Cited by 217Pancreatic and Hepatic Oncology ResearchCytokine Signaling Pathways and InteractionsCancer, Hypoxia, and Metabolism

The DOI matches its Crossref record; 65 of the 65 references it cites were found in a registry or an index.

Oncogenic KRAS-Driven Metabolic Reprogramming in Pancreatic Cancer Cells Utilizes Cytokines from the Tumor Microenvironment

Dey, Prasenjit, Li, Jun, Zhang, Jianhua, Chaurasiya, Surendra, Strom, Anders, Wang, Huamin, Liao, Wen-Ting, Cavallaro, Frederick, Denz, Parker, Bernard, Vincent, Yen, Er-Yen, Genovese, Giannicola, Gulhati, Pat, Liu, Jielin, Chakravarti, Deepavali, Deng, Pingna, Zhang, Tingxin, Carbone, Federica, Chang, Qing, Ying, Haoqiang, Shang, Xiaoying, Spring, Denise J., Ghosh, Bidyut, Putluri, Nagireddy, Maitra, Anirban, Wang, Y. Alan, DePinho, Ronald A.·2020·Cancer Discovery

DOI 10.1158/2159-8290.cd-19-0297

Published version of a preprint

Open this paper in CoChat — free account

Abstract

A hallmark of pancreatic ductal adenocarcinoma (PDAC) is an exuberant stroma comprised of diverse cell types that enable or suppress tumor progression. Here, we explored the role of oncogenic KRAS in protumorigenic signaling interactions between cancer cells and host cells. We show that KRAS mutation (KRAS*) drives cell-autonomous expression of type I cytokine receptor complexes (IL2rγ–IL4rα and IL2rγ–IL13rα1) in cancer cells that in turn are capable of receiving cytokine growth signals (IL4 or IL13) provided by invading Th2 cells in the microenvironment. Early neoplastic lesions show close proximity of cancer cells harboring KRAS* and Th2 cells producing IL4 and IL13. Activated IL2rγ–IL4rα and IL2rγ–IL13rα1 receptors signal primarily via JAK1–STAT6. Integrated transcriptomic, chromatin occupancy, and metabolomic studies identified MYC as a direct target of activated STAT6 and that MYC drives glycolysis. Thus, paracrine signaling in the tumor microenvironment plays a key role in the KRAS*-driven metabolic reprogramming of PDAC. Significance: Type II cytokines, secreted by Th2 cells in the tumor microenvironment, can stimulate cancer cell–intrinsic MYC transcriptional upregulation to drive glycolysis. This KRAS*-driven heterotypic signaling circuit in the early and advanced tumor microenvironment enables cooperative protumorigenic interactions, providing candidate therapeutic targets in the KRAS* pathway for this intractable disease.

Integrity signals

Registry

Crossref · 10.1158/2159-8290.cd-19-0297

Cites

65 of 65 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Fast gapped-read alignment with Bowtie 2
Langmead, B., & Salzberg, S. L. (2012) · Nature Methods · doi:10.1038/nmeth.1923 · Cited by 56,400
Differential gene and transcript expression analysis of RNA-seq experiments with TopHat and Cufflinks
Trapnell, C., Roberts, A., Goff, L. A., Pertea, G. M., Kim, D., Kelley, D. R., Pimentel, H., Salzberg, S. L., Rinn, J. L., & Pachter, L. S. (2012) · Nature Protocols · doi:10.1038/nprot.2012.016 · Cited by 12,145
Single Lgr5 stem cells build crypt-villus structures in vitro without a mesenchymal niche
Sato, T., Vries, R. G., Snippert, H. J., van de Wetering, M., Barker, N., Stange, D. E., van Es, J. H., Abo, A., Kujala, P., Peters, P. J., et al. (2009) · Nature · doi:10.1038/nature07935 · Cited by 7,204 · cited 3×
“Five microliters of cells (5 × 105) mixed with 5 μL Matrigel was injected.”
MethodInfluential
MYC on the Path to Cancer
Dang, C. V. (2012) · Cell · doi:10.1016/j.cell.2012.03.003 · Cited by 3,390 · cited 1×
“IL4 and IL13 Upregulate MYC to Promote Metabolic Reprogramming Oncogenic MYC is known to cooperate with KRAS* in driving many cancers and contributes to many cancer hallmarks (21, 22), including cancer cell survival (23, 24), cancer initiation and progression (24, 25), and metabolic reprogramming of bioenergetic pathw…”
Background
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-citation
Glutamine 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-citation
Chronic inflammation and cytokines in the tumor microenvironment
Landskron, G., De la Fuente, M., Thuwajit, P., Thuwajit, C., & Hermoso, M. A. (2014) · Journal of Immunology Research · doi:10.1155/2014/149185 · Cited by 1,765
Cytokines in cancer pathogenesis and cancer therapy
Dranoff, G. (2004) · Nature reviews. Cancer · doi:10.1038/nrc1252 · Cited by 1,660
Genetics and biology of pancreatic ductal adenocarcinomaPreprint
Hezel, A. F., Kimmelman, A. C., Stanger, B. Z., Bardeesy, N. M., & DePinho, R. A. (2006) · Genes & Development · doi:10.1101/gad.1415606 · Cited by 1,611
Self-citation
viSNE enables visualization of high dimensional single-cell data and reveals phenotypic heterogeneity of leukemia
Amir, E.-A. D., Davis, K. L., Tadmor, M. D., Simonds, E. F., Levine, J. H., Bendall, S. C., Shenfeld, D. K., Krishnaswamy, S., Nolan, G. P., & Pe'er, D. (2013) · Nature Biotechnology · doi:10.1038/nbt.2594 · Cited by 1,550 · cited 1×
“Data were analyzed with FlowJo (Tree Star) and viSNE (61).”
Method

Show all 65 references

Sorted by citations

Items 101–200 of 217

Construction and Validation of an Immune-Based Prognostic Model for Pancreatic Adenocarcinoma Based on Public Databases
Mao, M., Ling, H.-J., Lin, Y., Chen, Y., Xu, B., & Zheng, R. (2021) · Frontiers in Genetics · doi:10.3389/fgene.2021.702102 · Cited by 15
Co-dependencies in the tumor immune microenvironment
Chen, P., & Dey, P. (2022) · Oncogene · doi:10.1038/s41388-022-02406-7 · Cited by 15
“In pancreatic cancer, KRAS* has been shown to upregulate interleukin (IL) receptors that bind cognate cytokines produced by infiltrating immune cells, thereby enabling a cancer-immune cell paracrine circuit that drives anaerobic glycolysis in cancer cells [29].”
BackgroundSelf-citation
Pro-tumor Tfh2 cells induce detrimental IgG4 production and PGE2-dependent IgE inhibition in pancreatic cancer
Monte, L. B. D., Clemente, F., Ruggiero, E., Pini, R., Ceraolo, M. G., Lena, M. S., Balestrieri, C., Lazarevic, D., Belfiori, G., Crippa, S., et al. (2023) · EBioMedicine · doi:10.1016/j.ebiom.2023.104819 · Cited by 16
Molecular Alterations in Pancreatic Cancer: Transfer to the Clinic
Gil, Y. R., Sánchez, P. J., Velasco, R. M., García, A. G., & Lobo, V. J. S.-A. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22042077 · Cited by 18
“KRas drives the expression IL17 receptor and type I cytokine receptor complexes (IL2rγ-IL4rα and IL2rγ-IL3rα1) to establish a “hematopoietic-to-epithelial signaling axis” and enhance mPanIN progression and metabolic reprogramming [21,22].”
Background
The mycobiome-immune axis: The next frontier in pancreatic cancer
Li, X., & Saxena, D. (2022) · Cancer Cell · doi:10.1016/j.ccell.2022.01.009 · Cited by 15
Glycemic Control as an Early Prognostic Marker in Advanced Pancreatic Cancer
Alpertunga, I., Sadiq, R., Pandya, D. S., Lo, T., Dulgher, M., Evans, S., Bennett, B., Rennert, N. J., & Frank, R. C. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.571855 · Cited by 15
“In addition, oncogenic KRAS has also recently been shown to coopt the tumor microenvironment (TME) to sustain cancer cell glycolytic flux by directing paracrine signaling involving Type II cytokines secreted by Th2 cells in the TME (9).”
Background
Molecular characterization and prognostic implications of KRAS mutations in pancreatic cancer patients: insights from multi-cohort analysis
Jiang, Y., Mai, G., Zhao, X., Tang, M. X., Yang, P., Cheng, Q., Tian, H., Niu, Z., Wang, X., Wang, J., et al. (2025) · npj Precision Oncology · doi:10.1038/s41698-025-01087-1 · Cited by 15
“TheG12D/Q61mutationsmay enhanceRAF/MEK/ERKsignaling 21 or create an immunosuppressive tumor microenvironment 22,23 , promoting tumor proliferation, survival, and invasion.”
Self-citation
DNMT3A mutation promotes leukemia development through NAM-NAD metabolic reprogramming
Yang, X., Wang, X., Yang, Y., Li, Z., Chen, Y., Shang, S., & Wang, Y. (2023) · Journal of Translational Medicine · doi:10.1186/s12967-023-04323-z · Cited by 14
“Perturbations in metabolic pathways and changes in intermediate metabolites lead to changes in the epigenetic landscape by modulating the function of epigenetic enzymes, thereby conveying information about intracellular metabolic conditions to the nucleus [10].”
BackgroundSelf-citation
Identification of a novel prognostic signature for HCC and analysis of costimulatory molecule-related lncRNA AC099850.3
Wang, Q., Fang, Q., Huang, Y., Zhou, J., & Liu, M. (2022) · Scientific Reports · doi:10.1038/s41598-022-13792-z · Cited by 14
Serum Leptin Receptor and the rs1137101 Variant of the LEPR Gene Are Associated with Bladder Cancer
Alfaqih, M. A., Elsalem, L., Nusier, M. K., Mhedat, K., Khader, Y. S., & Ababneh, E. (2023) · Biomolecules · doi:10.3390/biom13101498 · Cited by 13
“Observations made from cell and/or animal models show that cytokines stimulate oncogenic signaling pathways and, hence, promote cancer cell proliferation [17].”
Background
Experimental models of pancreas cancer: what has been the impact for precision medicine?
Pantazopoulou, V., Kubota, C. S., Ogawa, S., Gulay, K. C. M., Lin, X., Song, H., Weitz, J., Tiriac, H., Lowy, A. M., & Engle, D. D. (2025) · Journal of Clinical Investigation · doi:10.1172/jci191945 · Cited by 16
“Models expressing a dox-ycycline-induced Kras (i Kras ) allow for more synchronous tumor growth, which enables the study of KRAS-dependent metabolic (102) and immune (103, 104) changes.”
The cross-talk between the macro and micro-environment in precursor lesions of pancreatic cancer leads to new and promising circulating biomarkers
Mottini, C., Auciello, F. R., Manni, I., Pilarsky, C. P., Caputo, D. D., Caracciolo, G., Rossetta, A., Gennaro, E. D., Budillon, A., Blandino, G., et al. (2024) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-024-03117-5 · Cited by 12
“Activated stromal cells as well as immune cells have already been found in the stroma of PanIN lesions [28, 29], underlining how the presence of these cell types may be crucial for the progression of early lesions to PC. Immune infiltration occurs in PanIN and IPMN [30, 31], thus facilitating…”
Background
Molecular, metabolic, and histological subtypes of pancreatic ductal adenocarcinoma and its tumor microenvironment: Insights into tumor heterogeneity and clinical implications
Ohara, Y., Liu, H., Moreno, P., Suzuki, S., & Hussain, S. P. (2025) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2025.108946 · Cited by 11
Development and validation of glycolysis‐related prognostic score for prediction of prognosis and chemosensitivity of pancreatic ductal adenocarcinoma
Zhang, X., Chen, Q., Liu, Q., Wang, Y., Wang, F., Zhao, Z., Zhao, G., Lau, W. Y., Gao, Y., & Liu, R. (2021) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.16573 · Cited by 11
Self-citation
Single-cell and spatial transcriptome profiling identifies the immunosuppressive spatial niche in KRAS -mutant colorectal cancer
Yang, S., Gu, C., Miao, X., Zuo, H., Xu, W. L., Zhang, Y., Tang, W., Zhu, J., Yuan, Z., Gu, X., et al. (2025) · Journal for ImmunoTherapy of Cancer · doi:10.1136/jitc-2025-013763 · Cited by 11
Blocking M2-Like Macrophage Polarization Using Decoy Oligodeoxynucleotide-Based Gene Therapy Prevents Immune Evasion for Pancreatic Cancer Treatment
Chen, C.-J., Wang, H., Hou, Y., Wu, Y.-Y., Shieh, C., & Shan, Y. (2024) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-23-0767 · Cited by 10
“As a multifunctional cytokine in the TME, IL4 not only participates in alternative macrophage priming but also accelerates pancreatic cancer progression (49).”
BackgroundSelf-citation
Drugging the Undruggable and beyond: Emerging precision oncology approaches to target acquired resistance to KRAS G12C and KRAS G12D inhibitors
Kale, R. R., Samant, C., Nandakumar, K., Pai, K. S. R., & Bhonde, M. (2025) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2025.151688 · Cited by 11
Precision immune regulation in KRAS-mutated cancers: the final piece of the puzzle?
Fu, S., Ma, J., Cai, C., Tan, J., Deng, X., Shen, H., Zeng, S., Chen, Y., & Han, Y. (2025) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-025-03444-1 · Cited by 11
Two rare cancers of the exocrine pancreas: to treat or not to treat like ductal adenocarcinoma?
Skorupan, N., Ghabra, S., Maldonado, J. A., Zhang, Y., & Alewine, C. (2023) · Journal of Cancer Metastasis and Treatment · doi:10.20517/2394-4722.2022.106 · Cited by 10
Molecular Pathology of Pancreatic Cancer
Karamitopoulou, E. (2022) · Cancers · doi:10.3390/cancers14061523 · Cited by 10
Surface-Engineered Monocyte Immunotherapy Combined Graphene Quantum Dots Effective Against Solid Tumor Targets
Xia, Q., Tang, Y., Li, W., Liang, T., Zhou, Y., Liu, J., & Liu, F. (2023) · International Journal of Nanomedicine · doi:10.2147/ijn.s404486 · Cited by 12
Self-citation
Oncogenic Kras G12D specific non-covalent inhibitor reprograms tumor microenvironment to prevent and reverse early pre-neoplastic pancreatic lesions and in combination with immunotherapy regresses advanced PDAC in a CD8 + T cells dependent mannerPreprint
Mahadevan, K. K., McAndrews, K. M., LeBleu, V. S., Yang, S., Lyu, H., Li, B., Sockwell, A. M., Kirtley, M. L., Morse, S. J., Diaz, B. A. M., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.02.15.528757 · Cited by 10
Self-citation
Type II Interleukin-4 Receptor Activation in Basal Breast Cancer Cells Promotes Tumor Progression via Metabolic and Epigenetic Modulation
Williams, D., Hargrove-Wiley, E., Bindeman, W. E., Valent, D., Miranda, A. X., Beckstead, J. A., & Fingleton, B. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25094647 · Cited by 9
“Type II IL4 receptor signaling has been previously associated with elevated glycolysis in breast cancer [15] and other cancer types [16].”
BackgroundMethodInfluential
KRAS-G12D inhibitor HRS-4642 plus chemotherapy in advanced KRASG12D-mutant pancreatic cancer: a phase 1b/2 trial
Cui, J., Jiang, K., Li, W., Ni, S., Zong, H., Du, J., He, Y., Liu, Z., Kong, G., Zhang, Y., et al. (2026) · Nature Medicine · doi:10.1038/s41591-026-04538-9 · Cited by 13
“Oncogenic KRAS mutations drive pathogenesis and shape the suppressive metabolic and immune tumor microenvironment of PDAC 8–10 , with the KRAS G12D variant representing the most prevalent KRAS alteration 11 , detectable in approximately 50% cases 12,13 .”
Positive Crosstalk Between Hedgehog and NF-κB Pathways Is Dependent on KRAS Mutation in Pancreatic Ductal Adenocarcinoma
Wang, Y., Wang, D., Dai, Y., Kong, X., Zhu, X., Fan, Y., Wang, Y., Wu, H., Jin, J., Yao, W., et al. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.652283 · Cited by 9
Self-citation
Orchestration of mesenchymal plasticity and immune evasiveness via rewiring of the metabolic program in pancreatic ductal adenocarcinoma
Hashimoto, A., Handa, H., Hata, S., & Hashimoto, S. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.1005566 · Cited by 9
The relationship of KRAS expression with KRAS status, prognosis, and tumor-infiltrated T lymphocytes in colorectal cancer
Zhou, Y., Zeng, Z., Li, Z., Ruan, L., Xie, H., Ye, F., Huang, L., Liu, H., & Kang, L. (2024) · Therapeutic Advances in Gastroenterology · doi:10.1177/17562848241249387 · Cited by 9
KRAS G12C inhibition and innate immune targeting
Tani, T., Kitajima, S., Conway, E. B., Knelson, E. H., & Barbie, D. A. (2021) · Expert Opinion on Therapeutic Targets · doi:10.1080/14728222.2021.1902991 · Cited by 9
“immune interactions via metabolic reprogramming, as elegantly shown in models of the pancreatic cancer stroma [22].”
Background
JNK inhibitor IX restrains pancreatic cancer through p53 and p21
Shi, J., Yang, X., Kang, Q., Lu, J., Denzinger, M., Kornmann, M., & Traub, B. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.1006131 · Cited by 9
“Furthermore, it has been shown that mutant KRAS causes alterations in associated pathways, thereby potentiating its deadly potential (27).”
Background
The Janus kinase 1 is critical for pancreatic cancer initiation and progression
Shrestha, H., Rädler, P. D., Dennaoui, R., Wicker, M. N., Rajbhandari, N., Sun, Y., Peck, A. R., Vistisen, K. S., Triplett, A. A., Beydoun, R., et al. (2024) · Cell Reports · doi:10.1016/j.celrep.2024.114202 · Cited by 8
“9 Despite differences in the RNA expression of selected genes related to cell adhesion (e.g., Vcam, Alcam, Claudins, and Syndecans that are part of this Kyoto Encyclopedia of Genes and Genomes [KEGG] gene cluster), the examination of nine markers of epithelial-mesenchymal transition (EMT) in seven…”
BRAF inhibitor resistance in melanoma: from resistance mechanisms to therapeutic innovations
Shang, Y., Cao, T., Li, J., Li, J., ZHANG, L., Ma, Q., Feng, L., & Zhao, H. (2026) · Molecular Biomedicine · doi:10.1186/s43556-026-00425-4 · Cited by 9
Self-citation
Clinical significance of pancreatic ductal metaplasia
Jiang, T., Fang, W., & Xie, K. (2022) · The Journal of Pathology · doi:10.1002/path.5883 · Cited by 8
“In KRAS-driven PDAC, upregulation of cytokine receptors induces MYC through the JAK1-STAT6 signaling pathway, driving metabolic reprogramming [197].”
Background
SP1‐Mediated Glycolytic Reprogramming Promotes Tumorigenesis and Progression in Pancreatic Cancer
Hang, H., Yu, M., Zhu, L., Tang, N., Fu, X., Cai, Z., Yan, M., Chen, Y., Yang, L., Wu, J., et al. (2025) · Advanced Science · doi:10.1002/advs.202510071 · Cited by 7
m6A demethylase FTO drives pancreatic ductal adenocarcinoma tumorigenesis and metastasis through remodeling PFKM mediated glycolysis
Tan, Z., Yang, J., Chen, Y., Zhu, H., Liu, X., He, X., Meng, Q., Xiao, M., Tang, R., Rong, Z., et al. (2025) · Cell Death and Disease · doi:10.1038/s41419-025-08049-2 · Cited by 7
“The Warburg effect, a hallmark of invasive cancer metabolism, accelerates glycolysis activation in PDAC partially through remodeling of the extracellular matrix [7, 8].”
Fucoxanthin suppresses pancreatic cancer progression by inducing bioenergetics metabolism crisis and promoting SLC31A1‑mediated sensitivity to DDP
Shangguan, F., Ma, N., Chen, Y., Zheng, Y., Ma, T., An, J., Lin, J., & Yang, H. (2025) · International Journal of Oncology · doi:10.3892/ijo.2025.5737 · Cited by 7
ZCCHC17 Served as a Predictive Biomarker for Prognosis and Immunotherapy in Hepatocellular Carcinoma
Liu, F., Liang, J., Long, P., Zhu, L., Hou, W., Wu, X., & Luo, C. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2021.799566 · Cited by 7
“Th2 cell function is hyperactive and then synthesizes and secretes many inhibitory cytokines under an imbalance of Th1/Th2 condition, which directly leads to the decline of the body’s immune function and causes the immune escape of tumor cells (26).”
Background
UBE2T is a prognostic biomarker and correlated with Th2 cell infiltrates in retinoblastoma
Wang, Z., Chen, N., Liu, C., Cao, G., Ji, Y., Yang, W., & Jiang, Q. L. (2022) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2022.04.096 · Cited by 7
Mitochondria-Related Transcriptome Characterization Associated with the Immune Microenvironment, Therapeutic Response and Survival Prediction in Pancreatic Cancer
Dong, J., Liu, J., Zhang, B., Liang, C., Hua, J., Meng, Q., Wei, M., Wang, W., Yu, X., & Xu, J. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24043270 · Cited by 7
“Previous researchers have found that type II helper cells infiltrate the pancreas early during tumorigenesis and drive PC progression by facilitating glycolysis and generating IL-4 and IL-13 [57].”
BackgroundSelf-citation
Comprehensive analysis of m6A reader YTHDF2 prognosis, immune infiltration, and related regulatory networks in hepatocellular carcinoma
Wang, H., Cai, H., & Li, L. (2023) · Heliyon · doi:10.1016/j.heliyon.2023.e23204 · Cited by 7
“As one type of T helper cell, Th2 cell can lead to the inhibition of the host immune system, and produce IL-4, consequently resulting in activation of several cancer-related pathways [38,39].”
BackgroundSelf-citation
CDK4 as a Prognostic Marker of Hepatocellular Carcinoma and CDK4 Inhibitors as Potential Therapeutics
Lai, F., Fang, Y., Cheng, C., Zhong, X., Zheng, W., Lan, S., Peng, Q., Cai, X., Cao, T., Zhong, C., et al. (2024) · Current Medicinal Chemistry · doi:10.2174/0109298673279399240102095116 · Cited by 6
Tumor microenvironment-like conditions alter pancreatic cancer cell metabolism and behavior
Gardner, G. L., & Stuart, J. A. (2024) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00452.2024 · Cited by 7
Targeting cytokines: Reshaping the pancreatic tumor microenvironment
Bandi, D. S. R., Chabattula, S. C., Pynam, H., Joseph, J. T., Sarvesh, S., Nagaraju, G. P., & El‐Rayes, B. F. (2025) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2025.11.003 · Cited by 6
The SMYD3-dependent H3K4me3 status of IGF2 intensifies local Th2 differentiation in CRSwNP via positive feedback
Yu, L., Wei, Y. Z., Lu, T., Li, Z., Lai, S., Yan, Y., Chen, C., & Wen, W. (2023) · Cell Communication and Signaling · doi:10.1186/s12964-023-01375-y · Cited by 6
“Consistent with published reports [39, 40], c-Myc, as a "bridge" linking MAT2A and IL-4/p-STAT6, might function as a mediator during this process, and its expression was found to be increased in the IL-4 group by Western blot analysis.”
Result
Epigenetic regulation of the tumor microenvironment: A leading force driving pancreatic cancer
Vera, R. E., Lamberti, M. J., González, A. L., & Fernández-Zapico, M. E. (2024) · Pancreatology · doi:10.1016/j.pan.2024.07.005 · Cited by 6
Propionyl-CoA carboxylase subunit B regulates anti-tumor T cells in a pancreatic cancer mouse modelPreprint
Han, H. V., Efem, R., Rosati, B., Lu, K., Maimouni, S., Jiang, Y., Montoya, V., Velden, A. W. M. V. D., Zong, W., & Lin, R. Z. (2024) · eLife · doi:10.7554/elife.96925.2 · Cited by 9
Organoids: technology refining, current applications and future directions
Cheng, X., Fang, Z., Sun, J., Liu, L., Yang, Y., Wang, J., Shuai, J., Zhou, X., Lin, P., Yang, G., et al. (2026) · Molecular Biomedicine · doi:10.1186/s43556-026-00422-7 · Cited by 6
“In recent years, research on regenerative medicine and organoids is not limited to traditional organoid transplantation, but also includes the optimization of regenerative medicine orga-noid culture systems [95] and the use of organoid models to explore specific genetic mechanisms [95, 96].”
CDK8 remodels the tumor microenvironment and promotes resistance to KRASG12D inhibitors and daraxonrasib in PDAC
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
“S3B) (Dey et al, 2020; Viale et al, 2014; Ying et al, 2012).”
Self-citation
Comparative Untargeted Metabolomic Profiling of Induced Mitochondrial Fusion in Pancreatic Cancer
Nguyen, N. D., Yu, M., Reddy, V. Y., Acevedo-Diaz, A., Mesarick, E. C., Jaoude, J. A., Yuan, M., Asara, J. M., & Taniguchi, C. M. (2021) · Metabolites · doi:10.3390/metabo11090627 · Cited by 5
Co-expression patterns explain how a basic transcriptional role for MYC modulates Wnt and MAPK pathways in colon and lung adenocarcinomas
Kucherlapati, M. H. (2022) · Cell Cycle · doi:10.1080/15384101.2022.2060454 · Cited by 5
“KRAS deregulation in pancreatic ductal adenocarcinoma has recently been linked to cytokines usage from the tumor microenvironment [100], providing CELL CYCLE 1631”
Background
TEDC2 plays an oncogenic role and serves as a therapeutic target of hepatocellular carcinoma
Li, Y., Guo, B., Wang, L., Zhou, F., Yu, Z., Huang, Y., Chen, R., Zhang, M., Zhang, K., Zheng, L., et al. (2023) · Digestive and Liver Disease · doi:10.1016/j.dld.2023.09.025 · Cited by 5
Anakinra-Loaded Sphingomyelin Nanosystems Modulate In Vitro IL-1-Dependent Pro-Tumor Inflammation in Pancreatic Cancer
Abal-Sanisidro, M., Michele, D. L., Roma, S., Ceraolo, M. G., de la Fuente, M., Monte, L. B. D., & Protti, M. P. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25158085 · Cited by 5
“Mouse models recapitulating the tumor-promoting Th2-and Th17-type inflammation, as reported in the human disease, have been described [29,66,67], and they could offer good models for exploring the new pharmaceutical preparations, comprising any additional/different side effects compared to the ones…”
Background
Thymic stromal lymphopoietin (TSLP) – pro-inflammatory cytokine and antimicrobial peptide
Döhner, K., John, O. P., & Werfel, T. (2026) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2026.120127 · Cited by 4
Selective Targeting of STAT6: Recent Advances and Future Perspectives
Liu, H., Ma, F., Wang, Z., Li, Z. A., Bian, J., Yuan, Z., & Wu, T. (2026) · Medicinal Research Reviews · doi:10.1002/med.70069 · Cited by 4
vNARs as Neutralizing Intracellular Therapeutic Agents: Glioblastoma as a Target
Manzanares-Guzmán, A., Lugo-Fabres, P. H., & Camacho-Villegas, T. A. (2024) · Antibodies · doi:10.3390/antib13010025 · Cited by 4
“IL13R α 1/IL-4R α binding to IL-13 prompts the activation of STAT-6 signaling, resulting in translocation to the nucleus [118].”
Background
CDK8 remodels the tumor microenvironment to resist the therapeutic efficacy of targeted KRAS G12D inhibition in pancreatic ductal adenocarcinomaPreprint
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-citation
Antioxidant capacity of the iron–sulfur cluster assembly protein IscU2 is mediated by aspartate metabolism to promote tumor survival
Yang, X., Liang, N., Liu, D., Yan, J., Yang, X., Lv, J., Xiao, S., Wei, X., Chen, X., Yang, Z., et al. (2025) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2025.110234 · Cited by 4
Molecular Imaging: Unveiling Metabolic Abnormalities in Pancreatic Cancer
Wang, H., Gui, Y., & Lv, K. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26115242 · Cited by 3
“This oncogene plays a central role in mediating metabolic reprogramming that fuels pancreatic carcinogenesis [9–11].”
Self-citation
Molecular pathology of intraductal papillary mucinous neoplasms of the pancreas: current understanding and perspectives on malignant progression
Makino, Y., Oyama, K., Sagara, A., Thege, F. I., & Maitra, A. (2025) · Journal of Gastroenterology · doi:10.1007/s00535-025-02328-7 · Cited by 4
“Another study showed that mutant RAS protein induces the expression of type I cytokine receptor complexes in cancer cells that enable them to receive cytokine growth signals (IL-4 or IL-13) from tumor microenvironment [111].”
Self-citation
The Warburg effect and beyond: Glycolytic reprogramming in cancer progression and emerging therapeutic strategies
Long, Y., Xu, J., Xu, Z., Su, Z., Li, W., & Li, J. (2026) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2026.119692 · Cited by 3
Self-citation
Oncogenic Kras targeting with MRTX1133 or Daraxonrasib specifically synergize with anti-CTLA4 to promote anti-tumor immunity in pancreatic cancer
Mahadevan, K. K., Maldonado, A. S., Li, B., Bickert, A. A., Perdyan, A., Kumbhar, S. V., Piya, S., Sockwell, A. M., Morse, S. J., Arian, K. A., et al. (2026) · Nature Communications · doi:10.1038/s41467-026-75960-3 · Cited by 12
Self-citation
STAT3 Inhibition Prevents Adaptive Resistance and Augments NK Cell Cytotoxicity to KRASG12C Inhibitors in Nonsmall Cell Lung Cancer
Pan, Z., Qian, Y., Wang, Y., Zhang, T.-S., Song, X., Ding, H., Li, R., Zhang, Y., Wang, Z., Wang, H., et al. (2025) · Cancer Science · doi:10.1111/cas.70017 · Cited by 3
Self-citation
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
“This subsequently upregulated glycolytic gene expression via the Janus kinase (JAK)-STAT /MYC signaling [92].”
Single-cell transcriptome analysis for cancer and biology of the pancreas: A review on recent progress
Tamaddon, M., Azimzadeh, M., Gifani, P., & Tavangar, S. M. (2023) · Frontiers in Genetics · doi:10.3389/fgene.2023.1029758 · Cited by 3
Fungal mycobiome-mediated immune response: a non-negligible promoter in pancreatic oncogenesis and chemoresistance
Jiang, Y., Donati, V. L., Peters, G. J., Giovannetti, E., & Deng, D. (2023) · Cancer Drug Resistance · doi:10.20517/cdr.2023.06 · Cited by 2
Antitumor effects of LPM5140276 and its potential combination with SHP2 inhibition in KRASG12D-mutant cancer
Hu, Z., Zou, F., Zhao, F., Yu, P., Zhu, H., Yu, L., Wang, W., & Ye, L. (2026) · Frontiers in Pharmacology · doi:10.3389/fphar.2025.1554356 · Cited by 2
Management of Advanced Pancreatic Cancer through Stromal Depletion and Immune Modulation
Liu, T., Cheng, S., Xu, Q., & Wang, Z. P. (2022) · Medicina · doi:10.3390/medicina58091298 · Cited by 2
“As part of this metabolic shift, redundant glycolytic intermediates enter various metabolic bypass pathways [38,39], and glutamine transportation is hyperactivated [40].”
Background
Identification of characteristic markers correlated with Th2 cell infiltration and metabolism molecular subtype in pancreatic adenocarcinoma
Xu, Z., Li, P., Wang, W., & Liu, L. (2022) · Journal of Gastrointestinal Oncology · doi:10.21037/jgo-22-333 · Cited by 1
“Accordingly, pancreatic adenocarcinoma patients were A previous study had reported that Th2 cells release IL2 and IL13 to activate the STAT6 and cMyc pathways and promote the development of Kras-initiated pancreatic cancer in mice (10).”
IMCell XMBD : A statistical approach for robust cell identification and quantification from imaging mass cytometry imagesPreprint
Xu, X., Su, N., Kong, Y., Zhang, L., Ding, X., Yang, W., & Yu, R. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.09.27.461899 · Cited by 2
Acinar-to-ductal metaplasia in the pancreas requires a glycolytic switch and functional mitochondriaPreprint
Neuß, T., Wirges, N., Chen, M., Usluer, S., Oellinger, R., Lier, S., Dudek, M., Madl, T., Jastroch, M., Steiger, K., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.06.27.495427 · Cited by 2
“Recent data from PDAC cells demonstrated that exogenous IL4 and IL13 influence the TCA cycle activity in a MYC-dependent manner (Dey et al., 2020).”
Background
Personalized Neoadjuvant Chemotherapy for Gastrointestinal Cancers: Shaping Imprecision to be Precise
Høgdall, D., Schou, J. V., Bromann, J. J. A., Andersen, J. B., & O’Rourke, C. J. (2025) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-24-4309 · Cited by 1
SMYD3 Promotes Immune Evasion in Clear Cell Renal Cell Carcinoma via SREBP1‐Mediated Transactivation of CD47
Liu, Z., Zhao, X., Zang, M., Yuan, H., Qin, X., Li, X., Zhao, S., Tan, R., Yan, K., Liu, L., et al. (2025) · Advanced Science · doi:10.1002/advs.202404200 · Cited by 1
IL-1 family members as regulators of lymphoid type-2 immunity in cancer
Roma, S., Colombo, F., Monte, L. B. D., & Protti, M. P. (2025) · Seminars in Immunology · doi:10.1016/j.smim.2025.102005 · Cited by 1
From “undruggable” to tractable: Therapeutic advances targeting Kristen rat sarcoma viral homolog glycine to cysteine mutation at codon 12 (KRAS G12C)-mutant cancers and emerging resistance mechanisms
Devanahally, S., & Dubey, S. (2026) · Cancer Pathogenesis and Therapy · doi:10.1016/j.cpt.2026.02.001 · Cited by 2
The Role of Glycolysis in Tumorigenesis—The Many Unresolved Issues
Marcucci, F., Wei, S., & Cordani, M. (2026) · Cells · doi:10.3390/cells15060499 · Cited by 1
“…concentration in the extracellular matrix [18], too low or too high glucose levels in the extracellular milieu [19,20], extracellular acetate [21], bacterial infections [22], antitumor therapeutics [23], reactive oxygen species (ROS) [24], or cytokines [25] can upregulate fermentative glycolysis.”
KRAS and MYC synergistic inhibition: a powerful strategy targeting KRAS-mutant cancers
Yan, M., Liu, K., Xu, J., Liu, Y., Ji, L., & Zhang, S. (2026) · Molecular Cancer · doi:10.1186/s12943-026-02659-w · Cited by 1
“Recent studies have highlighted the crucial role of MYC as a stress adaptation factor in KRAS-driven cancers, particularly under high metabolic demands driven by KRAS mutations [39].”
Advancing precision medicine in pancreatic cancer using novel biomarkers and clinical targets
Murthy, D., Seyhan, A. A., den Hollander, P., Lu, S., Kuburich, N. A., Gould, C., Karam, A., Sun, K., Schupp, P. G., Safran, H., et al. (2026) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2026.101476 · Cited by 2
Targeting stroma-mediated T-cell exclusion and functional exhaustion in pancreatic ductal adenocarcinoma through CXCR4 and PD-1 blockade
Deipenbrock, A., Hofer, L., Wilmes, B. E., Cetin, T., Esposito, I., Weyhe, D., Stegmaier, J., & Teusch, N. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1844781 · Cited by 2
“…are largely polarized toward a Th2 phenotype, promoting immunosuppression through the release of anti-in ﬂ am-matory cytokines such as IL-4 and IL-13, which polarize anti-in ﬂ ammatory M2 macrophages and support tumor cell metabolism through increased glycolysis via JAK-STAT signaling (14, 15).”
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
“KRAS is the predominant driver gene in PDAC and can link tumor-cell-intrinsic programs with stromal and immune-cell states by regulating cytokine production and metabolic remodeling (Dey et al., 2020).”
Influential
RRP8, associated with immune infiltration, is a prospective therapeutic target in hepatocellular carcinoma
You, K., Du, X., Zhao, Y., Wen, F., Lu, Z., & Fan, H. (2024) · Journal of Cancer Research and Clinical Oncology · doi:10.1007/s00432-024-05756-9 · Cited by 1
Visceral Surgery Profoundly Affects the Cellular and Humoral Components of the Anti-Tumour Immune Response in a Murine Pancreatic Adenocarcinoma Model
Loening, F., Kleinwort, A., Partecke, L. I., Schulze, T., & Menges, P. (2022) · Cancers · doi:10.3390/cancers14163850 · Cited by 1
“IL-4 and IL-13 have both been shown to supress the anti-tumoural immune response, and moreover to directly drive the proliferation of KRAS-mutant tumour cells [37].”
Background
A New Gene Therapy for Pancreatic Cancer: STAT6-CYBB Decoy Oligodeoxynucleotides Focusing on Inhibiting M2 MacrophagesPreprint
Chen, C.-J., Wang, H., Hou, Y., Wu, Y.-Y., Shieh, C., & Shan, Y. (2022) · Research Square · doi:10.21203/rs.3.rs-1690410/v1 · Cited by 1
Self-citation
ISG20L2 as a Novel Prognostic Biomarker Facilitates the Progression of Pancreatic Cancer via GlycolysisPreprint
Wei, J., Gao, X., Ren, B., Sun, D., & Liu, T. (2021) · Research Square · doi:10.21203/rs.3.rs-900506/v1
KRAS G12D can be targeted by potent salt-bridge forming inhibitorsPreprint
Mao, Z., Xiao, H., Shen, P., Yang, Y., Xue, J. W., Yang, Y., Shang, Y., Zhang, L., Li, X., Zhang, Y., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.12.13.472365
ISG20L2 as a Novel Prognostic Biomarker Facilitates the Progression of Pancreatic Cancer Via GlycolysisPreprint
Wei, J., Gao, X., Ren, B., Sun, D., & Liu, T. (2021) · Research Square · doi:10.21203/rs.3.rs-900506/v2
Construction and Verification of Prognosis Model Based on Autophagy-related Gene Signatures in Digestive System TumorPreprint
Zhang, Y., Wang, J., Liu, F., Wei, Y. Q., Cheng, Y. Q., & Wang, H. (2022) · Research Square · doi:10.21203/rs.3.rs-2159421/v1
Self-citation
Calligraphy tool offers clues to the origin of pancreatic cancer
Bednar, F., & di Magliano, M. P. (2023) · Nature · doi:10.1038/d41586-023-02518-4
PLPP2 as a metabolic and immune marker for predicting survival and enhancing response to anti-PD1 therapy in pancreatic cancerPreprint
Sheng, G., Du, X., Ni, B., Liu, Z., Wu, C., Meng, K., Xie, Y., & Yang, T. (2024) · Research Square · doi:10.21203/rs.3.rs-3952664/v1
Additional file 2 of DNMT3A mutation promotes leukemia development through NAM-NAD metabolic reprogramming
Yang, X., Wang, X., Yang, Y., Li, Z., Chen, Y., Shang, S., & Wang, Y. (2023) · Figshare · doi:10.6084/m9.figshare.23706967
Self-citation
Propionyl-CoA carboxylase subunit B regulates anti-tumor T cells in a pancreatic cancer mouse modelPreprint
Han, H. V., Efem, R., Rosati, B., Lu, K., Maimouni, S., Jiang, Y., Montoya, V., van der Velden, A. W. M., Zong, W., & Lin, R. Z. (2024) · eLife · doi:10.7554/elife.96925.1
Thymic Stromal Lymphopoietin and Malignancies
Ghasempour, P., Bagheri, A., Samieefar, N., & Rezaei, N. (2024) · Interdisciplinary cancer research · doi:10.1007/16833_2024_411
STAT5: Understanding the Biology of KRASG12D‐Driven Pancreatic Cancer
Papavassiliou, K. A., Adamopoulos, C., & Papavassiliou, A. G. (2024) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.70303
m6A Demethylase FTO Drives Pancreatic Ductal Adenocarcinoma Metastasis Through Remodeling PFKM Mediated GlycolysisPreprint
Tan, Z., Yang, J., Chen, Y., Zhu, H., Liu, X., He, X., Meng, Q., Xiao, M., Tang, R., Rong, Z., et al. (2025) · SSRN Electronic Journal · doi:10.2139/ssrn.5158499
Silencing the signal: The metastasis suppressor NDRG1 disrupts exosome-mediated crosstalk in pancreatic cancerPreprint
Chang, J., Alenizi, S., Milioli, H. H., Lay, W., Pounraj, S., Li, Y., Shiferaw, M. S., Beheshti, E. H., & Kovačević, Ž. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.10.15.682724
Pan-Cancer Expression Analysis of the Aminoadipate-semialdehyde synthase (AASS) Gene: Insights into its Potential Role in Oncogenic Metabolic ReprogrammingPreprint
Raza, H. (2025) · Research Square · doi:10.21203/rs.3.rs-8210982/v1
Additional file 5 of The SMYD3-dependent H3K4me3 status of IGF2 intensifies local Th2 differentiation in CRSwNP via positive feedback
Yu, L., Wei, Y., Lu, T., Li, Z., Lai, S., Yan, Y., Chen, C., & Wen, W. (2024) · Figshare · doi:10.6084/m9.figshare.26647515
Additional file 2 of The SMYD3-dependent H3K4me3 status of IGF2 intensifies local Th2 differentiation in CRSwNP via positive feedback
Yu, L., Wei, Y., Lu, T., Li, Z., Lai, S., Yan, Y., Chen, C., & Wen, W. (2024) · Figshare · doi:10.6084/m9.figshare.26647506
Additional file 1 of DNMT3A mutation promotes leukemia development through NAM-NAD metabolic reprogramming
Yang, X., Wang, X., Yang, Y., Li, Z., Chen, Y., Shang, S., & Wang, Y. (2023) · Figshare · doi:10.6084/m9.figshare.23706964
Self-citation
Additional file 1 of The SMYD3-dependent H3K4me3 status of IGF2 intensifies local Th2 differentiation in CRSwNP via positive feedback
Yu, L., Wei, Y., Lu, T., Li, Z., Lai, S., Yan, Y., Chen, C., & Wen, W. (2024) · Figshare · doi:10.6084/m9.figshare.26647503
Additional file 3 of The SMYD3-dependent H3K4me3 status of IGF2 intensifies local Th2 differentiation in CRSwNP via positive feedback
Yu, L., Wei, Y., Lu, T., Li, Z., Lai, S., Yan, Y., Chen, C., & Wen, W. (2024) · Figshare · doi:10.6084/m9.figshare.26647509
Additional file 6 of The SMYD3-dependent H3K4me3 status of IGF2 intensifies local Th2 differentiation in CRSwNP via positive feedback
Yu, L., Wei, Y., Lu, T., Li, Z., Lai, S., Yan, Y., Chen, C., & Wen, W. (2024) · Figshare · doi:10.6084/m9.figshare.26647518

Authors: Dey, P., Li, J., Zhang, J., Chaurasiya, S., Strom, A., Wang, H., Liao, W.-T., Cavallaro, F., Denz, P., Bernard, V., Yen, E.-Y., Genovese, G., Gulhati, P., Liu, J., Chakravarti, D., Deng, P., Zhang, T., Carbone, F., Chang, Q., Ying, H., Shang, X., Spring, D. J., Ghosh, B., Putluri, N., Maitra, A., Wang, Y. A., & DePinho, R. A.
Affiliations: The University of Texas MD Anderson Cancer Center (US)
University of Houston (US)
3Center for Nuclear Receptor and Cell Signaling, University of Houston, Houston, Texas.
1Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Roswell Park Comprehensive Cancer Center (US)
Baylor College of Medicine (US)
Corresponding author: DePinho, Ronald A.
ORCID: Dey, Prasenjit
Li, Jun
Zhang, Jianhua
Chaurasiya, Surendra
Wang, Huamin
Liao, Wen-Ting
Cavallaro, Frederick
Denz, Parker
Bernard, Vincent
Yen, Er-Yen
Genovese, Giannicola
Gulhati, Pat
Liu, Jielin
Chakravarti, Deepavali
Deng, Pingna
Zhang, Tingxin
Carbone, Federica
Chang, Qing
Ying, Haoqiang
Shang, Xiaoying
Spring, Denise J.
Putluri, Nagireddy
Maitra, Anirban
Wang, Y. Alan
DePinho, Ronald A.
Venue: Cancer Discovery
Publisher: American Association for Cancer Research (AACR)
Published: 2020-04-01
Volume: 10
Issue: 4
Pages: 608-625
ISSN: 2159-8274 (ISSN-L)
2159-8290
DOI: 10.1158/2159-8290.cd-19-0297
OpenAlex: W3006227213
Cited by: 213
References: 65
Citations by year: 2026: 30 · 2025: 33 · 2024: 33 · 2023: 33 · 2022: 40 · 2021: 36 · 2020: 8
FWCI: 10.65
Type: journal article
Language: en
Open access: closed
Locations: Cancer Discovery (publishedVersion)
PubMed (publishedVersion)
Funders: MD Anderson (P30CA16672)
Baylor College of Medicine (P30CA125123)
CPRIT (RP170005, RP140106170067, 170067)
NCI (P01 CA117969, R01 CA225955)
DOD (W81XWH-14-1-0429, K99/R00, 1K99 CA218891-01A1, U24 CA224020, R01 CA218004, R01 CA304969)
Topics: Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
Keywords: pancreatic ductal adenocarcinoma, oncogenic KRAS, tumor microenvironment, metabolic reprogramming, glycolysis, c-Myc, STAT6, IL-4, IL-13, Th2 cells, paracrine signaling, tumor stroma
MeSH terms: Animals, Humans, Oncogenes, Pancreatic Neoplasms, Transfection, Cytokines, Proto-Oncogene Proteins p21(ras), Mice, Tumor Microenvironment, Cellular Reprogramming

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

Oncogenic KRAS-Driven Metabolic Reprogramming in Pancreatic Cancer Cells Utilizes Cytokines from the Tumor Microenvironment

Abstract

Overview

Integrity signals

Verification

Claims the paper makes

Claims other papers make about this one

Citations

Cites

Cited by

Related

Metadata

Record

About these checks