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Table 1. AJCC staging for PDAC
Stage 0 Tis N0 M0
Stage IA T1 N0 M0
Stage IB T2 N0 M0
Stage IIA T3 N0 M0
Stage IIB T1, T2, T3 N1 M0
Stage III T1, T2, T3, N2 M0
T4 Any M0
Stage IV Any Any M1
T Primary Tumor
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor
Tis Carcinoma in situ, including:
High-grade pancreatic intraepithelial neoplasia
Intraductal papillary mucinous neoplasm with high-grade dysplasia
Intraductal tubulopapillary neoplasm with high-grade dysplasia
Mucinous cystic neoplasm with high-grade dysplasia
T1 Largest tumor diameter < 2 cm
T1a Largest tumor diameter ≤ 0.5 cm
T1b Largest tumor diameter > 0.5 cm and < 1 cm
T1c Largest tumor diameter 1-2 cm
T2 Largest tumor diameter > 2 cm and ≤ 4 cm
T3 Largest tumor diameter > 4 cm
T4 Tumor involves the celiac axis, superior mesenteric artery, and/or common hepatic artery, regardless of size
N Regional Lymph Nodes
Nx Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis in 1-3 regional lymph nodes
N2 Metastasis in ≥ 4 regional lymph nodes
M Distant Metastasis
M0 No distant metastasis
M1 Distant Metastasis

complete these potentially curative regimens will recur and die of their disease. Currently, neoadjuvant
[14]
strategies are being evaluated and may prove more beneficial in patients with resectable disease . Notably,
complete neoadjuvant treatment is considered the standard of care for patients with borderline resectable
and locally advanced diseases at many pancreatic cancer centers. The benefit of chemoradiation has not
been clearly established, but it is commonly incorporated in neoadjuvant paradigms, especially in cases of
borderline resectable or locally advanced disease . Locally advanced (Stage III that is T4) and metastatic
[15]
(Stage IV) PDAC are treated with palliative chemotherapy. Appropriate regimens for fit patients include
FOLFIRINOX or gemcitabine/nanoalbumin-bound (nab-) paclitaxel (GnP), which can extend median
survival to 11.5 months [1,16] . Single-agent gemcitabine can be given to patients with poorer performance
status to provide clinical benefit . Of note, PDAC is generally unresponsive to immunotherapy [18,19] .
[17]
Markers of response to immune checkpoint inhibitors - high microsatellite instability (MSI-H) and
mismatch repair deficiency (dMMR) - occur in less than 2% of PDAC patients [20,21] , but even in this small
group, responses to immunotherapy are lower when compared to other patients with MSI-H/dMMR solid
[22]
tumors .