Res Treat. 2009;116:595–602. [PMC free article] [PubMed]
13. Aebi S, Sun Z, Braun D, et al. Differential efficacy of three cycles of CMF followed by tamoxifen in patients with ER-positive and ER-negative tumors: long-term follow up on IBCSG Trial IX. Ann Oncol. 2011 [epub ahead of print 31 January 2011] doi:10.1093/annonc/mdq754. [PMC free article] [PubMed]
14. Albain KS, Barlow WE, Shak S, et al. Prognostic and predictive value of the 21-gene recurrence score assay in postmenopausal women with node-positive, oestrogen-receptor-positive breast cancer on chemotherapy: a retrospective analysis of a randomised trial. Lancet Oncol. 2010;11:55–65. [PMC free article] [PubMed]
15. Nguyen PL, Taghian AG, Katz MS, et al. Breast cancer subtype approximated by estrogen receptor, progesterone receptor, and HER-2 is associated with local and distant recurrence after breast-conserving therapy. J Clin Oncol. 2008;26:2373–2378. [PubMed]
16. Wo JY, Taghian AG, Nguyen PL, et al. The association between biological subtype and isolated regional nodal failure after breast-conserving therapy. Int J Radiat Oncol Biol Phys. 2010;77:188–196. [PubMed]
17. Tang G, Shak S, Paik S, et al. Comparison of the prognostic and predictive utilities of the 21-gene recurrence score assay and Adjuvant! for women with node-negative, ER-positive breast cancer: results from NSABP B-14 and NSABP B-20. Breast Cancer Res Treat. 2011;127:133–142. [PMC free article] [PubMed]
18. Goldhirsch A, Ingle JN, Gelber RD, et al. Thresholds for therapies: highlights of the St. Gallen International Expert Consensus on the Primary Therapy of Early Breast Cancer 2009. Ann Oncol. 2009;20:1319–1329. [PMC free article] [PubMed]
19. Krag DN, Anderson SJ, Julian TB, et al. Sentinel-lymph-node resection compared with conventional axillary-lymph-node dissection in clinically node-negative patients with breast cancer: overall survival findings from the NSABP B-32 randomised phase 3 trial. Lancet Oncol. 2010;11:927–933. [PMC free article] [PubMed]
20. Giuliano AE, Hunt KK, Ballman KV, et al. Axillary dissection vs no axillary dissection in women with invasive breast cancer and sentinel node metastasis. JAMA. 2011;305:569–575. [PubMed]
21. Vaidya JS, Joseph DJ, Tobias JS, et al. Targeted intraoperative radiotherapy versus whole breast radiotherapy for breast cancer (TARGIT-A trial): an international, prospective, randomised, non-inferiority phase 3 trial. Lancet. 2010;376:91–102. [PubMed]
22. Veronesi U, Orecchia R, Luini A, et al. Intraoperative radiotherapy during breast conserving surgery: a study on 1,822 cases treated with electrons. Breast Cancer Res Treat. 2010;124:141–151. [PubMed]
23. Whelan TJ, Pignol JP, Levine MN, et al. Long-term results of hypofractionated radiation therapy for breast cancer. N Engl J Med. 2010;362:513–520. [PubMed]
24. The START Trialists' Group. The UK Standardisation of Breast Radiotherapy (START) Trial B of radiotherapy hypofractionation for treatment of early breast cancer: a randomised trial. Lancet. 2008;371:1098–1107. [PMC free article] [PubMed]
25. Tutt A, Robson M, Garber JE, et al. Oral poly(ADP-ribose) polymerase inhibitor olaparib in patients with BRCA1 or BRCA2 mutations and advanced breast cancer: a proof-of-concept trial. Lancet. 2010;376:234–244. [PubMed]
26. Tutt A. PARP inhibitors—walking them through to adjuvant. Breast. 2011;20(Suppl 1):S1. (Abstr S01)
27. Baselga J. First results of the NeoALTTO trial (BIG 01-06/EGF 106903): a phase III, randomized, open label, neoadjuvant study of lapatinib, trastuzumab, and their combination plus paclitaxel in women with HER2-positive primary breast cancer. Presented at the San Antonio Breast Cancer Symposium. San Antonio, TX, 8–12 December 2010 (Abstr 291)
28. Gianni L. Neoadjuvant pertuzumab (P) and trastuzumab (H): antitumor and safety analysis of a randomized phase II study (‘NeoSphere’) Presented at the San Antonio Breast Cancer Symposium. San Antonio, Texas, 8–12 December 2010 (Abstr 1000)
29. Hudis CA. Trastuzumab—mechanism of action and use in clinical practice. N Engl J Med. 2007;357:39–51. [PubMed]
30. Goss P, Ingle J, Martino S, et al. Outcomes of women who were premenopausal at diagnosis of early stage breast cancer in the NCIC CTG MA17 Trial. Presented at the San Antonio Breast Cancer Symposium. San Antonio, Texas, 8–12 December 2010 (Abstr S 1-1)
31. Coleman RE. Adjuvant treatment with zoledronic acid in stage II/III breast cancer. The AZURE trial (BIG 01/04) Presented at the San Antonio Breast Cancer Symposium. San Antonio, Texas, 8–12 December 2010 (Abstr 226)
32. Gnant M, Mlineritsch B, Schippinger W, et al. Endocrine therapy plus zoledronic acid in premenopausal breast cancer. N Engl J Med. 2009;360:679–691. [PubMed]
33. Nielsen TO, Parker JS, Leung S, et al. A comparison of PAM50 intrinsic subtyping with immunohistochemistry and clinical prognostic factors in tamoxifen-treated estrogen receptor-positive breast cancer. Clin Cancer Res. 2010;16:5222–5232. [PMC free article] [PubMed]
34. Desmedt C, Haibe-Kains B, Wirapati P, et al. Biological processes associated with breast cancer clinical outcome depend on the molecular subtypes. Clin Cancer Res. 2008;14:5158–5165. [PubMed]
35. Sotiriou C, Pusztai L. Gene-expression signatures in breast cancer. N Engl J Med. 2009;360:790–800. [PubMed]
36. Iwamoto T, Bianchini G, Booser D, et al. Gene pathways associated with prognosis and chemotherapy sensitivity in molecular subtypes of breast cancer. J Natl Cancer Inst. 2011;103:264–272. [PubMed]
37. Sotiriou C. Molecular mechanisms which predict response to chemotherapy. Breast. 2011;20(Suppl 1):S3. (Abstr S05)
38. Andre F, Berrada N, Desmedt C. Implication of tumor microenvironment in the resistance to chemotherapy in breast cancer patients. Curr Opin Oncol. 2010;22:547–551. [PubMed]
39. Denkert C, Loibl S, Noske A, et al. Tumor-associated lymphocytes as an independent predictor of response to neoadjuvant chemotherapy in breast cancer. J Clin Oncol. 2010;28:105–113. [PubMed]
40. Fuentes G, Scaltriti M, Baselga J, et al. Synergy between trastuzumab and pertuzumab for human epidermal growth factor 2 (Her2) from colocalization: an in silico based mechanism. Breast Cancer Res. 2011;13:R54. [PMC free article] [PubMed]
41. Osborne CK, Schiff R. Mechanisms of endocrine resistance in breast cancer. Annu Rev Med. 2011;62:233–247. [PMC free article] [PubMed]
42. Daly MB, Axilbund JE, Buys S, et al. Genetic/familial high-risk assessment: breast and ovarian. J Natl Compr Canc Netw. 2010;8:562–594. [PubMed]
43. Garber J. Identifying and assessing women at high risk for breast cancer. Breast Cancer Res. 2009 11 Suppl 1: S1.
44. DeCensi A, Puntoni M, Goodwin P, et al. Metformin and cancer risk in diabetic patients: a systematic review and meta-analysis. Cancer Prev Res (Phila) 2010;3:1451–1461. [PubMed]
45. Bjelakovic G, Nikolova D, Gluud LL, et al. Mortality in randomized trials of antioxidant supplements for primary and secondary prevention: systematic review and meta-analysis. JAMA. 2007;297:842–857. [PubMed]
46. Cuzick J, DeCensi A, Arun B, et al. Preventive therapy for breast cancer: a consensus statement. Lancet Oncol. 2011;12:496–503. [PubMed]
47. Swain SM, Jeong JH, Geyer CE, Jr, et al. Longer therapy, iatrogenic amenorrhea, and survival in early breast cancer. N Engl J Med. 2010;362:2053–2065. [PMC free article] [PubMed]
48. International Breast Cancer Study Group. Colleoni M, Gelber S, et al. Tamoxifen after adjuvant chemotherapy for premenopausal women with lymph node-positive breast cancer: international Breast Cancer Study Group Trial 13-93. J Clin Oncol. 2006;24:1332–1341. [PubMed]
49. Swain SM, Jeong J-H, Wolmark N. Amenorrhea from breast cancer therapy - not a matter of dose. N Engl J Med. 2010;363:2268–2270. [PubMed]
50. Burstein HJ. Bevacizumab for advanced breast cancer: all tied up with a RIBBON? J Clin Oncol. 2011;29:1232–1235. [PubMed]
51. Lohsiriwat V, Curigliano G, Rietjens M, et al. Autologous fat transplantation in patients with breast cancer: “silencing” or “fueling” cancer recurrence? Breast. 2011 [epub ahead of print 4 February 2011] [PubMed]
52. Schramek D, Leibbrandt A, Sigl V, et al. Osteoclast differentiation factor RANKL controls development of progestin-driven mammary cancer. Nature. 2010;468:98–102. [PMC free article] [PubMed]
53. Gonzalez-Suarez E, Jacob AP, Jones J, et al. RANK ligand mediates progestin-induced mammary epithelial proliferation and carcinogenesis. Nature. 2010;468:103–107. [PubMed]
54. Asselin-Labat ML, Vaillant F, Sheridan JM, et al. Control of mammary stem cell function by steroid hormone signalling. Nature. 2010;465:798–802. [PubMed]
55. Iorio MV, Casalini P, Piovan C, et al. microRNA-205 regulates HER3 in human breast cancer. Cancer Res. 2009;69:2195–2200. [PubMed]
56. Tan W, Zhang W, Strasner A, et al. Tumour-infiltrating regulatory T cells stimulate mammary cancer metastasis through RANKL-RANK signalling. Nature. 2011;470:548–553. [PMC free article] [PubMed]
57. 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. 2006;24:3726–3734. [PubMed]
58. Knauer M, Mook S, Rutgers EJ, et al. The predictive value of the 70-gene signature for adjuvant chemotherapy in early breast cancer. Breast Cancer Res Treat. 2010;120:655–661. [PubMed]
59. Lazar AA, Cole BF, Bonetti M, et al. Evaluation of treatment-effect heterogeneity using biomarkers measured on a continuous scale: subpopulation treatment effect pattern plot. J Clin Oncol. 2010;28:4539–4544. [PMC free article] [PubMed]
60. Paik S. Is gene array testing to be considered routine now? Breast. 2011;20(Suppl 1):S9. (Abstr S23) [PubMed]
61. Perez EA, Suman VJ, Davidson NE, et al. Results of chemotherapy alone, with sequential or concurrent addition of trastuzumab in the NCCTG N9831 HER2-positive adjuvant breast cancer trial. Presented at the San Antonio Breast Cancer Symposium. San Antonio, Texas, 9–13 December 2009 (Abstr 80)
62. Gianni L, Eiermann W, Semiglazov V, et al. Neoadjuvant chemotherapy with trastuzumab followed by adjuvant trastuzumab versus neoadjuvant chemotherapy alone, in patients with HER2-positive locally advanced breast cancer (the NOAH trial): a randomised controlled superiority trial with a parallel HER2-negative cohort. Lancet. 2010;375:377–384. [PubMed]
63. Smith I. Is there a case for anti-HER2 treatment without chemotherapy? Breast. 2011;20(Suppl 1):S16. (Abstr S41)
64. Kaufman B, Mackey JR, Clemens MR, et al. Trastuzumab plus anastrozole versus anastrozole alone for the treatment of postmenopausal women with human epidermal growth factor receptor 2-positive, hormone receptor-positive metastatic breast cancer: results from the randomized phase III TAnDEM study. J Clin Oncol. 2009;27:5529–5537. [PubMed]
65. Schwartzberg LS, Franco SX, Florance A, et al. Lapatinib plus letrozole as first-line therapy for HER-2+ hormone receptor-positive metastatic breast cancer. Oncologist. 2010;15:122–129. [PMC free article] [PubMed]
66. Silver DP, Richardson AL, Eklund AC, et al. Efficacy of neoadjuvant cisplatin in triple-negative breast cancer. J Clin Oncol. 2010;28:1145–1153. [PMC free article] [PubMed]
67. Torrisi R, Cardillo A, Cancello G, et al. Phase II trial of combination of pegylated liposomal doxorubicin, cisplatin, and infusional 5-fluorouracil (CCF) plus trastuzumab as preoperative treatment for locally advanced and inflammatory breast cancer. Clin Breast Cancer. 2010;10:483–488. [PubMed]
68. Byrski T, Gronwald J, Huzarski T, et al. Pathologic complete response rates in young women with BRCA1-positive breast cancers after neoadjuvant chemotherapy. J Clin Oncol. 2010;28:375–379. [PubMed]
69. Ejlertsen B. Characteristics of breast cancer patients unlikely to benefit from adjuvant therapy. Breast. 2011;20:(Suppl 1):S14. (Abstr S37)
70. Early Breast Cancer Trialists' Collaborative Group. Adjuvant chemotherapy in oestrogen-receptor-poor breast cancer: patient-level meta-analysis of randomised trials. Lancet. 2008;371:29–40. [PubMed]
71. Muss HB, Berry DA, Cirrincione CT, et al. Adjuvant chemotherapy in older women with early-stage breast cancer. N Engl J Med. 2009;360:2055–2065. [PMC free article] [PubMed]
72. Albain KS, Barlow WE, Ravdin PM, et al. Adjuvant chemotherapy and timing of tamoxifen in postmenopausal patients with endocrine-responsive, node-positive breast cancer: a phase 3, open-label, randomised controlled trial. Lancet. 2009;374:2055–2063. [PMC free article] [PubMed]
73. Colleoni M. Adjuvant therapies for special types of breast cancer. Breast. 2011;20:(Suppl 1):S15. (Abstr S40) [PubMed]
74. Veronesi U, Saccozzi R, Del VM, et al. Comparing radical mastectomy with quadrantectomy, axillary dissection, and radiotherapy in patients with small cancers of the breast. N Engl J Med. 1981;305:6–11. [PubMed]
75. Fisher B, Bauer M, Margolese R, et al. Five-year results of a randomized clinical trial comparing total mastectomy and segmental mastectomy with or without radiation in the treatment of breast cancer. N Engl J Med. 1985;312:665–673. [PubMed]
76. Hammond ME, Hayes DF, Dowsett M, et al. American Society of Clinical Oncology/College of American Pathologists guideline recommendations for immunohistochemical testing of estrogen and progesterone receptors in breast cancer. J Clin Oncol. 2010;28:2784–2795. [PMC free article] [PubMed]
77. Wolff AC, Hammond ME, Schwartz JN, et al. American Society of Clinical Oncology/College of American Pathologists guideline recommendations for human epidermal growth factor receptor 2 testing in breast cancer. J Clin Oncol. 2007;25:118–145. [PubMed]
78. Wirapati P, Sotiriou C, Kunkel S, et al. Meta-analysis of gene expression profiles in breast cancer: toward a unified understanding of breast cancer subtyping and prognosis signatures. Breast Cancer Res. 2008;10:R65. [PMC free article] [PubMed]
79. Cheang MC, Voduc D, Bajdik C, et al. Basal-like breast cancer defined by five biomarkers has superior prognostic value than triple-negative phenotype. Clin Cancer Res. 2008;14:1368–1376. [PubMed]
80. Piccart-Gebhart MJ, Procter M, Leyland-Jones B, et al. Trastuzumab after adjuvant chemotherapy in HER2-positive breast cancer. N Engl J Med. 2005;353:1659–1672. [PubMed]
81. Romond EH, Perez EA, Bryant J, et al. Trastuzumab plus adjuvant chemotherapy for operable HER2-positive breast cancer. N Engl J Med. 2005;353:1673–1684. [PubMed]
82. Hammond ME, Hayes DF, Wolff AC. Clinical notice for American Society of Clinical Oncology-College of American Pathologists guideline recommendations on ER/PgR and HER2 testing in breast cancer. J Clin Oncol. 2011 29: e458. [PubMed]
83. Viale G, Regan MM, Mastropasqua MG, et al. Predictive value of tumor Ki-67 expression in two randomized trials of adjuvant chemoendocrine therapy for node-negative breast cancer. J Natl Cancer Inst. 2008;100:207–212. [PubMed]
84. Viale G, Giobbie-Hurder A, Regan MM, et al. Prognostic and predictive value of centrally reviewed Ki-67 labeling index in postmenopausal women with endocrine-responsive breast cancer: results from Breast International Group trial 1-98 comparing adjuvant tamoxifen with letrozole. J Clin Oncol. 2008;26:5569–5575. [PMC free article] [PubMed]
85. Dowsett M, Nielsen TO, A’Hern R, et al. J Natl Cancer Inst. Ki67 in breast cancer: recommendations from the International Ki67 in Breast Cancer Working Group. [PMC free article] [PubMed]
86. Janicke F, Schmitt M, Pache L, et al. Urokinase (uPA) and its inhibitor PAI-1 are strong and independent prognostic factors in node-negative breast cancer. Breast Cancer Res Treat. 1993;24:195–208. [PubMed]
87. 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. 2003;21:1431–1439. [PubMed]
88. Joensuu H, Bono P, Kataja V, et al. Fluorouracil, epirubicin, and cyclophosphamide with either docetaxel or vinorelbine, with or without trastuzumab, as adjuvant treatments of breast cancer: final results of the FinHer Trial. J Clin Oncol. 2009;27:5685–5692. [PubMed]
89. Kaufmann M, Hortobagyi GN, Goldhirsch A, et al. Recommendations from an international expert panel on the use of neoadjuvant (primary) systemic treatment of operable breast cancer: an update. J Clin Oncol. 2006;24:1940–1949. [PubMed]
90. Eidtmann H, de Boer R, Bundred N, et al. Efficacy of zoledronic acid in postmenopausal women with early breast cancer receiving adjuvant letrozole: 36-month results of the ZO-FAST Study. Ann Oncol. 2010;21:2188–2194. [PubMed]

Articles from Annals of Oncology are provided here courtesy of Oxford University Press
PubReader format: click here to try


Save items

Related citations in PubMed

See reviews...See all...

Cited by other articles in PMC

See all...


  • MedGen
    Related information in MedGen
  • PubMed
    PubMed citations for these articles
  • Substance
    PubChem chemical substance records that cite the current articles. These references are taken from those provided on submitted PubChem chemical substance records.

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...