This study was supported by National High Level Hospital Clinical Research Funding (2023-NHLHCRF-BQ-01) and the Youth Project of China-Japan Friendship Hospital (No.2020-1-QN-8).

The experimental animals were housed in the animal facility of the China-Japan Friendship Hospital, where the housing conditions met the animal feeding environment in line with China&#39;s national standard, Laboratory Animal-Requirements of Environment and Housing Facilities (GB14925-2010). All animal care procedures and experiments complied with the ARRIVE guidelines and were based on the 3R principles (reduction, replacement, refinement), adhering to the guidelines of the National Animal Welfare Law of China. BALB/c m...

<ol>
	<li>Thorlacius, G. E., Bjork, A., Wahren-Herlenius, M. Genetics and epigenetics of primary sjogren syndrome: Implications for future therapies. Nat Rev Rheumatol. 19 (5), 288-306 (2023).</li>
	<li>Bjordal, O., Norheim, K. B., Rodahl, E., Jonsson, R., Omdal, R. Primary Sjogren&#39;s syndrome and the eye. Surv Ophthalmol. 65 (2), 119-132 (2020).</li>
	<li>Zhong, H. et al. Hyperglobulinemia predicts increased risk of mortality in primary Sjogren&#39;s syndrome: Based on a Chinese multicentre registry. Mod Rheumatol. 34 (1), 137-143 (2023).</li>
	<li>Lin, W. et al. Interstitial lung disease in primary Sjogren&#39;s syndrome. BMC Pulm Med. 22 (1), 73 (2022).</li>
	<li>Aiyegbusi, O. et al. Renal disease in primary Sjogren&#39;s syndrome. Rheumatol Ther. 8 (1), 63-80 (2021).</li>
	<li>Liampas, A. et al. Primary sjogren syndrome-related peripheral neuropathy: A systematic review and meta-analysis. Eur J Neurol. 30 (1), 255-265 (2023).</li>
	<li>Wu, J. et al. Clinical and laboratory features of primary Sjogren&#39;s syndrome complicated with mild to severe thrombocytopenia. Ann Transl Med. 10 (6), 300 (2022).</li>
	<li>Zhong, H. et al. Primary Sjogren&#39;s syndrome is associated with increased risk of malignancies besides lymphoma: A systematic review and meta-analysis. Autoimmun Rev. 21 (5), 103084 (2022).</li>
	<li>Goulabchand, R. et al. Cancer incidence in primary Sjogren&#39;s syndrome: Data from the French hospitalization database. Autoimmun Rev. 20 (12), 102987 (2021).</li>
	<li>Witkowski Durand Viel, P. et al. Chronological interplay, clinical features, and treatments among patients with cancer and primary Sjogren&#39;s syndrome. Cancer Immunol Immunother. 72 (12), 4309-4322 (2023).</li>
	<li>Xu, Y. et al. The prevalence and clinical characteristics of primary Sjogren&#39;s syndrome patients with lung cancer: An analysis of ten cases in China and literature review. Thorac Cancer. 6 (4), 475-479 (2015).</li>
	<li>Shi, L., Du, X., Li, J., Zhang, G. Bioinformatics and systems biology approach to identify the pathogenetic link between psoriasis and cardiovascular disease. Clin Cosmet Investig Dermatol. 16, 2283-2295 (2023).</li>
	<li>Xu, R., Ma, L. L., Cui, S., Chen, L., Xu, H. Bioinformatics and systems biology approach to identify the pathogenetic link between heart failure and sarcopenia. Arq Bras Cardiol. 120 (10), e20220874 (2023).</li>
	<li>Lv, Y. et al. Bioinformatics and systems biology approach to identify the pathogenetic link of long COVID and myalgic encephalomyelitis/chronic fatigue syndrome. Front Immunol. 13, 952987 (2022).</li>
	<li>Barrett, T. et al. Ncbi geo: Archive for functional genomics data sets--update. Nucleic Acids Res. 41 (Database issue), D991-995 (2013).</li>
	<li>Stelzer, G. et al. The GeneCards suite: From gene data mining to disease genome sequence analyses. Curr Protoc Bioinformatics. 54, 1.30.1-1.30.33 (2016).</li>
	<li>Liu, S. et al. Three differential expression analysis methods for RNA sequencing: limma, EdgeR, DESeq2. J Vis Exp. 175, 62528 (2021).</li>
	<li>Zhou, Y. et al. Metascape provides a biologist-oriented resource for the analysis of systems-level datasets. Nat Commun. 10 (1), 1523 (2019).</li>
	<li>Szklarczyk, D. et al. The string database in 2023: Protein-protein association networks and functional enrichment analyses for any sequenced genome of interest. Nucleic Acids Res. 51 (D1), D638-D646 (2023).</li>
	<li>Shannon, P. et al. Cytoscape: A software environment for integrated models of biomolecular interaction networks. Genome Res. 13 (11), 2498-2504 (2003).</li>
	<li>Hill, W. et al. Lung adenocarcinoma promotion by air pollutants. Nature. 616 (7955), 159-167 (2023).</li>
	<li>Piao, C. H. et al. PM2.5 exposure regulates th1/th2/th17 cytokine production through NF-&#954;&#946; signaling in combined allergic rhinitis and asthma syndrome. Int Immunopharmacol. 119, 110254 (2023).</li>
	<li>Desjardins, P., Hansen, J. B., Allen, M. Microvolume protein concentration determination using the nanodrop 2000c spectrophotometer. J Vis Exp. 33, 1610 (2009).</li>
	<li>Luo, J. et al. Distinct clinical phenotypes of primary Sjogren&#39;s syndrome differ by onset age: A retrospective study of 742 cases and review of the literature. Clin Exp Rheumatol. 40 (12), 2373-2380 (2022).</li>
	<li>Luppi, F. et al. Lung complications of Sjogren syndrome. Eur Respir Rev. 29 (157), (2020).</li>
	<li>Berardicurti, O. et al. Interstitial lung disease and pulmonary damage in primary Sjogren&#39;s syndrome: A systematic review and meta-analysis. J Clin Med. 12 (7), 2586 (2023).</li>
	<li>Roca, F. et al. Interstitial lung disease in primary Sjogren&#39;s syndrome. Autoimmun Rev. 16 (1), 48-54 (2017).</li>
	<li>Fisher, D. A. et al. Diagnosis and treatment of lung cancer in the setting of interstitial lung disease. Radiol Clin North Am. 60 (6), 993-1002 (2022).</li>
	<li>Okudela, K. et al. Implications of thyroid transcription factor-1 gene methylation in carcinogenesis of interstitial pneumonia-related non-terminal respiratory unit lung adenocarcinoma. Int J Clin Exp Pathol. 15 (3), 120-130 (2022).</li>
	<li>Sekine, A. et al. Disease activity of lung cancer at the time of acute exacerbation of interstitial lung disease during cytotoxic chemotherapy. Thorac Cancer. 13 (17), 2443-2449 (2022).</li>
	<li>Glaviano, A. et al. PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer. Mol Cancer. 22 (1), 138 (2023).</li>
	<li>Ediriweera, M. K., Tennekoon, K. H., Samarakoon, S. R. Role of the PI3K/AKT/mTOR signaling pathway in ovarian cancer: Biological and therapeutic significance. Semin Cancer Biol. 59, 147-160 (2019).</li>
	<li>Hoxhaj, G. Manning, B. D. The PI3K-AKT network at the interface of oncogenic signalling and cancer metabolism. Nat Rev Cancer. 20 (2), 74-88 (2020).</li>
	<li>Liu, R. et al. PI3K/AKT pathway as a key link modulates the multidrug resistance of cancers. Cell Death Dis. 11 (9), 797 (2020).</li>
	<li>Manogaran, P., Beeraka, N. M., Paulraj, R. S., Sathiyachandran, P., Thammaiappa, M. Impediment of cancer by dietary plant-derived alkaloids through oxidative stress: Implications of PI3K/AKT pathway in apoptosis, autophagy, and ferroptosis. Curr Top Med Chem. 23 (10), 860-877 (2023).</li>
	<li>Acosta-Martinez, M. Cabail, M. Z. The PI3K/AKT pathway in meta-inflammation. Int J Mol Sci. 23 (23), 15330 (2022).</li>
	<li>Chen, G. Y. et al. Prediction of Rhizoma Drynariae targets in the treatment of osteoarthritis based on network pharmacology and experimental verification. Evid Based Complement Alternat Med. 2021, 5233462 (2021).</li>
	<li>Chen, G. Y. et al. Total flavonoids of Rhizoma Drynariae restore the MMP/TIMP balance in models of osteoarthritis by inhibiting the activation of the NF-&#954;&#946; and PI3K/AKT pathways. Evid Based Complement Alternat Med. 2021, 6634837 (2021).</li>
	<li>Chen, G. Y. et al. Network pharmacology analysis and experimental validation to investigate the mechanism of total flavonoids of Rhizoma Drynariae in treating rheumatoid arthritis. Drug Des Devel Ther. 16, 1743-1766 (2022).</li>
	<li>Yao, C. Narumiya, S. Prostaglandin-cytokine crosstalk in chronic inflammation. Br J Pharmacol. 176 (3), 337-354 (2019).</li>
	<li>Liu, P. et al. NOD-like receptor signaling in inflammation-associated cancers: From functions to targeted therapies. Phytomedicine. 64, 152925 (2019).</li>
	<li>Damasceno, L. E. A. et al. PKM2 promotes Th17 cell differentiation and autoimmune inflammation by fine-tuning stat3 activation. J Exp Med. 217 (10), e20190613 (2020).</li>
	<li>Banerjee, S., Biehl, A., Gadina, M., Hasni, S., Schwartz, D. M. JAK-STAT signaling as a target for inflammatory and autoimmune diseases: Current and future prospects. Drugs. 77 (5), 521-546 (2017).</li>
	<li>Jiramongkol, Y. Lam, E. W. FOXO transcription factor family in cancer and metastasis. Cancer Metastasis Rev. 39 (3), 681-709 (2020).</li>
	<li>Tong, X. et al. Targeting cell death pathways for cancer therapy: Recent developments in necroptosis, pyroptosis, ferroptosis, and cuproptosis research. J Hematol Oncol. 15 (1), 174 (2022).</li>
	<li>Ou, H. L. et al. Cellular senescence in cancer: From mechanisms to detection. Mol Oncol. 15 (10), 2634-2671 (2021).</li>
	<li>Felten, R. et al. Interleukin 6 receptor inhibition in primary Sjogren syndrome: A multicentre double-blind randomised placebo-controlled trial. Ann Rheum Dis. 80 (3), 329-338 (2021).</li>
	<li>Bardsen, K. et al. Interleukin-1-related activity and hypocretin-1 in cerebrospinal fluid contribute to fatigue in primary Sjogren&#39;s syndrome. J Neuroinflammation. 16 (1), 102 (2019).</li>
	<li>Barrera, M. J. et al. Tofacitinib counteracts il-6 overexpression induced by deficient autophagy: Implications in Sjogren&#39;s syndrome. Rheumatology (Oxford). 60 (4), 1951-1962 (2021).</li>
	<li>Liu, H., Zhou, Q., Xu, X., Du, Y., Wu, J. ASPM and TROAP gene expression as potential malignant tumor markers. Ann Transl Med. 10 (10), 586 (2022).</li>
	<li>Qian, X. et al. CCNB2 overexpression is a poor prognostic biomarker in Chinese NSCLC patients. Biomed Pharmacother. 74, 222-227 (2015).</li>
	<li>Mo, M. L. et al. Use of serum circulating CCNB2 in cancer surveillance. Int J Biol Markers. 25 (4), 236-242 (2010).</li>
	<li>Li, L. et al. NuSAP is degraded by APC/C-Cdh1 and its overexpression results in mitotic arrest dependent of its microtubules&#39; affinity. Cell Signal. 19 (10), 2046-2055 (2007).</li>
	<li>Fabbro, M. et al. Cdk1/Erk2- and Plk1-dependent phosphorylation of a centrosome protein, cep55, is required for its recruitment to midbody and cytokinesis. Dev Cell. 9 (4), 477-488 (2005).</li>
	<li>Jeffery, J., Sinha, D., Srihari, S., Kalimutho, M., Khanna, K. K. Beyond cytokinesis: The emerging roles of CEP55 in tumorigenesis. Oncogene. 35 (6), 683-690 (2016).</li>
	<li>Feng, Z. et al. Overexpression of abnormal spindle-like microcephaly-associated (ASPM) increases tumor aggressiveness and predicts poor outcome in patients with lung adenocarcinoma. Transl Cancer Res. 10 (2), 983-997 (2021).</li>
	<li>Zheng, H. et al. Comprehensive pan-cancer analysis reveals NuSAP1 is a novel predictive biomarker for prognosis and immunotherapy response. Int J Biol Sci. 19 (14), 4689-4708 (2023).</li>
	<li>Verstappen, G. M., Pringle, S., Bootsma, H., Kroese, F. G. M. Epithelial-immune cell interplay in primary sjogren syndrome salivary gland pathogenesis. Nat Rev Rheumatol. 17 (6), 333-348 (2021).</li>
	<li>El Rayes, T. et al. Lung inflammation promotes metastasis through neutrophil protease-mediated degradation of Tsp-1. Proc Natl Acad Sci U S A. 112 (52), 16000-16005 (2015).</li>
	<li>Zhao, L. et al. PM2.5 and serum metabolome and insulin resistance, potential mediation by the gut microbiome: A population-based panel study of older adults in china. Environ Health Perspect. 130 (2), 27007 (2022).</li>
	<li>Li, J. et al. PM2.5 exposure perturbs lung microbiome and its metabolic profile in mice. Sci Total Environ. 721 137432 (2020).</li>
	<li>Liao, J. H. et al. Network pharmacology-based strategy to investigate the mechanisms of artemisinin in treating primary sjogren&#39;s syndrome. BMC Immunol. 25 (1), 16 (2024).</li>
	<li>Hu, Q. et al. JAK/STAT pathway: Extracellular signals, diseases, immunity, and therapeutic regimens. Front Bioeng Biotechnol. 11, 1110765 (2023).</li>
	<li>Xue, C. et al. Evolving cognition of the JAK-STAT signaling pathway: Autoimmune disorders and cancer. Signal Transduct Target Ther. 8 (1), 204 (2023).</li>
</ol>

Although pSS is considered a disease primarily characterized by the invasion of exocrine glands, the damage of extra-glands cannot be ignored24. The lungs represent a target organ for pSS, and lung involvement is a common extra-glandular manifestation of pSS, typically involving lymphocytic infiltration of the bronchial mucosa and pulmonary interstitium25. Research indicates that at least 20% of pSS patients experience interstitial lung disease (ILD)26</su...

Primary Sj&#246;gren&#39;s syndrome (pSS) is an autoimmune disease characterized by lymphocytic infiltration of the exocrine glands and leads to the clinical symptoms of dry eyes (xerophthalmia) and dry mouth (xerostomia)1,2. pSS is also usually accompanied by extra-glandular manifestations of involvement, including hyperglobulinemia3, interstitial lung disease4, renal tubular acidosis5, neurological damage6, and thrombocytopenia7, which constitute the main adverse prognostic factors. In recent years, a line of studies has demonstrated that pSS is generally accompanied by an increased prevalence of cancer, including hematological malignancies and solid tumors8,9,10. Lung cancer is one of the most common pSS-related cancers, especially lung adenocarcinoma (LUAD)11.
Collectively, further investigation suggested that pSS with LUAD may have some underlying common pathogenesis. According to our current knowledge, no special studies yet explain the common mechanisms between the two diseases. Recently, bioinformatics analysis offer a potential possibility for us to reveal potentially shared disease mechanisms across species12,13,14. To further reveal the underlying mechanisms, bioinformatics analysis is used for the analysis of common targets and signaling pathways between pSS and LUAD, and animal models are subsequently established for experimental verification. Revealing these mechanisms may help provide an evidence base for clinical prevention of LUAD in pSS patients.
This study used the GEO and Genecard databases to retrieve the relevant genes associated with pSS and LUAD. Afterward, DEGs associated with pSS and LUAD were screened as pSS-LUAD-DEGs. We performed KEGG and GO enrichment analyses to elucidate the significant biological functions of pSS-LUAD-DEGs. PPI network construction was used to identify core targets, and we further assessed hub gene diagnostic accuracy through ROC curve analyses. We used NOD/Ltj mice as pSS animal models stimulated with particulate matter 2.5 (PM2.5) to generate an inflammatory reaction. QPCR, ELISA, and western blotting were performed to verify the study experimentally. Overall, the results here indicate that carcinogenesis induced by the pulmonary inflammatory microenvironment may be a critical reason for the high incidence of LUAD in pSS patients. It also suggests that the occurrence of LUAD in pSS patients may be prevented by blocking-related mechanisms.

<table border="1" fo:keep-together.within-page="1" fo:keep-with-next.within-page="always">
	<tbody>
		<tr>
			<td>3-Color Prestained Protein Marker</td>
			<td>Epizyme</td>
			<td>WJ103</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>Antibody Dilution Buffer</td>
			<td>Epizyme</td>
			<td>PS119</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>BCA Protein Quantification Kit</td>
			<td>Epizyme</td>
			<td>ZJ101</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>Cytoscape 3.7.1 software</td>
			<td>National Institute of General Medical Sciences (NIGMS), National Institutes of Health (NIH)</td>
			<td>Version 3.7.1.</td>
			<td>Open-source software for biological network analysis and visualization</td>
		</tr>
		<tr>
			<td>ECL Luminous Fluid</td>
			<td>Epizyme</td>
			<td>SQ203</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>Electrophoresis Buffer</td>
			<td>Epizyme</td>
			<td>PS105S</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>GraphPad Prism 10.0</td>
			<td>GraphPad</td>
			<td>Version 10.0</td>
			<td>Data analysis</td>
		</tr>
		<tr>
			<td>HRP-conjugated Goat anti-Rabbit IgG (H+L) (AS014)</td>
			<td>abclonal</td>
			<td>AS014</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>JAK2 Antibody</td>
			<td>Cell Signaling Technology</td>
			<td>3230T</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>Mouse IL-1&#946; ELISA Kit</td>
			<td>Beijing&#160;4A&#160;Biotech Co., Ltd</td>
			<td>CME0015</td>
			<td>ELISA</td>
		</tr>
		<tr>
			<td>Mouse IL-6 ELISA Kit</td>
			<td>Beijing&#160;4A&#160;Biotech Co., Ltd</td>
			<td>CME0006</td>
			<td>ELISA</td>
		</tr>
		<tr>
			<td>Phosphatase Inhibitor Cocktail (100&#215;)</td>
			<td>Epizyme</td>
			<td>GRF102</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>Phospho-JAK2 (Tyr1007/1008) Antibody</td>
			<td>Cell Signaling Technology</td>
			<td>3776S</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>Phospho-STAT3 (Tyr705) Antibody</td>
			<td>Cell Signaling Technology</td>
			<td>9145S</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>Protease Inhibitor Cocktail (100&#215;)</td>
			<td>Epizyme</td>
			<td>GRF101</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>Protein Free Rapid Blocking Buffer (5&#215;)</td>
			<td>Epizyme</td>
			<td>PS108</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>PVDF membrane</td>
			<td>Millipore</td>
			<td>IPVH00010</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>R software</td>
			<td>R Foundation for Statistical Computing</td>
			<td>Not Applicable</td>
			<td>Statistical analysis software and programming language used for data analysis, visualization, and machine learning applications</td>
		</tr>
		<tr>
			<td>Radio Immunoprecipitation Assay</td>
			<td>Epizyme</td>
			<td>PC101</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>Reverse Transcription System</td>
			<td>Promega</td>
			<td>A3500</td>
			<td>PCR</td>
		</tr>
		<tr>
			<td>SDS-PAGE</td>
			<td>Epizyme</td>
			<td>LK303</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>SDS-PAGE Protein Loading Buffer (5&#215;)</td>
			<td>Epizyme</td>
			<td>LT103</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>STAT3 Antibody</td>
			<td>Cell Signaling Technology</td>
			<td>9139S</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>SYBR Green Realtime PCR Master Mix</td>
			<td>TOYOBO</td>
			<td>QPK-201</td>
			<td>PCR</td>
		</tr>
		<tr>
			<td>TBST (10&#215;)</td>
			<td>Epizyme</td>
			<td>PS103</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>Western Blot Transfer Buffer (10&#215;)</td>
			<td>Epizyme</td>
			<td>PS109</td>
			<td>Western Blot</td>
		</tr>
		<tr>
			<td>&#946;-Actin Antibody</td>
			<td>abclonal</td>
			<td>AC026</td>
			<td>Western Blot</td>
		</tr>
	</tbody>
</table>

primary sjogren's syndrome associated with lung adenocarcinoma: probing the potential common pathogenic mechanisms and experimental verification

This study aimed to probe the potential common pathogenic mechanisms linking primary Sjogren's syndrome (pSS) and lung adenocarcinoma (LUAD) through bioinformatics analysis and experimental verification. The relevant genes associated with pSS and LUAD were retrieved from the Gene Expression Omnibus (GEO) database and Genecard database. Subsequently, differentially expressed genes (DEGs) associated with pSS and LUAD were screened as pSS-LUAD-DEGs. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analyses were performed to elucidate the significant biological functions of pSS-LUAD-DEGs. Core targets were identified by constructing the protein-protein interaction (PPI) network, further assessing hub gene diagnostic accuracy through Receiver Operating Characteristic (ROC) curve analyses. In this study, NOD/Ltj mice served as pSS animal models and were stimulated with particulate matter 2.5 (PM2.5) to generate an inflammatory reaction. Quantitative real-time polymerase chain reaction (qPCR), enzyme-linked immunosorbent assay (ELISA), and western blotting were employed for relevant molecular biology experiment verification. The results revealed through KEGG and GO enrichment analyses indicate that inflammation plays a critical role in linking pSS and LUAD. IL6, CCNA2, JAK2, IL1B, ASPM, CCNB2, NUSAP1, and CEP55 were determined as key targets of pSS-LUAD. BALB/c mice and NOD/Ltj mice exhibited enhanced expression of inflammatory cytokines IL-6 and IL-1&#946; in lung tissues following 21 days of stimulation with PM2.5, activating the JAK2/STAT3 signaling pathway and up-regulating the expression of tumor-associated genes CCNA2, CCNB2, and CEP55, with NOD/Ltj mice exhibiting more pronounced changes than BALB/c mice. This protocol demonstrates that carcinogenesis induced by the pulmonary inflammatory microenvironment may be a key reason for the high incidence of LUAD in pSS patients. Additionally, blocking-related mechanisms may help prevent the occurrence of LUAD in pSS patients.

A total of 3290 DEGs were identified from the 23348 genes in GSE84884 (pSS), including 2659 up-regulated genes and 631 down-regulated genes (Figure 1A). For GSE51092 (pSS), a total of 3290 DEGs were identified from the 11409 genes, including 667 up-regulated genes and 587 down-regulated genes (Figure 1B). The GeneCards database obtained 102 ovarian pSS-related DEGs, and the correlation score of screening criteria was &#8805;20. The union and deduplication of the...

This manuscript describes the operational procedures and precautions to probe the potential common pathogenic mechanisms linking primary Sjogren's syndrome and lung adenocarcinoma through bioinformatics analysis and experimental verification.

Primary Sjogren's Syndrome Associated with Lung Adenocarcinoma: Probing the Potential Common Pathogenic Mechanisms and Experimental Verification

This study aimed to probe the potential common pathogenic mechanisms linking primary Sjogren's syndrome (pSS) and lung adenocarcinoma (LUAD) through ...