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Mutant p53 Drives Pancreatic Cancer Metastasis through Cell-Autonomous PDGF Receptor β Signaling
Open accessAbstract
Missense mutations in the p53 tumor suppressor inactivate its antiproliferative properties but can also promote metastasis through a gain-of-function activity. We show that sustained expression of mutant p53 is required to maintain the prometastatic phenotype of a murine model of pancreatic cancer, a highly metastatic disease that frequently displays p53 mutations. Transcriptional profiling and functional screening identified the platelet-derived growth factor receptor b (PDGFRb) as both necessary and sufficient to mediate these effects. Mutant p53 induced PDGFRb through a cell-autonomous mechanism involving inhibition of a p73/NF-Y complex that represses PDGFRb expression in p53-deficient, noninvasive cells. Blocking PDGFRb signaling by RNA interference or by small molecule inhibitors prevented pancreatic cancer cell invasion in vitro and metastasis formation in vivo. Finally, high PDGFRb expression correlates with poor disease-free survival in pancreatic, colon, and ovarian cancer patients, implicating PDGFRb as a prognostic marker and possible target for attenuating metastasis in p53 mutant tumors.
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“altered p53 function has a multitude of tumor-promoting effects on neoplastic cells, including increased genomic instability30, reprogrammed cellular metabolism57,58, and enhanced metastatic propensity59.”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [59]
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Self-citationCore Signaling Pathways in Human Pancreatic Cancers Revealed by Global Genomic Analyses
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Novel Molecular Subtypes of Serous and Endometrioid Ovarian Cancer Linked to Clinical Outcome
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Mutant p53: one name, many proteinsPreprint
Freed-Pastor, W. A., & Prives, C. L. (2012) · Genes & Development · doi:10.1101/gad.190678.112 · Cited by 1,290 · cited 3×
“Mutations in the p53 tumor suppressor gene represent the most common genetic lesions in cancer (Freed-Pastor and Prives, 2012).”
InfluentialSelf-citationGain of function of a p53 hot spot mutation in a mouse model of Li-Fraumeni syndrome
Lang, G. A., Iwakuma, T., Suh, Y.-A., Liu, G., Rao, V. A., Parant, J. M., Valentin-Vega, Y. A., Terzian, T., Caldwell, L. C., Strong, L. C., et al. (2004) · Cell · doi:10.1016/j.cell.2004.11.006 · Cited by 1,069 · cited 4×
“…with previous studies showing that (1) loss of p73 in a p53 null background might be functionally equivalent to the expression of mutant p53 (Lang et al., 2004); (2) aberrant transcriptional regulation by mutant p53 is mediated through the transcriptional activator NF-Y (Di Agostino et al.,…”
InfluentialTranscriptome analysis by strand-specific sequencing of complementary DNA
Parkhomchuk, D., Borodina, T. A., Amstislavskiy, V. S., Banaru, M., Hallen, L., Krobitsch, S., Lehrach, H. R., & Солдатов, А. В. (2009) · Nucleic Acids Research · doi:10.1093/nar/gkp596 · Cited by 934
Mutant p53 disrupts mammary tissue architecture via the mevalonate pathway
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“, 2009), the mevalonate pathway (Freed-Pastor et al., 2012), or microRNA”
Self-citationMutant p53 drives invasion by promoting integrin recycling
Muller, P. A. J., Caswell, P. T., Doyle, B., Iwanicki, M. P., Tan, E. H., Karim, S., Lukashchuk, N., Gillespie, D. A., Ludwig, R. L., Gosselin, P., et al. (2009) · Cell · doi:10.1016/j.cell.2009.11.026 · Cited by 796
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Mutant p53 Gain-of-Function in CancerPreprint
Oren, M., & Rotter, V. (2009) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a001107 · Cited by 778 · cited 4×
“009), which generally represents tumors with p53 mutation (Oren and Rotter, 2010) (Figures 7D and S6A).”
InfluentialSmith, J. J., Deane, N. G., Wu, F., Merchant, N. B., Zhang, B., Jiang, A., Lu, P., Johnson, J. C., Schmidt, C. R., Bailey, C. E., et al. (2009) · Gastroenterology · doi:10.1053/j.gastro.2009.11.005 · Cited by 720
Assessing TP53 status in human tumours to evaluate clinical outcome
Soussi, T., & Béroud, C. (2001) · Nature reviews. Cancer · doi:10.1038/35106009 · Cited by 659 · cited 1×
“Accordingly, human tumors with mutant p53 are associated with poor patient prognosis (Soussi and Béroud, 2001) and drug resistance (Masciarelli et al., 2013).”
Mutant p53 drives metastasis and overcomes growth arrest/senescence in pancreatic cancer
Morton, J. P., Timpson, P., Karim, S. A., Ridgway, R. A., Athineos, D., Doyle, B., Jamieson, N. B., Oien, K. A., Lowy, A. M., Brunton, V. G., et al. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0908428107 · Cited by 657 · cited 2×
“To understand the impact of p53 mutations on cell invasion and metastasis in this well-defined genetic system, we employed a murine KPC pancreatic cancer cell line that lost the remaining p53 wild-type allele during disease progression (Morton et al., 2010).”
PDGF-BB induces intratumoral lymphangiogenesis and promotes lymphatic metastasis
Cao, R., Björndahl, M. A., Religa, P., Clasper, S., Garvin, S., Galter, D., Meister, B., Ikomi, F., Tritsaris, K., Dissing, S., et al. (2004) · Cancer Cell · doi:10.1016/j.ccr.2004.08.034 · Cited by 526
PDGF receptors as cancer drug targets
Pietras, K., Sjöblom, T., Rubin, K., Heldin, C., & Östman, A. (2003) · Cancer Cell · doi:10.1016/s1535-6108(03)00089-8 · Cited by 467 · cited 2×
“Oncogenic properties of mutated or amplified PDGFRa have been extensively studied in several tumor types, whereas PDGFRb has been exclusively linked to tumor angiogenesis via paracrine effects (Pietras et al., 2003; Cao et al., 2004).”
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“First, we verified the interaction between p73 and mutant p53 proteins by reciprocal coimmunoprecipitation (Figure 4A), and, consistentwithprevious reports, p73binding toa ‘‘conformation’’ p53 mutant (R175H) appeared stronger than to a ‘‘DNA-binding’’ p53 mutant (R273H) (Gaiddon et al., 2001; Muller et al., 2009).”
InfluentialSelf-citationTAp63 suppresses metastasis through coordinate regulation of Dicer and miRNAs
Su, X., Chakravarti, D., Cho, M. S., Liu, L.-Z., Gi, Y. J., Lin, Y.-L., Leung, M. L., El‐Naggar, A. K., Creighton, C. J., Suraokar, M. B., et al. (2010) · Nature · doi:10.1038/nature09459 · Cited by 429 · cited 2×
“Such efforts have identified proteins involved in integrin recycling (Muller et al., 2009), the mevalonate pathway (Freed-Pastor et al., 2012), or microRNA (miRNA) biogenesis (Su et al., 2010) as potential mediators of mutant p53 action in invasion and metastasis.”
Di Agostino, S., Strano, S., Emiliozzi, V., Zerbini, V., Mottolese, M., Sacchi, A., Blandino, G., & Piaggio, G. (2006) · Cancer Cell · doi:10.1016/j.ccr.2006.08.013 · Cited by 418 · cited 2×
“Although studies suggest that mutant p53 can directly bind to NF-Y to regulate its transcriptional activity (Di Agostino et al., 2006), we failed to observe any physical interaction between mutant p53 and NF-Y in our cells.”
Russo, A., Bazan, V., Iacopetta, B., Kerr, D., Soussi, T., & Gebbia, N. (2005) · Journal of Clinical Oncology · doi:10.1200/jco.2005.00.471 · Cited by 416 · cited 1×
“Other tumor types for which p53 mutations are predictive of metastatic disease are colorectal and ovarian cancer (Russo et al., 2005; Levesque et al., 1995).”
Longati, P., Jia, X., Eimer, J., Wagman, A., Witt, M.-R., Rehnmark, S., Verbeke, C., Toftgård, R., Löhr, M., & Heuchel, R. L. (2013) · BMC Cancer · doi:10.1186/1471-2407-13-95 · Cited by 394 · cited 2×
“…mediate cellular iron efflux (Montalbetti et al., 2013); SNED1 is a stromal marker that induces cisplatinresistance in head and neck squamous carcinoma (Longati et al., 2013); and PDGFRb is a receptor tyrosine kinase that mediates PDGF-regulated proliferation, survival, and chemotaxis (Dai, 2010).”
Hemann, M. T., Fridman, J. S., Zilfou, J. T., Hernando, E., Paddison, P. J., Cordon‐Cardo, C., Hannon, G. J., & Lowe, S. W. (2003) · Nature Genetics · doi:10.1038/ng1091 · Cited by 354
Self-citationDong, P., Karaayvaz, M., Jia, N., Kaneuchi, M., Hamada, J., Watari, H., Sudo, S., Ju, J., & Sakuragi, N. (2012) · Oncogene · doi:10.1038/onc.2012.334 · Cited by 307 · cited 2×
“In addition, mutant p53 has also been reported to drive invasion by regulating several miRNAs, such as miR155 and miR130b (Neilsen et al., 2013; Dong et al., 2013).”
Two hot spot mutant p53 mouse models display differential gain of function in tumorigenesis
Hanel, W. G., Marchenko, N. D., Xu, S., Yu, S., Weng, W., & Moll, U. M. (2013) · Cell Death and Differentiation · doi:10.1038/cdd.2013.17 · Cited by 278 · cited 1×
“…more aggressive and metastatic tumors compared to those arising in their p53 heterozygous or null counterparts (Lang et al., 2004; Olive et al., 2004, Hanel et al., 2013), suggesting that the mutant forms of p53 exert gain-of-function activities independent of their effects on wild-type p53.”
Zuber, J., McJunkin, K., Fellmann, C., Dow, L. E., Taylor, M. J., Hannon, G., & Lowe, S. (2010) · Nature Biotechnology · doi:10.1038/nbt.1720 · Cited by 277
Self-citationZhang, G., Schetter, A. J., He, P., Funamizu, N., Gaedcke, J., Ghadimi, Β. M., Ried, T., Hassan, R., Yfantis, H. G., Lee, D. H., et al. (2012) · PLoS ONE · doi:10.1371/journal.pone.0031507 · Cited by 257
Are interactions with p63 and p73 involved in mutant p53 gain of oncogenic function?
Li, Y., & Prives, C. L. (2007) · Oncogene · doi:10.1038/sj.onc.1210311 · Cited by 174 · cited 1×
“Several pro-oncogenic properties of mutant p53 depend on its ability to physically interact with and inhibit the p53 family members, p63 and p73 (Li and Prives, 2007).”
BackgroundSelf-citationMutant p53 drives invasion in breast tumors through up-regulation of miR-155
Neilsen, P. M., Noll, J. E., Mattiske, S., Bracken, C. P., Gregory, P. A., Schulz, R. B., Lim, S. P., Kumar, R., Suetani, R. J., Goodall, G. J., et al. (2012) · Oncogene · doi:10.1038/onc.2012.305 · Cited by 171 · cited 2×
“In addition, mutant p53 has also been reported to drive invasion by regulating several miRNAs, such as miR155 and miR130b (Neilsen et al., 2013; Dong et al., 2013).”
Positive feedback between Dia1, LARG, and RhoA regulates cell morphology and invasionPreprint
Kitzing, T. M., Sahadevan, A. S., Brandt, D. T., Knieling, H., Hannemann, S., Fackler, O., Großhans, J., & Grosse, R. (2007) · Genes & Development · doi:10.1101/gad.424807 · Cited by 166 · cited 2×
“previously described (Goulimari et al., 2005; Kitzing et al., 2007).”
Self-citationMammalian iron transporters: Families SLC11 and SLC40
Montalbetti, N., Simonin, A., Kovács, G., & Hediger, M. A. (2013) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2013.01.002 · Cited by 151 · cited 2×
“that has been shown to mediate cellular iron efflux (Montalbetti et al., 2013); SNED1 is a stromal marker that induces cisplatinresistance in head and neck squamous carcinoma (Longati et al.”
Masciarelli, S., Fontemaggi, G., Agostino, S. D., Donzelli, S., Carcarino, E., Strano, S., & Blandino, G. (2013) · Oncogene · doi:10.1038/onc.2013.106 · Cited by 144
Structural Biology of the Tumor Suppressor p53 and Cancer‐Associated Mutants
Joerger, A. C., & Fersht, A. R. (2007) · Advances in cancer research · doi:10.1016/s0065-230x(06)97001-8 · Cited by 131 · cited 2×
“…disable this property of p53 and, consequently, its antiproliferative effects. p53 mutations typically occur within the DNA-binding region and involve either DNA contact residues or residues important for conformational structure, both resulting in loss of DNA binding (Joerger and Fersht, 2007).”
Levesque, M. A., Katsaros, D., Yu, H., Zola, P., Sismondi, P., Giardina, G., & Diamandis, E. P. (1995) · Cancer · doi:10.1002/1097-0142(19950315)75:6 · Cited by 123
Garofalo, M., Jeon, Y.-J., Nuovo, G. J., Middleton, J. D., Secchiero, P., Joshi, P., Alder, H., Nazaryan, N., Leva, G. D., Romano, G., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0067581 · Cited by 122 · cited 1×
“Additionally, miR34a expression levels were not dependent on p53 status in our system (data not shown), even though this miRNA acts as negative regulator of PDGFRb in lung cancer (Garofalo et al., 2013).”
BackgroundTopBP1 Mediates Mutant p53 Gain of Function through NF-Y and p63/p73
Liu, K., Ling, S., & Lin, W.-C. (2011) · Molecular and Cellular Biology · doi:10.1128/mcb.05574-11 · Cited by 122 · cited 1×
“The discrepancy could reflect different extraction conditions or biological settings, because the mutant p53/NF-Y interaction has been shown to occur upon DNA damage (Liu et al., 2011).”
Wolff, N. C., Richardson, J. A., Egorin, M. J., & Ilaria, R. L. (2003) · Blood · doi:10.1182/blood-2002-10-3059 · Cited by 112 · cited 1×
“To this end, mice were treated with a dose of 50 mg/kg imatinib by oral gavage twice daily, a regimen previously shown to produce therapeutic concentrations of imatinib in mice (Wolff et al., 2003).”
MethodMehta, S., Christopherson, K. W., Bhat‐Nakshatri, P., Goulet, R. J., Broxmeyer, H. E., Kopelovich, L., & Nakshatri, H. (2006) · Oncogene · doi:10.1038/sj.onc.1210120 · Cited by 109 · cited 1×
“Studies in other systems, primarily breast cancer, have suggested that CXCR4, cyclin-G2, and the mevalonate pathway are important mediators of the prometastatic activities of mutant p53 (Mehta et al., 2007; Adorno et al., 2009; FreedPastor et al., 2012).”
Gα12/13 Is Essential for Directed Cell Migration and Localized Rho-Dia1 Function
Goulimari, P., Kitzing, T. M., Knieling, H., Brandt, D. T., Offermanns, S., & Grosse, R. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m508690200 · Cited by 104 · cited 2×
“previously described (Goulimari et al., 2005; Kitzing et al., 2007).”
Self-citationPDGFRB Promotes Liver Metastasis Formation of Mesenchymal-Like Colorectal Tumor Cells
Steller, E. J. A., Raats, D., Köster, J., Rutten, B., Govaert, K. M., Emmink, B. L., Snoeren, N., van Hooff, S. R., Holstege, F. C. P., Maas, C., et al. (2013) · Neoplasia · doi:10.1593/neo.121726 · Cited by 101 · cited 1×
“High levels of PDGFRb expression have recently been associated with tumor recurrence in primary colorectal cancer, another gastrointestinal tumor in which p53 is frequently mutated (Steller et al., 2013).”
Lewis, N. L., Lewis, L. D., Eder, J. P., Reddy, N. J., Guo, F., Pierce, K. J., Olszanski, A. J., & Cohen, R. B. (2009) · Journal of Clinical Oncology · doi:10.1200/jco.2009.21.8487 · Cited by 96 · cited 1×
“We used the compound crenolanib, a small molecule inhibitor of type III tyrosine kinases, potent against PDGFRa, PDGFRb, and FLT3, but not against other known receptor tyrosine kinases (VEGFR, FGFR), serine/threonine (RAF), or tyrosine kinases (ABL1) (Lewis et al., 2009).”
Targeting Mutant p53 in Human Tumors
Lehmann, B. D., & Pietenpol, J. A. (2012) · Journal of Clinical Oncology · doi:10.1200/jco.2012.44.0412 · Cited by 74 · cited 2×
“However, mutant p53 is neither a targetable cell-surface protein nor a druggable enzyme (Levine and Oren, 2009), and novel therapeutic modalities, such as RNAi or restoring wild-type p53 conformations, have yet to show efficacy in clinical studies (Lehmann and Pietenpol, 2012).”
A role for Chk1 in blocking transcriptional elongation of p21 RNA during the S-phase checkpointPreprint
Beckerman, R., Donner, A. J., Mattia, M., Peart, M. J., Manley, J. L., Espinosa, J. M., & Prives, C. L. (2009) · Genes & Development · doi:10.1101/gad.1795709 · Cited by 69
Self-citationIsolation and Characterization of the Mouse PDGF β-Receptor Promoter
Ballagi, A. E., Ishizaki, A., Nehlin, J. O., & Funa, K. (1995) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1995.1642 · Cited by 42 · cited 2×
“…Inc. conserved CCAAT binding motif for NF-Y, a well-characterized heterotrimeric transcriptional activator (NF-YA, NF-YB, and NF-YC) of PDGFRB, where the NF-YB subunit interacts with p73 but is devoid of transcriptional activity (Ballagi et al., 1995; Ishisaki et al., 1997; Serra et al., 1998).”
Dai, Y. (2010) · Expert Opinion on Therapeutic Patents · doi:10.1517/13543776.2010.493559 · Cited by 37 · cited 2×
“, 2013); and PDGFRb is a receptor tyrosine kinase that mediates PDGF-regulated proliferation, survival, and chemotaxis (Dai, 2010).”
Conservation and divergence of NF-Y transcriptional activation function
Serra, E. C., Zemzoumi, K., Lardans, V., Dissous, C., di Silvio, A., & Mantovani, R. (1998) · Nucleic Acids Research · doi:10.1093/nar/26.16.3800 · Cited by 37 · cited 1×
“…Inc. conserved CCAAT binding motif for NF-Y, a well-characterized heterotrimeric transcriptional activator (NF-YA, NF-YB, and NF-YC) of PDGFRB, where the NF-YB subunit interacts with p73 but is devoid of transcriptional activity (Ballagi et al., 1995; Ishisaki et al., 1997; Serra et al., 1998).”
Hackzell, A., Uramoto, H., Izumi, H., Kohno, K., & Funa, K. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m204483200 · Cited by 33 · cited 2×
“Because a previous report indicated that p73 can repress the transcription of PDGFRB (Hackzell et al., 2002), and because our KPC cells expressed p73, but not p63, as determined by RNA-seq (data not shown), we aimed to understand whether the physical interaction of mutant p53 with p73 might impair the ability of p73 t…”
Ishisaki, A., Murayama, T., Ballagi, A. E., & Funa, K. (1997) · European Journal of Biochemistry · doi:10.1111/j.1432-1033.1997.t01-2-00142.x · Cited by 21 · cited 1×
“…Inc. conserved CCAAT binding motif for NF-Y, a well-characterized heterotrimeric transcriptional activator (NF-YA, NF-YB, and NF-YC) of PDGFRB, where the NF-YB subunit interacts with p73 but is devoid of transcriptional activity (Ballagi et al., 1995; Ishisaki et al., 1997; Serra et al., 1998).”
Hoehler, T., von Wichert, G., Schimanski, C. C., Kanzler, S., Moehler, M. H., Hinke, A., Seufferlein, T. T. W., Siebler, J., Hochhaus, A., Arnold, D., et al. (2013) · British Journal of Cancer · doi:10.1038/bjc.2013.409 · Cited by 18 · cited 1×
“Although further studies will be required to explore this notion, pharmacological inhibition of PDGFRb with the tyrosine kinase inhibitor imatinib, in combination with standard chemotherapy, has shown promise in treating metastatic colorectal cancer patients (Hoehler et al., 2013).”
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(2017) · doi:10.1038/s41467-017-02391-6 · Cited by 1,108
“…mutations and loss are in line with the recent discovery that TP53 mutations can act in an oncogenic manner in addition to disrupting its tumor suppressor activity, which has been shown for individual cancer types (Olive et al. 2004; Zhang et al. 2013; Weissmueller et al. 2014; Zhu et al. 2015).”
BackgroundKrebs, A. M., Mitschke, J., Losada, M. L., Schmalhofer, O., Boerries, M., Busch, H. S., Böttcher, M., Mougiakakos, D., Reichardt, W., Bronsert, P., et al. (2017) · Nature Cell Biology · doi:10.1038/ncb3513 · Cited by 1,008
Self-citation
Metadata
- Authors
- Weissmueller, S., Manchado, E., Saborowski, M., Morris, J. P., Wagenblast, E., Davis, C. A., Moon, S.-H., Pfister, N. T., Tschaharganeh, D. F., Kitzing, T., Aust, D., Markert, E. K., Wu, J., Grimmond, S. M., Pilarsky, C., Prives, C., Biankin, A. V., & Lowe, S. W.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Cold Spring Harbor Laboratory (US)
- Columbia University (US)
- Technische Universität Dresden (DE)
- Institute for Advanced Study (US)
- Garvan Institute of Medical Research (AU)
- The University of Queensland (AU)
- Corresponding author
- Lowe, Scott W.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2014-04
- Volume
- 157
- Issue
- 2
- Pages
- 382-394
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4001090
- OpenAlex
- W2088441464
- Cited by
- 466
- References
- 61
- Citations by year
- 2026: 11 · 2025: 17 · 2024: 16 · 2023: 42 · 2022: 42 · 2021: 54 · 2020: 43 · 2019: 32 · 2018: 48 · 2017: 59 · 2016: 50 · 2015: 33 · 2014: 18
- FWCI
- 25.71
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (submittedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (submittedVersion)
- Funders
- Cancer Research UK (17263)
- National Cancer Institute (P01CA087497, P01CA129243, CA 013106, P01CA013106, P30CA008748)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mechanisms of cancer metastasis
- Keywords
- mutant p53, pancreatic cancer, metastasis, PDGF receptor beta, gain-of-function p53, cell invasion, prognostic factors, small molecule inhibitors, RNA interference, tumor suppressor inactivation
- MeSH terms
- Animals, Disease Models, Animal, Humans, Neoplasm Metastasis, Pancreatic Neoplasms, Tumor Suppressor Protein p53, Receptor, Platelet-Derived Growth Factor beta, Gene Expression Profiling, Carcinoma, Pancreatic Ductal, Mice
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