SMAD4 Y353C promotes the progression of PDAC
Open accessAbstract
Background: SMAD4 is frequently inactivated and associated with a poor prognosis in pancreatic ductal adenocarcinoma (PDAC). Abnormal SMAD4 expression also plays an important role in the malignant progression of PDAC. Methods: We investigated SMAD4 status in PDAC by immunohistochemical methods to explore the relationships between SMAD4 expression and clinicopathological features and then detected SMAD4 mutations by Sanger sequencing in 95 patients with PDAC to identify new mutation sites in PDAC. We further evaluated the effects of a missense mutation, Y353C, in the SMAD4 MH2 domain, on cell proliferation and migration in vitro. Results: Immunohistochemistry showed that the expression of SMAD4 in PDAC carcinoma tissue was significantly lower than that in normal pancreatic tissue, and negative SMAD4 expression was closely related to tumour diameter, staging, lymph node metastasis and differentiation. Sanger sequencing analysis showed that the rate of SMAD4 mutation was 11.8% in 85 PDAC cases, and the novel SMAD4 Y353C missense mutation identified in this study promoted cell migration and invasion without affecting cell proliferation in vitro. Furthermore, SMAD4 Y353C resulted in reduced expression of E-cadherin and increased expression of Vimentin compared with wild-type SMAD4 overexpression. Conclusion: This study supports the key role of SMAD4 as a tumour suppressor gene in PDAC and shows that SMAD4 Y353C is associated with poor progression of PDAC.
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In a study involving 95 PDAC cases, SMAD4 Y353C mutation was identified in 75.7% of carcinoma tissues, correlating significantly with malignant phenotypes.
“In a study involving 95 PDAC cases, SMAD4 Y353C mutation, a novel mutation, was identified in 75.7% of carcinoma tissues, correlating significantly with malignant phenotypes.”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [70]
The Results (pages not specified) describe a study of 95 PDAC cases and identify Y353C as a novel mutation. But 75.7% refers to SMAD4 expression measurements, not the prevalence of Y353C; sequencing found SMAD4 mutations of any kind in 11.8% of 85 cases. The reported association with malignant clinical features concerns loss of SMAD4 expression, while Y353C was tested for effects on cell behaviour in vitro. (LLM, conf=0.90)
Experimental — accuracy not yet measuredDespite associations with malignant phenotypes, SMAD4 Y353C did not affect overall survival rate.
“Despite associations with malignant phenotypes, SMAD4 Y353C did not affect the overall survival rate.”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [70]
The Discussion reports that SMAD4 Y353C promoted cell migration and invasion, supporting its association with malignant phenotypes. The Results section on overall survival reports no statistically significant relationship for loss of SMAD4 expression in 73 patients (P = 0.053), not for the Y353C mutation specifically. The Conclusion says the relationship between Y353C and overall survival requires further study. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn PDAC, SMAD4 mutations promote tumor progression and metastasis, induce resistance to radiotherapy and correlate with poor prognosis.
“As aforementioned, in PDAC, SMAD4 mutations have profound implications, promoting tumor progression and metastasis, inducing resistance to radiotherapy and correlating with poor prognosis.”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [70]
The Results and Discussion (page not provided) report that SMAD4 Y353C promoted migration and invasion in PDAC cell lines, while loss of SMAD4 expression was associated with lymph node metastasis and other malignant features. The paper discusses reports linking SMAD4 alterations to poor prognosis, but its own cohort found no association between SMAD4 expression loss and overall survival. No passage found supports the claim that SMAD4 mutations induce resistance to radiotherapy. (LLM, conf=0.90)
Experimental — accuracy not yet measuredSMAD4 loss is associated with poor prognosis and shorter survival, but its impact on chemotherapy response may vary based on treatment regimens and disease stages.
“While SMAD4 loss is associated with poor prognosis and shorter survival, its impact on chemotherapy response may vary, based on specific treatment regimens and disease stages [64,70,71].”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [70]
The Background (page unavailable) reports that low SMAD4 expression has been linked to poor outcomes, and the Discussion cites a study finding shorter median survival with SMAD4 alterations. This paper’s own Results found no significant association between SMAD4 loss and overall survival (P = 0.053). Our copy does not address whether chemotherapy response varies by regimen or disease stage. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSMAD4 Y353C promoted EMT, increased cell migration and invasion, and altered E-cadherin and Vimentin expression.
“SMAD4 Y353C promoted epithelial–mesenchymal transition (EMT), increased cell migration and invasion, and altered E-cadherin and Vimentin expression.”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [70]
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Cites
Siegel, R. L., Miller, K. D., & Jemal, A. (2016) · CA: A Cancer Journal for Clinicians · doi:10.3322/caac.21332 · Cited by 16,003 · see citing works
Sørlie, T., Perou, C., Tibshirani, R., Aas, T., Geisler, S., Johnsen, H., Hastie, T., Eisen, M., van de Rijn, M., Jeffrey, S., et al. (2001) · Proceedings of the National Academy of Sciences of the United States of America · doi:10.1073/pnas.191367098 · Cited by 11,695 · see citing works
The Epithelial-Mesenchymal Transition Generates Cells with Properties of Stem Cells
Mani, S. A., Guo, W., Liao, M.-J., Eaton, E. N., Ayyanan, A., Zhou, A. Y., Brooks, M. W., Reinhard, F., Zhang, C. C., Shipitsin, M. V., et al. (2008) · Cell · doi:10.1016/j.cell.2008.03.027 · Cited by 8,679 · see citing works
FOLFIRINOX versus Gemcitabine for Metastatic Pancreatic Cancer
Conroy, T., Desseigne, F., Ychou, M., Bouché, O., Guimbaud, R., Bécouarn, Y., Adenis, A., Raoul, J.-L., Gourgou-Bourgade, S., de la Fouchardière, C., et al. (2011) · New England Journal of Medicine · doi:10.1056/nejmoa1011923 · Cited by 7,810 · see citing works
Core Signaling Pathways in Human Pancreatic Cancers Revealed by Global Genomic Analyses
Jones, S., Zhang, X., Parsons, D. W., Lin, J. C.-H., Leary, R. J., Angenendt, P., Mankoo, P., Carter, H., Kamiyama, H., Jimeno, A., et al. (2008) · Science · doi:10.1126/science.1164368 · Cited by 3,969 · see citing works
Transitions between epithelial and mesenchymal states: acquisition of malignant and stem cell traits
Polyak, K., & Weinberg, R. A. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2620 · Cited by 3,302 · see citing works
Hermann, P. C., Huber, S. L., Herrler, T., Aicher, A., Ellwart, J. W., Guba, M. O., Bruns, C. J., & Heeschen, C. (2007) · Cell stem cell · doi:10.1016/j.stem.2007.06.002 · Cited by 2,898 · see citing works
<i>DPC4</i> , A Candidate Tumor Suppressor Gene at Human Chromosome 18q21.1
Hahn, S. A., Schutte, M., Shamsul Hoque, A. T. M., Moskaluk, C. A., da Costa, L. T., Rozenblum, E., Weinstein, C. L., Fischer, A., Yeo, C. J., Hruban, R. H., et al. (1996) · Science · doi:10.1126/science.271.5247.350 · Cited by 2,337 · see citing works
Transcriptional control by the TGF‐β/Smad signaling system
Massagué, J., & Wotton, D. (2000) · The EMBO Journal · doi:10.1093/emboj/19.8.1745 · Cited by 1,969 · see citing works
Signal Transduction by the TGF-β Superfamily
Attisano, L., & Wrana, J. L. (2002) · Science · doi:10.1126/science.1071809 · Cited by 1,271 · see citing works
TGFβ–SMAD signal transduction: molecular specificity and functional flexibility
Schmierer, B., & Hill, C. S. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2297 · Cited by 1,258 · see citing works
DPC4 gene in various tumor types.
Schutte, M. E. M., Hruban, R. H., Hedrick, L., Cho, K. R., Nadasdy, G. M., Weinstein, C. L., Bova, G. S., Isaacs, W. B., Cairns, P., Nawroz, H., et al. (1996) · PubMed · Cited by 672 · see citing works
TGF-β – an excellent servant but a bad master
Kubiczkova, L., Sedlarikova, L., Hajek, R., & Sevcikova, S. (2012) · Journal of Translational Medicine · doi:10.1186/1479-5876-10-183 · Cited by 511 · see citing works
Infante, J. R., Matsubayashi, H., Sato, N., Tonascia, J., Klein, A. P., Riall, T. S., Yeo, C. J., Iacobuzio–Donahue, C. A., & Goggins, M. (2007) · Journal of Clinical Oncology · doi:10.1200/jco.2006.07.8824 · Cited by 403 · see citing works
<i>SMAD4</i> Gene Mutations Are Associated with Poor Prognosis in Pancreatic Cancer
Blackford, A., Serrano, O. K., Wolfgang, C. L., Parmigiani, G., Jones, S., Zhang, X., Parsons, D. W., Lin, J. C.-H., Leary, R. J., Eshleman, J. R., et al. (2009) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-09-0227 · Cited by 371 · see citing works
Fuxe, J., Vincent, C. T., & de Herreros, A. G. (2010) · Cell Cycle · doi:10.4161/cc.9.12.12050 · Cited by 311 · see citing works
(2001) · PubMed · Cited by 309 · see citing works
Immunohistochemical Labeling for Dpc4 Mirrors Genetic Status in Pancreatic Adenocarcinomas
Wilentz, R. E., Su, G. H., Dai, J. L., Sparks, A. B., Argani, P., Sohn, T. A., Yeo, C. J., Kern, S. E., & Hruban, R. H. (2000) · American Journal Of Pathology · doi:10.1016/s0002-9440(10)64703-7 · Cited by 304 · see citing works
Crystal Structure of a Phosphorylated Smad2
Wu, J.-W., Hu, M., Chai, J., Seoane, J., Huse, M., Li, C., Rigotti, D. J., Kyin, S., Muir, T. W., Fairman, R., et al. (2001) · Molecular Cell · doi:10.1016/s1097-2765(01)00421-x · Cited by 300 · see citing works
Homozygous deletion map at 18q21.1 in pancreatic cancer.
Hahn, S. A., Hoque, A. T., Moskaluk, C. A., da Costa, L. T., Schutte, M. E. M., Rozenblum, E., Seymour, A. B., Weinstein, C. L., Yeo, C. J., Hruban, R. H., et al. (1996) · PubMed · Cited by 265 · see citing works
Nieto, M. A., & Cano, A. (2012) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2012.05.003 · Cited by 263 · see citing works
Qian, Z. R., Rubinson, D. A., Nowak, J. A., Morales-Oyarvide, V., Dunne, R. F., Kozak, M. M., Welch, M. W., Brais, L. K., Da Silva, A., Li, T., et al. (2018) · JAMA Oncology · doi:10.1001/jamaoncol.2017.3420 · Cited by 260 · see citing works
Philip, P. A., Mooney, M., Jaffe, D., Eckhardt, G., Moore, M. J., Meropol, N. J., Emens, L. A., O'Reilly, E. M., Korc, M., Ellis, L. M., et al. (2009) · Journal of Clinical Oncology · doi:10.1200/jco.2009.21.9022 · Cited by 240 · see citing works
Oshima, M., Okano, K., Muraki, S., Haba, R., Maeba, T., Suzuki, Y., & Yachida, S. (2013) · Annals of Surgery · doi:10.1097/sla.0b013e3182827a65 · Cited by 236 · see citing works
Moore, P. S., Orlandini, S., Zamboni, G., Capelli, P., Rigaud, G., Falconi, M., Bassi, C., Lemoine, N. R., & Scarpa, A. (2001) · British Journal of Cancer · doi:10.1054/bjoc.2000.1567 · Cited by 197 · see citing works
KRAS Mutant Pancreatic Cancer: No Lone Path to an Effective Treatment
Zeitouni, D., Pylayeva‐Gupta, Y., Der, C. J., & Bryant, K. L. (2016) · Cancers · doi:10.3390/cancers8040045 · Cited by 179 · see citing works
Sullivan, J. P., Minna, J. D., & Shay, J. W. (2010) · Cancer and Metastasis Reviews · doi:10.1007/s10555-010-9216-5 · Cited by 176 · see citing works
<i>DPC4</i>/Smad4 Expression and Outcome in Pancreatic Ductal Adenocarcinoma
Biankin, A. V., Morey, A. L., Lee, C.-S., Kench, J. G., Biankin, S. A., Hook, H. C., Head, D. R., Hugh, T. B., Sutherland, R. L., & Henshall, S. M. (2002) · Journal of Clinical Oncology · doi:10.1200/jco.2002.12.063 · Cited by 163 · see citing works
Kim, S. K., Fan, Y.-H., Papadimitrakopoulou, V. A., Clayman, G. L., Hittelman, W. N., Hong, W. K., Lotan, R., & Mao, L. (1996) · PubMed · Cited by 159 · see citing works
Pancreatic Cancer Death Rates by Race Among US Men and Women, 1970–2009
Ma, J., Siegel, R. L., & Jemal, A. (2013) · JNCI Journal of the National Cancer Institute · doi:10.1093/jnci/djt292 · Cited by 145 · see citing works
Bonavida, B., & Baritaki, S. (2010) · Nitric Oxide · doi:10.1016/j.niox.2010.10.001 · Cited by 136 · see citing works
Itatani, Y., Kawada, K., Fujishita, T., Kakizaki, F., Hirai, H., Matsumoto, T., Iwamoto, M., Inamoto, S., Hatano, E., Hasegawa, S., et al. (2013) · Gastroenterology · doi:10.1053/j.gastro.2013.07.033 · Cited by 125 · see citing works
Saha, D., Datta, P. K., & Beauchamp, R. D. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m100069200 · Cited by 117 · see citing works
Infiltrating immune cells and gene mutations in pancreatic ductal adenocarcinoma
Wang, W.-Q., Liu, L., Xu, H.-X., Wu, C.-T., Xiang, J.-F., Xu, J., Liu, C., Long, J., Ni, Q.-X., & Yu, X. (2016) · British journal of surgery · doi:10.1002/bjs.10187 · Cited by 111 · see citing works
Shin, S. H., Kim, S. C., Hong, S.-M., Kim, Y. H., Song, K.-B., Park, K.-M., & Lee, Y.-J. (2013) · Pancreas · doi:10.1097/mpa.0b013e31825b6ab0 · Cited by 107 · see citing works
Li, L., Li, Z., Kong, X., Xie, D., Jia, Z., Jiang, W., Cui, J., Du, Y., Wei, D., Huang, S., et al. (2014) · Gastroenterology · doi:10.1053/j.gastro.2014.04.048 · Cited by 102 · see citing works
Hayashi, H., Kohno, T., Ueno, H., Hiraoka, N., Kondo, S., Saito, M., Shimada, Y., Ichikawa, H., Kato, M., Shibata, T., et al. (2017) · Pancreas · doi:10.1097/mpa.0000000000000760 · Cited by 88 · see citing works
Yang, K., Li, Y., Lian, G., Lin, H., Shang, C., Zeng, L., Chen, S., Li, J., Huang, C., Huang, K., et al. (2018) · International Journal of Cancer · doi:10.1002/ijc.31248 · Cited by 88 · see citing works
Self-citationBosscher, K. D., Hill, C. S., & Nicolás, F. J. (2004) · Biochemical Journal · doi:10.1042/bj20031886 · Cited by 76 · see citing works
Prognostic Value of SMAD4 in Pancreatic Cancer: A Meta-Analysis
Shugang, X., Hongfa, Y., Jianpeng, L., Xu, Z., Jingqi, F., Xiangxiang, L., & Wei, L. (2016) · Translational Oncology · doi:10.1016/j.tranon.2015.11.007 · Cited by 72 · see citing works
SMAD4 Loss triggers the phenotypic changes of pancreatic ductal adenocarcinoma cells
Chen, Y.-W., Hsiao, P., Weng, C., Kuo, K., Kuo, T., Wu, D., Hung, W., & Cheng, K. (2014) · BMC Cancer · doi:10.1186/1471-2407-14-181 · Cited by 67 · see citing works
Genetics and Biology of Pancreatic Ductal Adenocarcinoma
Dunne, R. F., & Hezel, A. F. (2015) · Hematology/Oncology Clinics of North America · doi:10.1016/j.hoc.2015.04.003 · Cited by 67 · see citing works
Promoter methylation correlates with reduced Smad4 expression in advanced prostate cancer
Aitchison, A., Veerakumarasivam, A., Vias, M., Kumar, R., Hamdy, F. C., Neal, D. E., & Mills, I. G. (2008) · The Prostate · doi:10.1002/pros.20730 · Cited by 60 · see citing works
Shin, S. H., Kim, H. J., Hwang, D. W., Lee, J. H., Song, K. B., Jun, E., Shim, I. K., Hong, S.-M., Kim, H. J., Park, K.-M., et al. (2017) · Oncotarget · doi:10.18632/oncotarget.14901 · Cited by 57 · see citing works
Hua, Z. (2003) · World Journal of Gastroenterology · doi:10.3748/wjg.v9.i12.2764 · Cited by 55 · see citing works
Cf, Q., & Fl, Z. (2017) · PubMed · Cited by 55 · see citing works
Singh, P., Srinivasan, R., & Wig, J. D. (2012) · Pancreas · doi:10.1097/mpa.0b013e318247d6af · Cited by 53 · see citing works
Chen, S., Zhang, J., Chen, J.-Z., Chen, H., Qiu, F., Yan, M.-L., Chen, Y., Peng, C., Tian, Y., & Wang, Y.-D. (2017) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2017.03.123 · Cited by 51 · see citing works
Nagata, N., Kawazoe, A., Mishima, S., Wada, T., Shimbo, T., Sekine, K., Watanabe, K., Imbe, K., Kojima, Y., Kumazawa, K., et al. (2015) · Radiology · doi:10.1148/radiol.2015150131 · Cited by 46 · see citing works
Du, M., Chen, W., Zhang, W., Tian, X., Wang, T., Wu, J., Gu, J., Zhang, N., Lü, Z., Qian, L., et al. (2018) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2018.01.120 · Cited by 31 · see citing works
Targeting the ERK pathway reduces liver metastasis of Smad4-inactivated colorectal cancer
Ai, X., Wu, Y., Zhang, W., Zhang, Z., Jin, G.-N., Zhao, J., Yu, J., Lin, Y., Zhang, W., Liang, H., et al. (2013) · Cancer Biology & Therapy · doi:10.4161/cbt.26427 · Cited by 28 · see citing works
Ormanns, S., Haas, M., Remold, A., Krüger, S., Holdenrieder, S., Kirchner, T., Heinemann, V., & Boeck, S. H. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18051094 · Cited by 22 · see citing works
Grelet, S., Andries, V., Polette, M., Gilles, C., Staes, K., Martin, A., Kileztky, C., Terryn, C., Dalstein, V., Cheng, C., et al. (2015) · The Journal of Pathology · doi:10.1002/path.4549 · Cited by 21 · see citing works
Kang, C. M., Hwang, H. K., Park, J., Kim, C., Cho, S.-K., Yun, M., & Lee, W. J. (2016) · Medicine · doi:10.1097/md.0000000000003452 · Cited by 19 · see citing works
Zhang, X., Cao, J., Pei, Y., Zhang, J., & Wang, Q. (2016) · Oncology Letters · doi:10.3892/ol.2016.4427 · Cited by 18 · see citing works
Wright, G. P., Chesla, D. W., & Chung, M. H. (2015) · The American Journal of Surgery · doi:10.1016/j.amjsurg.2015.11.002 · Cited by 9 · see citing works
DPC 4/SMAD 4 in non-pancreatic tumors with frequent LOH 18q21 and in hematological malignancies
Verbeek, W., Spirin, K. S., Hatta, Y., Miller, C. J., Kawamata, N., Takeuchi, S., Koike, M., Asou, H., Simpson, J., & Koeffler, H. P. (1997) · International Journal of Oncology · doi:10.3892/ijo.10.2.257 · Cited by 8 · see citing works
Flagged first, then by citations
1 of the 58 references couldn’t be matched to a known paper.
Cited by
Sorted by citations
Mutational drivers of cancer cell migration and invasion
Novikov, N. M., Zolotareva, S. Y., Gautreau, A. M., & Denisov, E. V. (2020) · British Journal of Cancer · doi:10.1038/s41416-020-01149-0 · Cited by 303 · see citing works
Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer
Stefanoudakis, D., Frountzas, M., Schizas, D., Michalopoulos, N. V., Drakaki, A., & Toutouzas, K. G. (2024) · Current Issues in Molecular Biology · doi:10.3390/cimb46040177 · Cited by 110 · see citing works
SMAD4 and the TGFβ Pathway in Patients with Pancreatic Ductal Adenocarcinoma
Dardare, J., Witz, A., Merlin, J.-L., Gilson, P., & Harlé, A. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21103534 · Cited by 101 · see citing works
TGFβ Signaling in the Pancreatic Tumor Microenvironment
Principe, D. R., Timbers, K. E., Atia, L. G., Koch, R. M., & Rana, A. (2021) · Cancers · doi:10.3390/cancers13205086 · Cited by 86 · see citing works
Shao, H., Zhang, Y., Yan, J., Ban, X., Fan, X., Chang, X., Lu, Z., Wu, Y., Zong, L., Mo, S., et al. (2021) · OncoTargets and Therapy · doi:10.2147/ott.s288936 · Cited by 46 · see citing works
SMAD4 represses FOSL1 expression and pancreatic cancer metastatic colonization
Dai, C., Rennhack, J. P., Arnoff, T. E., Thaker, M., Younger, S. T., Doench, J. G., Huang, A. Y., Yang, A., Aguirre, A. J., Wang, B. L., et al. (2021) · Cell Reports · doi:10.1016/j.celrep.2021.109443 · Cited by 46 · see citing works
Javed, A. A., Mahmud, O., Fatimi, A. S., Habib, A., Grewal, M., He, J. W., Wolfgang, C. L., & Besselink, M. G. (2024) · Annals of Surgical Oncology · doi:10.1245/s10434-024-15281-1 · Cited by 40 · see citing works
Giannis, D., Moris, D., & Barbas, A. S. (2021) · Cancers · doi:10.3390/cancers13051071 · Cited by 37 · see citing works
Yao, H.-J., Song, W., Cao, R., Ye, C., Zhang, L., Chen, H., Wang, J., Shi, Y., Li, R. P., Li, Y., et al. (2022) · Nature Communications · doi:10.1038/s41467-022-33037-x · Cited by 33 · see citing works
Self-citationGao, Y., Chen, S., Vafaei, S., & Zhong, X. (2020) · Frontiers in Oncology · doi:10.3389/fonc.2020.557638 · Cited by 30 · see citing works
Xiong, W., He, W., Wang, T., He, S., Xu, F., Wang, Z., Wang, X., Guo, H., Ling, J., Zhang, H., et al. (2022) · Advanced Science · doi:10.1002/advs.202103029 · Cited by 29 · see citing works
Self-citationRacu, M.-L., Lebrun, L., Schiavo, A. A., Campenhout, C. V., Clercq, S. D., Absil, L., Minguijón, E., Maris, C., Decaestecker, C., Salmon, I. J., et al. (2022) · Cancers · doi:10.3390/cancers14040973 · Cited by 29 · see citing works
Fanijavadi, S., Thomassen, M., & Jensen, L. H. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26020515 · Cited by 24 · see citing works
Yao, H.-J., Luo, L., Li, R. Q., Zhao, Y., Zhang, L., Pešić, M., Cai, L., & Li, L. (2024) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2024.189220 · Cited by 19 · see citing works
Self-citationXu, Y. X., & Zhu, Q. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24054820 · Cited by 16 · see citing works
Molecular pathways in periampullary cancer: An overview
Apurva, A., Sattar, R. S. A., Ali, A., Nimisha, Sharma, A. K., Kumar, A., Santoshi, S., & Saluja, S. S. (2022) · Cellular Signalling · doi:10.1016/j.cellsig.2022.110461 · Cited by 11 · see citing works
ZHAO, X., HUANG, X., Dang, C., WANG, X., qi, Y., & Li, H. L. (2024) · Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics · doi:10.32604/or.2024.046679 · Cited by 8 · see citing works
Mafficini, A., Brosens, L. A. A., Piredda, M. L., Conti, C., Mattiolo, P., Turri, G., Mastrosimini, M. G., Cingarlini, S., Crinò, S. F., Fassan, M., et al. (2022) · Familial Cancer · doi:10.1007/s10689-022-00289-x · Cited by 6 · see citing works
Hou, J., Kang, N., Liu, N., Tan, D., Zhang, S., Liu, J., & Xie, Y. (2022) · Annals of Translational Medicine · doi:10.21037/atm-22-1085 · Cited by 5 · see citing works
Self-citationTan, W. L., Subha, S. T., Mohtarrudin, N., & Cheah, Y. K. (2023) · Molecular Biology Reports · doi:10.1007/s11033-023-08421-5 · Cited by 4 · see citing works
Shih, C., Chattopadhyay, A. S., Wu, C., Tien, Y., & Lu, T. (2021) · BMC Bioinformatics · doi:10.1186/s12859-021-04243-z · Cited by 1 · see citing works
Ni, P., Du, K., Nov, P., Kou, Q., Li, Y., Zheng, C., Fu, W., & Li, J. (2025) · Research Square · doi:10.21203/rs.3.rs-6697879/v1
Self-citationManjunath, G. K., Kanchi, L. P., Dakal, T. C., Beura, A., & Kumar, A. (2026) · Functional & Integrative Genomics · doi:10.1007/s10142-026-01921-0
Varzaru, B., Croitoru, A. E., Sorop, A., Lupescu, I. G., Dima, S., Iacob, R. A., Becheanu, G., & Gheorghe, C. (2026) · Reports — Medical Cases Images and Videos · doi:10.3390/reports9030285
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- Wang, Z., Li, Y., Zhan, S., Zhang, L., Zhang, S., Tang, Q., Li, M., Tan, Z., Liu, S., & Xing, X.
- Affiliations
- Affiliated Hospital of Qingdao University (CN)
- Corresponding author
- Liu, Shiguo
- Xing, Xiaoming
- Venue
- BMC Cancer
- Published
- 2019-11-04
- Volume
- 19
- Issue
- 1
- Pages
- 1037-1037
- ISSN
- 1471-2407 (ISSN-L)
- PMC
- PMC6829834
- OpenAlex
- W2984610317
- Cited by
- 25
- References
- 58
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 4 · 2023: 2 · 2022: 6 · 2021: 6 · 2020: 3
- FWCI
- 1.57
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- BMC Cancer (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- China National Funds for Distinguished Young Scientists (1)
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Keywords
- SMAD4, pancreatic ductal adenocarcinoma, tumor suppressor, cell migration, cell invasion, E-cadherin, vimentin, clinicopathological features, lymph node metastasis, tumor progression
- MeSH terms
- Cell Movement, Female, Humans, Immunohistochemistry, Male, Middle Aged, Pancreatic Neoplasms, Vimentin, Cadherins, Gene Expression Regulation, Neoplastic, Mutation, Missense, Carcinoma, Pancreatic Ductal, Cell Line, Tumor, Cell Proliferation, Smad4 Protein, Carcinogenesis
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