The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.
Tumor Microenvironment Remodeling Enables Bypass of Oncogenic KRAS Dependency in Pancreatic Cancer
Open accessPublished version of a preprint
Abstract
Oncogenic KRAS (KRAS*) is a key tumor maintenance gene in pancreatic ductal adenocarcinoma (PDAC), motivating pharmacologic targeting of KRAS* and its effectors. Here, we explored mechanisms involving the tumor microenvironment (TME) as a potential basis for resistance to targeting KRAS*. Using the inducible KrasG12D;Trp53−/− PDAC mouse model, gain-of-function screens of epigenetic regulators identified HDAC5 as the top hit enabling KRAS* independent tumor growth. HDAC5-driven escaper tumors showed a prominent neutrophil-to-macrophage switch relative to KRAS*-driven tumors. Mechanistically, HDAC5 represses Socs3, a negative regulator of chemokine CCL2, resulting in increased CCL2, which recruits CCR2+ macrophages. Correspondingly, enforced Ccl2 promotes macrophage recruitment into the TME and enables tumor recurrence following KRAS* extinction. These tumor-associated macrophages in turn provide cancer cells with trophic support including TGFβ to enable KRAS* bypass in a SMAD4-dependent manner. Our work uncovers a KRAS* resistance mechanism involving immune cell remodeling of the PDAC TME. Significance: Although KRAS* is required for PDAC tumor maintenance, tumors can recur following KRAS* extinction. The capacity of PDAC cancer cells to alter the TME myeloid cell composition to support KRAS*-independent tumor growth illuminates novel therapeutic targets that may enhance the effectiveness of therapies targeting KRAS* and its pathway components. See related commentary by Carr and Fernandez-Zapico, p. 910. This article is highlighted in the In This Issue feature, p. 890
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In the citing paper
“This discovery gains significance considering the ability of KRAS G12D to boost GM-CSF production in PDAC cancer cells, thereby attracting immunosuppressive myeloid cells that can dampen the activity of CD8 T-cells [54].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [54]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“YAP, a pivotal EMT regulator gene, can restore oncogenicity in murine tumors that have lost KRAS [54,131].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [54]
The cited source says what the claim attributes to it.
In the citing paper
“In HDAC5-rich tumors, these macrophages increase TGFβ production, triggering pSMAD3/SMAD4 signaling in cancer cells, and bypassing the need for KRAS.”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [54]
The cited source says what the claim attributes to it.
In the citing paper
“Specifically, HDAC5 suppresses SOCS3, boosting CCL2 and CCL7 expression.”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [54]
The cited source says what the claim attributes to it.
In the citing paper
“Gain-of-function screens of epigenetic regulators in KRAS-mutant PDAC models identified HDAC5 as a driver of resistance to KRAS inhibition within the tumor microenvironment [54].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [54]
The cited source says what the claim attributes to it.
In the citing paper
“Furthermore, studies of the iKras mouse model have highlighted myriad mechanisms to enable bypass of oncogenic KRAS addiction, including the adoption of a KRAS-independent cell state dependent on oxidative phosphorylation (5), induction of SMARCB–MYC-network-driven mesenchymal reprogramming (38), activation of the TGFβ-SMAD3/4 axis via TME remodeling (39), and USP21-mediated upregulation of macrop”
From Mechanisms of Resistance to Oncogenic KRAS Inhibition in Pancreatic Cancer (2024) · cites this paper as [39]
In the citing paper
“In a KRASG12D mutation driven PDAC mice model, immune suppressive cytokines IL-4 and IL-13 and remodeling of the myeloid cell composition in TME have been demonstrated40,41.”
From Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma (2024) · cites this paper as [40]
In the citing paper
“Overexpression of the histone deacetylase HDAC5 also enables bypass of KRAS extinguishment through cytokine-mediate remodeling of the tumor microenvironment (86).”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [86]
In the citing paper
“Inhibitors of the HDAC5-SMAD4 pathways in combination with KRAS (G12D) inhibition have synergistic antitumor effects in an isogenic PDAC model [146].”
From Targeting KRAS mutant cancers: from druggable therapy to drug resistance (2022) · cites this paper as [146]
In the citing paper
“These tumor-associated macrophages (TAMs) provide cancer cells with TGFβ that promotes KRAS mutation-independent PDAC cell growth after KRAS mutation-targeted inhibition.”
From Targeting KRAS mutant cancers: from druggable therapy to drug resistance (2022) · cites this paper as [146]
In the citing paper
“Histone deacetylase 5 (HDAC5)-induced bypass promotes macrophage recruitment into the TME and enables tumor recurrence following the extinction of KRAS (G12D) [146].”
From Targeting KRAS mutant cancers: from druggable therapy to drug resistance (2022) · cites this paper as [146]
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Citations
Cites
Subramanian, A., Tamayo, P., Mootha, V. K., Mukherjee, S., Ebert, B. L., Gillette, M. A., Paulovich, A., Pomeroy, S. L., Golub, T. R., Lander, E. S., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0506580102 · Cited by 53,625
Mootha, V. K., Lindgren, C. M., Eriksson, K.-F., Subramanian, A., Sihag, S., Lehar, J., Puigserver, P., Carlsson, E., Ridderstråle, M., Laurila, E., et al. (2003) · Nature Genetics · doi:10.1038/ng1180 · Cited by 10,197
Genomic analyses identify molecular subtypes of pancreatic cancer
Bailey, P., Chang, D. K., Nones, K., Johns, A. L., Patch, A.-M., Gingras, M.-C., Miller, D. K., Christ, A. N., Bruxner, T. J. C., Quinn, M. C., et al. (2016) · Nature · doi:10.1038/nature16965 · Cited by 3,621 · cited 3×
“485 Additionally, we propose that SMAD4 status, which is a frequent deletion event in PDAC (2), 486 should be assessed as patient inclusion criteria for clinical trials testing KRAS* inhibitors.”
BackgroundMethodTargeting RAS signalling pathways in cancer therapy
Downward, J. (2003) · Nature reviews. Cancer · doi:10.1038/nrc969 · Cited by 3,350
A survey of best practices for RNA-seq data analysis
Conesa, A., Madrigal, P., Tarazona, S., Gomez-Cabrero, D., Cervera, A., McPherson, A., Szcześniak, M. W., Gaffney, D. J., Elo, L. L., Zhang, X., et al. (2016) · Genome Biology · doi:10.1186/s13059-016-0881-8 · Cited by 2,794
Haberland, M., Montgomery, R. L., & Olson, E. N. (2008) · Nature Reviews Genetics · doi:10.1038/nrg2485 · Cited by 2,600
Data-Driven Phenotypic Dissection of AML Reveals Progenitor-like Cells that Correlate with Prognosis
Levine, J. H., Simonds, E. F., Bendall, S. C., Davis, K. L., Amir, E.-A. D., Tadmor, M. D., Litvin, O., Fienberg, H. G., Jager, A., Zunder, E. R., et al. (2015) · Cell · doi:10.1016/j.cell.2015.05.047 · Cited by 2,303
Oncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism
Ying, H., Kimmelman, A. C., Lyssiotis, C. A., Hua, S., Chu, G. C., Fletcher-Sananikone, E., Locasale, J. W., Son, J., Zhang, H., Coloff, J. L., et al. (2012) · Cell · doi:10.1016/j.cell.2012.01.058 · Cited by 2,043
Self-citationGlutamine supports pancreatic cancer growth through a KRAS-regulated metabolic pathway
Son, J., Lyssiotis, C. A., Ying, H., Wang, X., Hua, S., Ligorio, M., Perera, R. M., Ferrone, C. R., Mullarky, E., Shyh-Chang, N., et al. (2013) · Nature · doi:10.1038/nature12040 · Cited by 1,990
Self-citationMacropinocytosis of protein is an amino acid supply route in Ras-transformed cells
Commisso, C., Davidson, S. M., Soydaner-Azeloglu, R. G., Parker, S. J., Kamphorst, J. J., Hackett, S., Grabocka, E., Nofal, M., Drebin, J. A., Thompson, C. B., et al. (2013) · Nature · doi:10.1038/nature12138 · Cited by 1,683
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Items 101–154 of 154
Lin, Q., Morales-Giron, A. A., Sander, C., Curtis, J. M., Barnes, H., Patel, P. S., de la Cruz, F. F., Riedl, J. M., Matsubara, H., Nakamura, H., et al. (2026) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-25-1788 · Cited by 6
McAndrews, K. M., Mahadevan, K. K., Li, B., Comptdaer, A. M., Sockwell, A. M., Morse, S. J., Kelly, P. J., Patel, S. I., Kirtley, M. L., Diaz, B. A. M., et al. (2026) · The EMBO Journal · doi:10.1038/s44318-026-00854-5 · Cited by 10
Self-citationXiao, B., Zhang, Y., Lu, Z., Chen, W., An, Y., Zu, G., Xu, X., Wu, D., Yang, H., Qin, Y., et al. (2022) · Acta Biochimica et Biophysica Sinica · doi:10.3724/abbs.2022111 · Cited by 5
Yang, H., Zhang, W., Ding, J., Hu, J., Sun, Y. E., Peng, W., Chu, Y., Xie, L., Mei, Z., Shao, Z., et al. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.970588 · Cited by 5
KRAS Inhibition Activates an Actionable CD24 “Do Not Eat Me” Signal in Pancreatic Cancer
Wei, Y., Liu, M., Yen, E.-Y., Yao, J., Xun, Z., Nguyen, P. T.-M., Wang, X., Yang, Z., Yousef, A. M. G., Pan, D. N., et al. (2025) · Cancer Research · doi:10.1158/0008-5472.can-25-2024 · Cited by 5
Self-citationRecent advances in targeted drug delivery for the treatment of pancreatic ductal adenocarcinoma
Song, H., & Jiang, C. (2022) · Expert Opinion on Drug Delivery · doi:10.1080/17425247.2022.2045943 · Cited by 4
Faraoni, E. Y., Thosani, N. C., O’Brien, B. J., Strickland, L. N., Mota, V., Chaney, J., Cen, P., Rowe, J. H., Cardenas, J. C., Poulsen, K. L., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.01.07.475451 · Cited by 4
McAndrews, K. M., Mahadevan, K. K., Li, B., Sockwell, A. M., Morse, S. J., Kelly, P. J., Patel, S. I., Kirtley, M. L., Diaz, B. A. M., Lyu, H., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.01.29.635543 · Cited by 4
Self-citationZhang, S., Cui, M., Huang, X., Feng, X., Xiao, R., Liu, Q., Bai, J., Han, X., Liu, X., Xu, W., et al. (2026) · Cell Reports Medicine · doi:10.1016/j.xcrm.2026.102660 · Cited by 3
Intratumor heterogeneity in KRAS signaling shapes treatment resistance
Petrenko, O., Kirillov, V., D’Amico, S., & Reich, N. C. (2024) · iScience · doi:10.1016/j.isci.2024.111662 · Cited by 3
KRAS mutations in colorectal cancer: impacts on tumor microenvironment and therapeutic implications
Emami, A., Sharif, P. M., & Rezaei, N. (2025) · Expert Opinion on Therapeutic Targets · doi:10.1080/14728222.2025.2500426 · Cited by 3
Wu, Q., He, X., Liu, J., Ou, C., Li, Y., & Fu, X. (2023) · Cancer Cell International · doi:10.1186/s12935-023-03061-y · Cited by 3
STAT3 is a genetic modifier of TGF-beta induced EMT in KRAS mutant pancreatic cancer
D’Amico, S., Kirillov, V., Petrenko, O., & Reich, N. C. (2024) · eLife · doi:10.7554/elife.92559 · Cited by 11
An integrated model for predicting KRAS dependency
(2023) · doi:10.1371/journal.pcbi.1011095 · Cited by 3
Zheng, W., Sun, Z., Wang, W., Han, J. E., Islam, M. T., Li, W., Yuan, Q., Chen, C., Xi, S., Li, Z., et al. (2026) · Journal of Advanced Research · doi:10.1016/j.jare.2026.01.082 · Cited by 2
Bree, B. A. V., & Eichner, L. J. (2026) · Science Advances · doi:10.1126/sciadv.aee7295 · Cited by 2
Xu, Z., Wang, W., Liu, L., & Lou, W. (2022) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2022.188751 · Cited by 2
Road Map to Defeat Pancreatic Cancer
Ferguson, L. P., & Tuveson, D. A. (2025) · Annual Review of Cancer Biology · doi:10.1146/annurev-cancerbio-060624-044323 · Cited by 2
Identification Of key prognostic genes in ovarian cancer using WGCNA and LASSO analysis
Zhong, Y. M., & Ouyang, L. (2022) · All Life · doi:10.1080/26895293.2022.2087107 · Cited by 2
STAT3 is a genetic modifier of TGF-beta induced EMT in KRAS mutant pancreatic cancerPreprint
D’Amico, S., Kirillov, V., Petrenko, O., & Reich, N. C. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.09.01.555946 · Cited by 2
Novel paradigms in KRAS targeting: Unveiling strategies to combat drug resistance
Luo, X., Zhou, F., Tang, Y., Liu, X., Xiao, R., Gu, M., Bai, J., Jiang, D., Yang, G., You, L., et al. (2025) · Chinese Medical Journal · doi:10.1097/cm9.0000000000003776 · Cited by 2
KRAS-driven cytokine–metabolic crosstalk shapes immune exclusion in pancreatic ductal adenocarcinoma
Huang, C., Mai, G., Li, Y., Liu, H., & Huang, W. (2026) · Frontiers in Genetics · doi:10.3389/fgene.2026.1899014 · Cited by 1
It Takes a Village to Overcome KRAS Dependence in Pancreatic Cancer
Carr, R. M., & Fernández-Zapico, M. E. (2020) · Cancer Discovery · doi:10.1158/2159-8290.cd-20-0490 · Cited by 1
Plaugher, D. R., & Murrugarra, D. (2024) · npj Systems Biology and Applications · doi:10.1038/s41540-024-00398-6 · Cited by 2
Jiang, H., Courau, T., Lupin-Jimenez, L. C., Borison, J., Ritchie, A. J., Mayer, A. T., Krummel, M. F., & Collisson, E. A. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.11.05.370569 · Cited by 1
Liu, Y., Deguchi, Y., Wei, D., Moussalli, M. J., Li, D., Wang, H., Valentin, L. A., Colby, J. K., Liu, F., Wang, J., et al. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.12.04.412320 · Cited by 1
Qu, G., Li, D., Xue, F., Zhu, M., Guo, W., & Xu, W. (2022) · Research Square · doi:10.21203/rs.3.rs-2335487/v1 · Cited by 1
Plaugher, D. R., & Murrugarra, D. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.01.27.577546 · Cited by 1
Pascual-Sabater, S., Varhadi, S., Vona, C. D., Celma, M., Fillat, C., & de la Luna, S. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.11.26.690756 · Cited by 1
Mimicking Multicellular Features of the Tumor Microenvironment
Curvello, R., & Loessner, D. (2022) · Royal Society of Chemistry eBooks · doi:10.1039/9781839166013-00141
Wu, Q., He, X., Liu, J., Ou, C., Li, Y., & Fu, X. (2023) · Research Square · doi:10.21203/rs.3.rs-2903186/v1
Supplementary Figure S10 from Comutations and KRASG12C Inhibitor Efficacy in Advanced NSCLC
Negrao, M. V., Araújo, H. A., Lamberti, G., Cooper, A. J., Akhave, N. S., Zhou, T., Delasos, L., Hicks, J. K., Aldea, M. D., Minuti, G., et al. (2023) · doi:10.1158/2159-8290.23310275
Self-citationSupplementary Figure S10 from Comutations and KRASG12C Inhibitor Efficacy in Advanced NSCLC
Negrao, M. V., Araújo, H. A., Lamberti, G., Cooper, A. J., Akhave, N. S., Zhou, T., Delasos, L., Hicks, J. K., Aldea, M. D., Minuti, G., et al. (2023) · doi:10.1158/2159-8290.23310275.v1
Self-citationSupplementary Figure S10 from Comutations and KRASG12C Inhibitor Efficacy in Advanced NSCLC
Negrao, M. V., Araújo, H. A., Lamberti, G., Cooper, A. J., Akhave, N. S., Zhou, T., Delasos, L., Hicks, J. K., Aldea, M. D., Minuti, G., et al. (2023) · doi:10.1158/2159-8290.23641387
Self-citationSupplementary Figure S10 from Comutations and KRASG12C Inhibitor Efficacy in Advanced NSCLC
Negrao, M. V., Araújo, H. A., Lamberti, G., Cooper, A. J., Akhave, N. S., Zhou, T., Delasos, L., Hicks, J. K., Aldea, M. D., Minuti, G., et al. (2023) · doi:10.1158/2159-8290.23641387.v1
Self-citationPeng, X., Lv, S., Fan, Y., Zhang, J., Liu, H., Liu, Y., & Feng, W. (2023) · Journal of Pancreatology · doi:10.1097/jp9.0000000000000164
Self-citationSTAT3 is a genetic modifier of TGF-beta induced EMT in KRAS mutant pancreatic cancerPreprint
D’Amico, S., Kirillov, V., Petrenko, O., & Reich, N. C. (2024) · eLife · doi:10.7554/elife.92559.1
Wang, X., Chen, H., Zhu, Y., Pan, Z., Cao, J., Li, Z., Tian, Y., Mohammed, D., Zhang, X., Liu, Y., et al. (2024) · SSRN Electronic Journal · doi:10.2139/ssrn.4831845
Zhu, C., & Liang, Y. (2024) · International Conference on Bioinformatics and Intelligent Computing (BIC) · doi:10.1145/3665689.3665766
Acetylation of E2F1 at K125 facilitates cell apoptosis under serum stress
Fang, Z., Gong, C., Hu, Y., Cui, T., Lin, M., Lin, S., & Ye, M. (2024) · Translational Oncology · doi:10.1016/j.tranon.2024.102259
Liu, Y., Fu, Y., Liu, T., Wang, J., Zhang, Z., Shi, Y., Cao, Z., Yang, G., Chen, H., Luo, W., et al. (2025) · Molecular Carcinogenesis · doi:10.1002/mc.23936
Self-citationKRAS, APC, and TP53 mutations define opposing immune archetypes in stage III colorectal cancerPreprint
Chaiboonchoe, A., Tanjak, P., Suwatthanarak, T., Thanormjit, K., Acharayothin, O., Vorasan, N., Sakamula, R., Likhityungyuen, T., Suktitipat, B., Korphaisarn, K., et al. (2025) · Research Square · doi:10.21203/rs.3.rs-7903094/v1
Single-dose DSS-induced inflammation enhances colorectal tumorigenesis in APC and KRAS mutant mice
Ishibashi, K., Urabe, Y., Uda, T., Sako, Y., Gurita, T., Masuda, S., Hatsushika, Y., Nakamura, T., Konishi, H., Tsuboi, A., et al. (2025) · Scientific Reports · doi:10.1038/s41598-025-25577-1
Wu, Q., He, X., Liu, J., 欧春麟, Li, Y., & Fu, X. (2024) · Figshare · doi:10.6084/m9.figshare.24225255
Parker, A. L., Bowman, E. D., Zingone, A., Ryan, B. M., Cooper, W. A., Kohonen-Corish, M., Harris, C. C., & Cox, T. R. (2022) · Figshare · doi:10.6084/m9.figshare.21591114
Wu, Q., He, X., Liu, J., 欧春麟, Li, Y., & Fu, X. (2023) · Figshare · doi:10.6084/m9.figshare.24225214
PPARδ: An underappreciated tumor accelerator in pancreatic ductal adenocarcinoma
Niu, D., Wei, D., Liu, Y., Yao, J. C., Shureiqi, I., & Zuo, X. (2026) · Cancer Letters · doi:10.1016/j.canlet.2026.218385
Ketogenic supplementation enhances KRASG12D inhibitor efficacy in pancreatic ductal adenocarcinoma
Duong, L., Lee, J., Qin, Y., Barupala, N. P., Fishel, M. L., Lü, X., Wan, J., Turk, A. A., & Lü, X. (2026) · Cancer Letters · doi:10.1016/j.canlet.2026.218490
Li, R., Xu, X., Zhang, W., & Zhan, Y.-Y. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1843505
Xavier, C. B., Shah, P. A., Yakimova, D., Kravets, A., Belousov, D. M., Kudryavtseva, K., Massaro, M., Paradiso, F., Kotlov, N., Zhao, D., et al. (2026) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-26-0344 · Cited by 1
Kawczak, P., Kawczak, K., & Bączek, T. (2026) · Journal of Clinical Medicine · doi:10.3390/jcm15145521
Salih, R., Sirajudeen, F., & Rahmani, M. (2026) · Journal of Advanced Research · doi:10.1016/j.jare.2026.08.030
Li, J., Li, Y., Zhang, K., Wu, Z., & Han, K. (2026) · Microchemical Journal · doi:10.1016/j.microc.2026.119412
Self-citationMariano, M. P., Sgarilli, E., Mijnlieff, D., Visuvasam, B., Blesio, A., Digiacomo, G., Cavazzoni, A., Ferracin, M., & Giovannetti, E. (2026) · Cancer Drug Resistance · doi:10.20517/cdr.2026.52
Metadata
- Authors
- Hou, P., Kapoor, A., Zhang, Q., Li, J., Wu, C.-J., Li, J., Lan, Z., Tang, M., Ma, X., Ackroyd, J. J., Kalluri, R., Zhang, J., Jiang, S., Spring, D. J., Wang, Y. A., & DePinho, R. A.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- Corresponding author
- Wang, Y. Alan
- DePinho, Ronald A.
- ORCID
- Venue
- Cancer Discovery
- Published
- 2020-07-01
- Volume
- 10
- Issue
- 7
- Pages
- 1058-1077
- ISSN
- 2159-8274 (ISSN-L)
- 2159-8290
- PMC
- PMC7334087
- OpenAlex
- W3019483263
- Cited by
- 154
- References
- 57
- Citations by year
- 2026: 17 · 2025: 20 · 2024: 29 · 2023: 30 · 2022: 26 · 2021: 25 · 2020: 7
- FWCI
- 7.94
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cancer Discovery (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (P30 CA016672, P01 CA117969, R01 CA225955, R01 CA231349)
- Hirshberg Foundation for Pancreatic Cancer Research
- Emerson Collective
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Keywords
- pancreatic ductal adenocarcinoma, KRAS, tumor microenvironment, HDAC5, epigenetic regulators, tumor-associated macrophages, MCP-1, CCR2, SOCS3, TGF-beta, SMAD4, tumor recurrence
- MeSH terms
- Humans, Oncogenes, Pancreatic Neoplasms, Proto-Oncogene Proteins p21(ras), Tumor Microenvironment
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