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适用于：乳腺浸润性癌，乳腺导管原位癌。 T-----原发肿瘤 TX 原发肿瘤无法评估； T0 无原发肿瘤证据； Tis（DCIS） 导管原位癌； Tis（Paget） 乳头Paget病，乳腺实质中无浸润癌和/或原位癌。伴有Paget病的乳腺实质肿瘤应根据实质病变的大小和特征进行分期，并对paget病加以注明； T1 肿瘤最大径≤20mm； T1mi 微小浸润癌，肿瘤最大径≤1mm； T1a 1mm＜肿瘤最大径≤5mm； T1b 5mm＜肿瘤最大径≤10mm； T1c 10mm＜肿瘤最大径≤20mm； T2 20mm＜肿瘤最大径≤50mm； T3 肿瘤最大径＞50mm； T4 任何肿瘤大小，侵及胸壁或皮肤（溃疡或者卫星结节形成）； T4a 侵及胸壁，单纯的胸肌受累不在此列； T4b 没有达到炎性乳癌诊断标准的皮肤的溃疡和/或卫星结节和/或水肿（包括橘皮样变）； T4c 同时存在T4a和T4b； T4d 炎性乳癌； pN-----区域淋巴结 pNX 区域淋巴结无法评估（先行切除或未切除）； pN0 无区域淋巴结转移证据或者只有孤立的肿瘤细胞群(ITCs)； pN0（i ） 区域淋巴结中可见孤立的肿瘤细胞群(ITCs≤0.2mm)； pN0(mol ) 无ITCs ,但PCR阳性（RT-PCR）； pN1 pN1mi 微转移（ 最大直径>0.2mm，或单个淋巴结单张组织切片中肿瘤细胞数量超过200个，但最大直径≤2mm）； pN1a 1-3枚腋窝淋巴结转移，至少1处转移灶＞2mm； pN1b 内乳淋巴结转移（包括微转移） pN1c pN1a pN1b； pN2 4-9个患侧腋窝淋巴结转移；或临床上发现患侧内乳淋巴结转移而无腋窝淋巴结转移； pN2a 4-9个患侧腋窝淋巴结转移，至少1处转移灶>2mm； pN2b 有临床转移征象的同侧内乳淋巴结转移，但无腋窝淋巴结转移； pN3 10个或10个以上患侧腋窝淋巴结转移；或锁骨下淋巴结转移；或临床表现有患侧内乳淋巴结转移伴1个以上腋窝淋巴结转移；或3个以上腋窝淋巴结转移伴无临床表现的镜下内乳淋巴结转移；或锁骨上淋巴结转移； pN3a 10个或10个以上同侧腋窝淋巴结转移（至少1处转移灶>2mm）或锁骨下淋巴结（Ⅲ区腋窝淋巴结）转移； pN3b 有临床征象的同侧内乳淋巴结转移，并伴1个以上腋窝淋巴结转移；或3个以上腋窝淋巴结转移，通过前哨淋巴结活检发现内乳淋巴结转移，但无临床征象； pN3c 同侧锁骨上淋巴结转移； M-----远处转移 M0 无临床或者影像学证据； cM0（i ） 无临床或者影像学证据，但是存在通过外周血分子检测，骨髓穿刺，或非区域淋巴结区软组织发现≤0.2mm的转移灶，无转移症状或体征； M1 临床有转移征象，并且组织学证实转移灶大于0.2mm；
Rapid advances in both clinical and laboratory science and in translational research have raised questions about the ongoing relevance of TNM staging, especially in breast cancer. The TNM system was developed in 1959 in the absence of effective systemic therapy and based on limited understanding of the biology of breast cancer as well as the then-widely accepted paradigm of orderly progression for the tumor to regional nodes and thence to distant sites, which supported the use of the Halsted radical mastectomy introduced in the late 1800s. The TNM system was generated to reflect the risk of distant recurrence and death subsequent to local therapy, which at the time was almost universally aggressive surgery (radical mastectomy) and postoperative radiation to the chest wall. Therefore, the primary objective of TNM staging was to provide a standard nomenclature for prognosis of patients with newly diagnosed breast cancer, and its main clinical utility was to prevent apparently futile therapy in those patients who were destined to die rapidly in spite of aggressive local treatments. Over the succeeding decades, remarkable progress challenged this Halstedian view of tumor progression with the understanding of the potential for distant systemic spread of all invasive cancers irrespective of node involvement and with demonstration of the value of adjuvant systemic therapy. This led to (1) more limited surgical management, with breastconserving surgery being preferred for most patients with early-stage breast cancers and total mastectomy with axillary dissection for more advanced disease; (2) reduction in the extent of axillary staging, with sentinel lymph node biopsy becoming the leading approach for patients with clinically negative axillae; (3) dramatic improvements in the delivery and safety of radiation treatment; (4) the recognition that early (adjuvant) systemic therapy reduces the chance of recurrence and mortality; (5) the increasing implementation of preoperative (or neoadjuvant) systemic therapies for treatment of larger operable tumors and locally advanced breast cancer; and (6) a better understanding of biologic markers of prognosis and, perhaps more important, of prediction of response to selective categories of systemic therapy, such as those targeting cancer cells positive for ER and HER2 overexpression or amplification.3 Heretofore, TNM staging based solely on the anatomic extent of disease has been used as a prognostic guide to select whether to apply systemic therapy. Based on such progress, biologic factors—such as grade, hormone receptor expression, HER2 overexpression/amplification, and genomic panels—have become as or more important than the anatomic extent of disease to define prognosis, select the optimal combination of systemic therapies,3 and increasingly, influence the selection of locoregional treatments.4 Much of this biological information had started to appear at the time the 6th and 7th editions of the AJCC Cancer Staging Manual were being developed, but published information with high enough level of evidence to incorporate biomarkers into the TNM classification was lacking or incomplete. As an example, it has been known for several decades that the expression of the ER in primary breast cancer conferred a more favorable prognosis than its absence to groups of patients in various clinical stages. However, precise analysis to demonstrate that within specific TNM stages, the presence of ER modified prognosis was not available. Similar statements can be made about grade, markers of proliferation, and HER2. Population-based registries have started to collect information about hormone receptors only within the past 10–15 years, and information about HER2 was not integrated into national databases (National Cancer Database [NCDB]; National Program of Cancer Registries [NPCR]; Surveillance, Epidemiology, and End Results [SEER]; and others) until 2010. In the meantime, clinical practice evolved rapidly, integrating modern biological knowledge into the selection of systemic treatments.5 ER, PR, grade, and HER2 started to be collected by most clinical laboratories, and clinicians integrated these concepts into prognostication and selection of therapies. The widespread adoption of the concept of biologic intrinsic subtypes led to different treatment strategies for the three major biological subsets of breast cancer: (1) hormone receptor-positive (ER and/or PR positive), HER2-negative tumors (also referred to as luminal-type); (2) HER2-amplified or overexpressed breast cancers; and (3) breast cancers that do not express hormone receptors or HER2 (also known as triple-negative tumors).3 More recently, it also was recognized that in the presence of HER2 overexpression/amplification, the presence or absence of hormone receptor expression was associated with different prognoses and responsiveness to anti-HER2 therapy. Based on that observation, the HER2-positive population is now approached differently based on the expression of hormone receptors. These advances raise two questions. (1) Is anatomic-based TNM staging still relevant for breast cancer? (2) What, exactly, is the objective of TNM staging for patients with this disease? The answer to the first question is twofold: The TNM staging classification based solely on anatomical/histological parameters is clearly relevant to that part of the world where that is the only information available to practitioners. It also remains useful as the foundational basis of staging classification for areas of the world where biological information is an integral part of the initial evaluation. However, in these regions, staging needs to expand to incorporate the prognostic and predictive value of biomarkers. The second question, on the objective of TNM staging, has three potential answers: (1) to provide continuity to breast cancer investigators, in regards to studying categories of patients that accurately reflect prior groupings over the last six decades, (2) to permit current investigators |
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