Survival Analysis Based on Clinicopathological Data from a Single Institution: Chemotherapy Intensity Would Be Enhanced in Patients with Positive Hormone Receptors and Positive HER2 in China Who Cannot Afford the Target Therapy
Background. Immunohistochemical markers were often used to classify breast cancer into subtypes. The aim of this study was to estimate death and tumor progression for patients with the major subtypes of breast cancer as classified using immunohistochemical assay and to investigate the patterns of benefit from the therapies over the past years. Methods. The study population included primary, operable 199 invasive ductal breast cancer patients, with the median age of 51.1？years old. All patients underwent local and/or systemic treatments. The clinicopathological characteristics and clinical outcomes were retrospectively reviewed. The expression of estrogen receptor, progesterone receptor, human epidermal growth factor receptor 2, and Ki67 was analyzed by immunohistochemistry. All patients were classified into the following categories: luminal A, luminal B, HER2 overexpression, and triple-negative subtypes. Result. The median follow-up time was 33 months. Luminal A tumors had the lowest rate of tumor progression (0%, ), while luminal B, HER2 over-expression, and triple-negative subtypes were associated with an increased risk of tumor progression (15.4, 19.2, 15.4%). Clinicopathological subtypes retained independent prognostic significance ( ). There were significant differences by Cox model analyzed in age, menopause, lymph node metastasis, and HER2 for the event of death and tumor progression ( ), and there were significant differences only in chemotherapy for the event, respectively ( ). Conclusion. Clinicopathological subtypes of breast cancer could robustly identify the risk of death and tumor progression and were significant in making therapeutic decision. HER2 was the important poor indicator. The chemotherapy intensity would be enhanced for patients with luminal B, especially for HER2 over-expression subgroup. 1. Introduction The 12th St. Gallen International Breast Cancer Conference (2011) Expert Panel adopted a new approach towards classifying 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 factors rather than gene expression array criteria, including luminal A (LA) and luminal B (LB) breast tumors, overexpression of human epidermal growth factor receptor 2 (HER2), and triple-negative breast cancer (TNBC) [1]. Clinicopathological subtypes are becoming increasingly relevant to both the diagnosis of breast cancer patients with different prognoses and their therapies [2]. Hormone
References
[1]
A. Goldhirsch, W. C. Wood, A. S. Coates, R. D. Gelber, B. Thürlimann, and H.-J. Senn, “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,” Annals of Oncology, vol. 22, no. 8, pp. 1736–1747, 2011.
[2]
H. Mersin, K. Gülben, U. Berbero？lu et al., “Prognostic factors affecting postmastectomy locoregional recurrence in patients with early breast cancer: are intrinsic subtypes effective?” World Journal of Surgery, vol. 35, no. 10, pp. 2196–2202, 2011.
[3]
K. R. Bauer, M. Brown, R. D. Cress, C. A. Parise, and V. Caggiano, “Descriptive analysis of estrogen receptor (ER)-negative, progesterone receptor (PR)-negative, and HER2-negative invasive breast cancer, the so-called triple-negative phenotype: a population-based study from the California Cancer Registry,” Cancer, vol. 109, no. 9, pp. 1721–1728, 2007.
[4]
W. Chen, Z. Jiang, Z. Shao, Q. Sun, and K. Shen, “An economic evaluation of adjuvant trastuzumab therapy in HER2-positive early breast cancer,” Value in Health, vol. 12, no. 3, pp. S82–S84, 2009.
[5]
J. M. Harvey, G. M. Clark, C. K. Osborne, and D. C. Allred, “Estrogen receptor status by immunohistochemistry is superior to the ligand-binding assay for predicting response to adjuvant endocrine therapy in breast cancer,” Journal of Clinical Oncology, vol. 17, no. 5, pp. 1474–1481, 1999.
[6]
M. C. U. Cheang, S. K. Chia, D. Voduc et al., “Ki67 index, HER2 status, and prognosis of patients with luminal B breast cancer,” Journal of the National Cancer Institute, vol. 101, no. 10, pp. 736–750, 2009.
[7]
C. Desantis, R. Siegel, P. Bandi, and A. Jemal, “Breast cancer statistics, 2011,” CA Cancer Journal for Clinicians, vol. 61, no. 6, pp. 409–418, 2011.
[8]
C. La Vecchia, C. Bosetti, F. Lucchini et al., “Cancer mortality in Europe, 2000–2004, and an overview of trends since 1975,” Annals of Oncology, vol. 21, no. 6, pp. 1323–1360, 2009.
[9]
F. C. Geyer, D. N. Rodrigues, B. Weigelt, and J. S. Reis-Filho, “Molecular classification of estrogen receptor-positive/luminal breast cancers,” Advances in Anatomic Pathology, vol. 19, no. 1, pp. 39–53, 2012.
[10]
F. Rastelli, S. Biancanelli, A. Falzetta et al., “Triple-negative breast cancer: current state of the art,” Tumori, vol. 96, no. 6, pp. 875–888, 2010.
[11]
Y. Akasbi, S. Bennis, F. Abbass et al., “Clinicopathological, therapeutic and prognostic features of the triple-negative tumors in moroccan breast cancer patients (experience of Hassan II university hospital in Fez),” BMC Research Notes, vol. 4, article 500, 2011.
[12]
S. J. Howell, A. M. Wardley, and A. C. Armstrong, “Re: Ki67 index, HER2 status, and prognosis of patients with luminal B breast cancer,” Journal of the National Cancer Institute, vol. 101, no. 24, pp. 1730–1731, 2009.
[13]
G. Tancini and A. Rossi, “Surgery and chemotherapy in early breast cancer,” Schweizerische Medizinische Wochenschrift, vol. 107, no. 28, pp. 1005–1007, 1977.
[14]
H. Jinno, T. Ikeda, K. Kubouchi, K. Fujiwara, and M. Kitajima, “Adjuvant chemotherapy for breast cancer–a current controversy,” Gan To Kagaku Ryoho, vol. 31, no. 2, pp. 176–180, 2004.
[15]
J. Chilcott, M. Lloyd Jones, and A. Wilkinson, “Docetaxel for the adjuvant treatment of early node-positive breast cancer: a single technology appraisal,” Health Technology Assessment, vol. 13, supplement 1, pp. 7–13, 2009.
