Table 4.

Proteomic analysis of saliva and salivary gland tissue in SS patients with and without non-Hodgkin MALT lymphoma.

Author (year)	No. of subjects	Materials and methods	Findings
Hu S. et al., 2009 (44)	9 pSS 6 pSS/MALT 8 non-pSS controls	Parotid gland tissue 2-DGE, Weighted gene co-expression network analysis (WGCNA)	Six highly associated hub genes (involved in proteasome degradation, apoptosis, signal peptides (MHC) class I, complement activation, cell growth and death, and integrin-mediated cell adhesion) distinguished pSS from non-pSS control subjects. Eight hub genes (involved in translation, ribosome, protease degradation, signal peptides (MHC) class I, G13 signaling pathway, complement activation, and integrin-mediated cell adhesion) distinguished pSS/MALT from pSS.
Cui L. et al., 2017 (41)	6 pSS 6 pSS/MALT 6 HC	SWS 2-DGE/MS, ELISA	↑ α-enolase, cofilin-1, annexin A2 and Rho GDP-dissociation inhibitor 2 (RGI2) in pSS and pSS/MALT. ↑ α-enolase, cofilin-1 and RGI2 in pSS/MALT compared to pSS. The combination of the latter 3 antibodies yielded AUC 0.94 (86% sensitivity, 93% specificity in pSS vs HC) and AUC 0.86 (75% sensitivity, 94% specificity in pSS vs pSS/MALT)
Jazzar AA. et al., 2018 (42)	14 pSS/MALT (SS-M) 18 pSS high-risk of MALT (SS-HR) 19 pSS low-risk of MALT 19 pSS non-risk 14 SNOX, 18 HC	UWS parotid saliva LC-MS/MS ELISA	↑ levels of S100A8(calgranulin A) and S100A9 (calgranulin B) in parotid saliva of SS-HR and SS-M patients compared to HC. ↑ levels of S100A8/A9 in UWS in SS subgroups compared to HC and SNOX. The median concentration in SS-M were higher than in HC, SNOX and non-risk pSS patients. S100A8 and -A9 were 20-fold higher in UWS than parotid saliva.