適用于：乳腺浸潤性癌，乳腺導(dǎo)管原位癌。

T-----原發(fā)腫瘤

TX     原發(fā)腫瘤無法評(píng)估；

T0     無原發(fā)腫瘤證據(jù)；

Tis（DCIS）    導(dǎo)管原位癌；

Tis（Paget）   乳頭Paget病，乳腺實(shí)質(zhì)中無浸潤癌和/或原位癌。伴有Paget病的乳腺實(shí)質(zhì)腫瘤應(yīng)根據(jù)實(shí)質(zhì)病變的大小和特征進(jìn)行分期，并對(duì)paget病加以注明；

T1     腫瘤最大徑≤20mm；

T1mi     微小浸潤癌，腫瘤最大徑≤1mm；

T1a     1mm＜腫瘤最大徑≤5mm；

T1b     5mm＜腫瘤最大徑≤10mm；

T1c     10mm＜腫瘤最大徑≤20mm；

T2     20mm＜腫瘤最大徑≤50mm；

T3     腫瘤最大徑＞50mm；

T4     任何腫瘤大小，侵及胸壁或皮膚（潰瘍或者衛(wèi)星結(jié)節(jié)形成）；

T4a     侵及胸壁，單純的胸肌受累不在此列；

T4b     沒有達(dá)到炎性乳癌診斷標(biāo)準(zhǔn)的皮膚的潰瘍和/或衛(wèi)星結(jié)節(jié)和/或水腫（包括橘皮樣變）；

T4c     同時(shí)存在T4a和T4b；

T4d     炎性乳癌；

pN-----區(qū)域淋巴結(jié)

pNX     區(qū)域淋巴結(jié)無法評(píng)估（先行切除或未切除）；

pN0     無區(qū)域淋巴結(jié)轉(zhuǎn)移證據(jù)或者只有孤立的腫瘤細(xì)胞群(ITCs)；

pN0（i ）     區(qū)域淋巴結(jié)中可見孤立的腫瘤細(xì)胞群(ITCs≤0.2mm)；

pN0(mol )      無ITCs ,但PCR陽性（RT-PCR）；

pN1         

pN1mi     微轉(zhuǎn)移（ 最大直徑>0.2mm，或單個(gè)淋巴結(jié)單張組織切片中腫瘤細(xì)胞數(shù)量超過200個(gè)，但最大直徑≤2mm）；

pN1a     1-3枚腋窩淋巴結(jié)轉(zhuǎn)移，至少1處轉(zhuǎn)移灶＞2mm；

pN1b     內(nèi)乳淋巴結(jié)轉(zhuǎn)移（包括微轉(zhuǎn)移）

pN1c     pN1a pN1b；

pN2     4-9個(gè)患側(cè)腋窩淋巴結(jié)轉(zhuǎn)移；或臨床上發(fā)現(xiàn)患側(cè)內(nèi)乳淋巴結(jié)轉(zhuǎn)移而無腋窩淋巴結(jié)轉(zhuǎn)移；

pN2a     4-9個(gè)患側(cè)腋窩淋巴結(jié)轉(zhuǎn)移，至少1處轉(zhuǎn)移灶>2mm；

pN2b     有臨床轉(zhuǎn)移征象的同側(cè)內(nèi)乳淋巴結(jié)轉(zhuǎn)移，但無腋窩淋巴結(jié)轉(zhuǎn)移；

pN3     10個(gè)或10個(gè)以上患側(cè)腋窩淋巴結(jié)轉(zhuǎn)移；或鎖骨下淋巴結(jié)轉(zhuǎn)移；或臨床表現(xiàn)有患側(cè)內(nèi)乳淋巴結(jié)轉(zhuǎn)移伴1個(gè)以上腋窩淋巴結(jié)轉(zhuǎn)移；或3個(gè)以上腋窩淋巴結(jié)轉(zhuǎn)移伴無臨床表現(xiàn)的鏡下內(nèi)乳淋巴結(jié)轉(zhuǎn)移；或鎖骨上淋巴結(jié)轉(zhuǎn)移；

pN3a     10個(gè)或10個(gè)以上同側(cè)腋窩淋巴結(jié)轉(zhuǎn)移（至少1處轉(zhuǎn)移灶>2mm）或鎖骨下淋巴結(jié)（Ⅲ區(qū)腋窩淋巴結(jié)）轉(zhuǎn)移；

pN3b     有臨床征象的同側(cè)內(nèi)乳淋巴結(jié)轉(zhuǎn)移，并伴1個(gè)以上腋窩淋巴結(jié)轉(zhuǎn)移；或3個(gè)以上腋窩淋巴結(jié)轉(zhuǎn)移，通過前哨淋巴結(jié)活檢發(fā)現(xiàn)內(nèi)乳淋巴結(jié)轉(zhuǎn)移，但無臨床征象；

pN3c     同側(cè)鎖骨上淋巴結(jié)轉(zhuǎn)移；

M-----遠(yuǎn)處轉(zhuǎn)移

M0     無臨床或者影像學(xué)證據(jù)；

cM0（i ）     無臨床或者影像學(xué)證據(jù)，但是存在通過外周血分子檢測，骨髓穿刺，或非區(qū)域淋巴結(jié)區(qū)軟組織發(fā)現(xiàn)≤0.2mm的轉(zhuǎn)移灶，無轉(zhuǎn)移癥狀或體征；

M1     臨床有轉(zhuǎn)移征象，并且組織學(xué)證實(shí)轉(zhuǎn)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