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Journal articles on the topic 'P53FL'

Author: Grafiati

Published: 6 September 2023

Last updated: 31 July 2025

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1

Haaland, Ingvild, Sigrun M. Hjelle, Håkon Reikvam, et al. "p53 Protein Isoform Profiles in AML: Correlation with Distinct Differentiation Stages and Response to Epigenetic Differentiation Therapy." Cells 10, no. 4 (2021): 833. http://dx.doi.org/10.3390/cells10040833.

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p53 protein isoform expression has been found to correlate with prognosis and chemotherapy response in acute myeloid leukemia (AML). We aimed to investigate how p53 protein isoforms are modulated during epigenetic differentiation therapy in AML, and if p53 isoform expression could be a potential biomarker for predicting a response to this treatment. p53 full-length (FL), p53β and p53γ protein isoforms were analyzed by 1D and 2D gel immunoblots in AML cell lines, primary AML cells from untreated patients and AML cells from patients before and after treatment with valproic acid (VPA), all-trans

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2

Ghosh, Arnab, Judith Michel, Divya Venkatesh, et al. "Abstract 250: Activating canonical p53 functions in tumor-associated macrophages improves immune checkpoint blockade efficacy." Cancer Research 82, no. 12_Supplement (2022): 250. http://dx.doi.org/10.1158/1538-7445.am2022-250.

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Abstract Canonical p53-activated pathways can influence a microenvironment that promotes antitumor immune surveillance via tumor-associated macrophages (TAMs). We examined whether p53 activity in the tumor microenvironment (TME) influences antitumor immunity and show that p53 signaling induced pharmacologically with APR-246 (eprenetapopt) can augment the efficacy of immune checkpoint blockade (ICB) in preclinical models, a strategy that is also being tested in patients (NCT04383938). We first investigated the effects of combining APR-246 with ICB in wildtype C57BL6 (B6) mice bearing syngeneic

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3

Pourebrahimabadi, Rasoul, Zoe Alaniz, Lauren B. Ostermann, et al. "p53 Mediated Bone Marrow Mesenchymal Stem Cell Expansion Supports Acute Myeloid Leukemia Development." Blood 134, Supplement_1 (2019): 523. http://dx.doi.org/10.1182/blood-2019-127245.

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Acute myeloid leukemia (AML) is a heterogeneous disease that develops within a complex microenvironment. Reciprocal interactions between the bone marrow mesenchymal stem/stromal cells (BM-MSCs) and AML cells can promote AML progression and resistance to chemotherapy (Jacamo et al., 2014). We have recently reported that BM-MSCs derived from AML patients (n=103) highly express p53 and p21 compared to their normal counterparts (n=73 p&lt;0.0001) (Hematologica, 2018). To assess the function of p53 in BM-MSCs, we generated traceable lineage specific mouse models targeting Mdm2 or Trp53 alleles

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Pourebrahim, Rasoul, Peter P. Ruvolo, Steven M. Kornblau, Carlos E. Bueso-Ramos, and Michael Andreeff. "Genetic Dissection of p53 Driven Senescence of Bone Marrow Mesenchymal Cells in Acute Myeloid Leukemia." Blood 132, Supplement 1 (2018): 2625. http://dx.doi.org/10.1182/blood-2018-99-117585.

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Abstract Acute myeloid leukemia (AML) is a genetically heterogeneous malignancy characterized by bone marrow infiltration of abnormally proliferating leukemic blasts which results in fatal anemia, bleeding and infectious complications due to compromised normal hematopoiesis. Patients with complete remission (CR) but incomplete blood cell count recovery (CRi) have significantly shorter survival compared to CR patients. Although there is a correlation between CRi and minimal residual disease (MRD), the two variables were shown to be independent risk factors for relapse development (1). The mecha

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5

Verdeil, Gregory, Marine Leblond, Claire Imbratta, and Daniel E. Speiser. "Combination of anti-CD40 and anti-PD1 revert M2 polarization to limit tumor growth in a genetically engineered blander cancer mouse model." Journal of Immunology 202, no. 1_Supplement (2019): 194.3. http://dx.doi.org/10.4049/jimmunol.202.supp.194.3.

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Abstract Bladder cancer (BCa) represents the fourth most common cancer in men with a poor patient prognosis for advanced disease. About 75% of patients present non-muscle invasive BCa (NMIBC) and 25% present muscle invasive BCa (MIBC) or metastatic disease. Although BCG immunotherapy is a common treatment of BCa, the dynamics of immune cell infiltration and its relevance for disease outcome are still not well understood. We took advantage of a genetic based mouse model of MIBC to obtain a profound understanding of the immune contexture over tumor development. P53Fl/Fl/PTENFl/Fl mice were injec

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6

Guo, Xiaofeng, Yan Liu, Jessica L. Kim, et al. "Effect of cyclical intermittent hypoxia on Ad5CMVCre induced solitary lung cancer progression and spontaneous metastases in the KrasG12D+; p53fl/fl; myristolated p110fl/fl ROSA-gfp mouse." PLOS ONE 14, no. 2 (2019): e0212930. http://dx.doi.org/10.1371/journal.pone.0212930.

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7

Du, Ziwei, Miltiadis Tsesmelis та Thomas Wirth. "Abstract A059: NF-κB inducing kinase (NIK) deletion accelerates the progression of pancreatic cancer". Cancer Research 82, № 22_Supplement (2022): A059. http://dx.doi.org/10.1158/1538-7445.panca22-a059.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is the most common type of pancreatic cancer and the leading cause of cancer-related deaths. The canonical NF-κB pathway displays critical functions in the development of PDAC. However, the relationship between the non-canonical NF-κB pathway and PDAC is still obscure. Here, we analyzed the role of the non-canonical NF-κB signaling in precancerous lesions and PDAC development by deleting NF-κB inducing kinase (NIK), an essential kinase for the activation of the non-canonical pathway. We used KC mice (Pdx1-cre/LSL-KrasG12D) that develop pancreati

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8

Lanfranca, Mirna Perusina, Ilona Kryczek, Andrew Rhim, et al. "IL-22 Promotes Pancreatic Cancer Tumorigenesis through Induction of Stemness and Epithelial to Mesenchymal Transition." Journal of Immunology 198, no. 1_Supplement (2017): 66.22. http://dx.doi.org/10.4049/jimmunol.198.supp.66.22.

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Abstract Elevated levels of Interleukin 22 (IL-22) and its receptor (IL-22R) are associated with poor prognosis in pancreatic ductal adenocarcinoma (PDAC) and the underlying mechanism is currently unknown. Our aim is to investigate the role of the IL-22 axis in PDAC initiation and progression. Impact of IL-22 on tumor initiation was assayed by subcutaneous and intravenous inoculation of PDAC cells into wild-type and IL-22−/− mice. The PKCY (Pdx1-Cre; KrasG12D; p53fl/+; RosaYFP) model of pancreas cancer was used to study the in-vivo presence and significance of IL-22 in spontaneous tumors. Resu

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9

Shimazu, Yosuke, Agila Somasundaram, Daniel Brat, and Oren Becher. "PDTM-13. A NOVEL DIFFUSE MIDLINE GLIOMA MODEL INITIATED IN OLIG2-EXPRESSING PROGENITORS OF THE NEONATAL BRAIN." Neuro-Oncology 21, Supplement_6 (2019): vi189. http://dx.doi.org/10.1093/neuonc/noz175.789.

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Abstract Diffuse intrinsic pontine glioma (DIPG) is an incurable brain tumor that arises in the pons of children. Recent studies using single cell RNA-seq and enhancer analysis of DIPG tumor cells, together with analysis of the developing human pons, strongly suggest that an oligodendrocyte progenitor cell is the most likely cell-of-origin for DIPG. Here we describe a novel mouse model by expressing PDGF-B, with H3.3K27M or H3.3 wild-type in Olig2-expressing progenitors via injection into the 4th ventricle using Olig2-tva-cre;p53fl/fl mice. H3.3K27M tumors have high rate of Ki-67, Sox2, and Ol

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10

Singh, Ranjodh, Vanessa Bellat, Melinda Wang, et al. "Volume of distribution and clearance of peptide-based nanofiber after convection-enhanced delivery." Journal of Neurosurgery 129, no. 1 (2018): 10–18. http://dx.doi.org/10.3171/2017.2.jns162273.

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OBJECTIVEDrug clearance may be a limiting factor in the clinical application of convection-enhanced delivery (CED). Peptide-based nanofibers (NFPs) have a high aspect ratio, and NFPs loaded with drugs could potentially maintain effective drug concentrations for an extended period sufficient for cancer therapy. The objective of this study was to assess the volume of distribution (Vd) and clearance of variable lengths of NFPs when administered using CED.METHODSNFPs composed of multiple methoxypolyethylene glycol (mPEG)-conjugated constructs (mPEG2000-KLDLKLDLKLDL-K(FITC)-CONH2, for which FITC is

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11

Cockle, Julia, Lynn Bjerke, Alan Mackay, et al. "IMMU-12. Exploring and modulating the tumour immune microenvironment to facilitate the selection of immunotherapies for paediatric-type diffuse high-grade glioma." Neuro-Oncology 24, Supplement_1 (2022): i83—i84. http://dx.doi.org/10.1093/neuonc/noac079.305.

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Abstract Immune cells have the potential to selectively eradicate high-risk brain tumours such as paediatric-type diffuse high-grade glioma (PDHGG). We aim to characterize the tumour immune microenvironment (TIME) of intra-cranial syngeneic mouse models of diffuse hemispheric glioma, H3G34 (DHG-H3G34) and diffuse midline glioma, H3K27 (DMG-H3K27). We also demonstrate how an oncolytic reovirus (Reolysin) can “heat-up” the TIME of our syngeneic models. Orthotopic immunocompetent mouse models of DHG-H3G34 (C57BL/6, NRASG12V + shp53 + shATRX +/- H3.3G34R) and DMG-H3K27 (Nestin-Tv-a/p53fl/fl, RCAS-

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12

Chattenton, Dani, Ian Rivens, Zheng Jiang, et al. "DDEL-06. Drug Delivery to the Pons Using Short-Pulse Focused Ultrasound and Microbubble Exposure for the Treatment of Diffuse Midline Glioma." Neuro-Oncology 24, Supplement_1 (2022): i35. http://dx.doi.org/10.1093/neuonc/noac079.127.

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Abstract Despite advances in understanding diffuse midline glioma (DMG-H3K27), including DIPG, there are still no effective treatments available, and the dismal clinical prognosis remains. This is partly because of tumour spread behind an intact blood brain barrier (BBB), preventing drug delivery and the reason for many drugs failing in the clinic. The use of focused ultrasound and intravenous microbubbles enables temporary increases in BBB permeability, allowing drugs to enter the targeted brain region. Building on recent research demonstrating that short pulses (&lt;5 µs) of ultrasound c

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13

Seblani, Maggie, Markella Zannikou, Joseph Duffy, et al. "EXTH-63. A NOVEL MOUSE MODEL OF DIFFUSE MIDLINE GLIOMA FOR TARGETED IMMUNOTHERAPY." Neuro-Oncology 23, Supplement_6 (2021): vi177. http://dx.doi.org/10.1093/neuonc/noab196.702.

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Abstract In children, diffuse midline gliomas retain poor outcomes, failing to have a durable response to conventional therapies. Immunotherapies hold promise, with the integration of the host's immune system fundamental to their design. Here, we describe a novel genetically engineered immunocompetent model that incorporates interleukin 13 receptor alpha 2 (IL13Rα2), a tumor-associated antigen, to evaluate the antitumor activity of IL13Rα2-CAR T cell and bispecific T cell engager (BiTE) therapies in preclinical studies. The RCAS-Tva delivery system was utilized to induce gliomagenesis through

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14

Timpson, Paul, Brooke Pereira, Shona Ritchie, katie Gordon, and Thomas Cox. "Abstract PR-09: Temporally resolved proteomics identifies nidogen-2 as a co-target in pancreatic cancer that modulates fibrosis and therapy response." Cancer Research 84, no. 17_Supplement_2 (2024): PR—09—PR—09. http://dx.doi.org/10.1158/1538-7445.pancreatic24-pr-09.

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Abstract Pancreatic cancer (PC) is highly lethal, with a five-year survival rate of ∼13%. PC is characterised by progressive cancer-associated fibrosis. We and others have shown that targeting cancer fibrosis can improve chemotherapy efficacy and impair metastasis in pre-clinical models. As such, we aimed to use integrated temporal proteomics to dissect the matrix signatures of pancreatic tumours from the highly-metastatic KPC (Pdx1-Cre; LSL-K-rasG12D/+; LSL-p53R172H/+) and poorly-metastatic KPflC (Pdx1-Cre; LSL-K-rasG12D/+; LSL-p53fl/+) mouse models, with an aim to identify new metastatic dri

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15

Jaeger, Alex M., Andrew Weeden, and Anika Ali. "Abstract LB351: A novel mouse model to interrogate the functional relationship between protein synthesis and antigen presentation in cancer." Cancer Research 83, no. 8_Supplement (2023): LB351. http://dx.doi.org/10.1158/1538-7445.am2023-lb351.

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Abstract Antigen presentation is a fundamental component of cancer immunity. Cytotoxic CD8+ T cells, the primary mediators of cell killing, recognize peptide antigens presented in the context of Major Histocompatibility Complex Class I (MHC-I). MHC-I presents an astoundingly diverse array of peptides, collectively known as the immunopeptidome. The biosynthesis of the immunopeptidome, which integrates gene expression, protein synthesis, and proteolytic processing, is not well understood. Additionally, most studies interrogating the immunopeptidome use cultured cells in vitro, which lack physiol

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16

Peter, Levke-Sophie, Lea Altendorf, Karoline Hack, et al. "STEM-03. A NOVEL MOUSE MODEL OF CHOROID PLEXUS CARCINOMA UNRAVELS SEQUENTIAL DEDIFFERENTIATION OF HINDBRAIN CHOROID PLEXUS TISSUE AND REVEALS NEW THERAPEUTIC PROSPECTS." Neuro-Oncology 26, Supplement_4 (2024): 0. http://dx.doi.org/10.1093/neuonc/noae064.774.

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Abstract BACKGROUND Choroid Plexus tumors constitute 10-20% of brain tumors in the first year of life. Among those, Choroid Plexus Carcinomas (CPC) pose a significant challenge due to their aggressiveness, resulting in poor survival rates and long-term adverse effects stemming from intense therapeutic approaches. Although loss of p53 and Sonic hedgehog signaling have been implicated in CPC development, a deeper biological understanding is needed to expand mechanistic insights and advance targeted therapies. METHODS We generated a novel mouse model with a simultaneous loss of TP53 and overexpre

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17

Hwang, Elizabeth E., Alex Lee, Stanley Leung, Marcus Breese, and Alejandro Sweet-Cordero. "Abstract 1107: Notch activation drives resistance to Kras(G12C) inhibition in lung adenocarcinoma." Cancer Research 82, no. 12_Supplement (2022): 1107. http://dx.doi.org/10.1158/1538-7445.am2022-1107.

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Abstract Approximately one-third of lung adenocarcinoma (LUAD) tumors contain driver mutations in the Kras GTPase, most commonly occurring as Kras(G12C) activating mutations. Despite the promising development of covalent G12C small molecule inhibitors, early-phase clinical trial data indicate most patients will likely demonstrate disease progression through either intrinsic or acquired resistance. Thus, there is an urgent need to identify such resistance mechanisms to targeting Kras. Our lab previously discovered a unique requirement for Notch3 in tumor-propagating cells from the KrasLSL-G12D

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18

Zhang, Jingfang, Yangang Liu, Guangyao Kong, et al. "Loss Of p53 Promotes Transformation Of Oncogenic Nras-Induced Chronic Myelomonocytic Leukemia To An Acute Phase." Blood 122, no. 21 (2013): 3790. http://dx.doi.org/10.1182/blood.v122.21.3790.3790.

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Abstract Chronic myelomonocytic leukemia (CMML) primarily occurs in the elderly with the median age ranging from 65 to 75 years. As defined by WHO, CMML is characterized by persistent monocytosis in peripheral blood, hepatosplenomegaly, and the absence of BCR-ABL fusion gene. CMML is a devastating cancer for multiple reasons, one of which is that approximately 20% of CMML cases evolve into acute myeloid leukemia (AML) soon after their first diagnosis. However, little is known about the cellular and molecular mechanisms underlying this malignant transformation. Recently, our lab developed a CMM

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Churchhouse, A. M., C. V. Billard, M. J. Arends, and K. B. Myant. "P036 A novel p53-mediated mouse model of inflammatory bowel disease-associated colorectal cancer." Journal of Crohn's and Colitis 14, Supplement_1 (2020): S150. http://dx.doi.org/10.1093/ecco-jcc/jjz203.165.

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Abstract Background Current mouse models of colitis-associated cancer often utilise a combination of APC mutation, Dextran sulphate sodium (DSS) and azoxymethane administration. However, only 13% of human inflammatory bowel disease (IBD)-associated cancers is associated with an APC mutation1. Instead, they are frequently associated with mutation of p53 (occurring in 63% of human cancers1). Whilst some models of IBD-associated cancer using either global p53 loss or mutant p53 have been described, we felt that a more pathophysiologically relevant model would be represented using p53 loss solely

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Date, Yuki, Tomoya Ueno та Kosei Ito. "Abstract 5732: p53 deficiency causes Myc dysregulation through a novel TGFβ-facilitated promoter switching mechanism to instigate osteosarcoma development". Cancer Research 82, № 12_Supplement (2022): 5732. http://dx.doi.org/10.1158/1538-7445.am2022-5732.

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Abstract p53 deficiency and Myc dysregulation, driven by genetic and epigenetic alterations, respectively, are frequently associated with cancer. Previously, we reported that the combination of p53 inactivation and Myc overexpression, mediated by Runx transcription factors (TFs), leads to osteosarcoma (OS), the most common primary bone cancer. However, the mechanisms leading to Myc upregulation by Runx in a p53-deficient microenvironment remain unclear. TGFβ is a main driver of the epithelial-to-mesenchymal transition and its signal-dependent TFs, Smads, are known to associate with lineage-det

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Raizada, Devesh, Felicia Lazure, Stanislav Drapela, et al. "Abstract PR004: Age-induced chronic accumulation of glucocorticoids drives therapy resistance in lung cancer." Cancer Research 84, no. 22_Supplement (2024): PR004. http://dx.doi.org/10.1158/1538-7445.tumbody-pr004.

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Abstract Non-small cell lung cancer (NSCLC), a highly aggressive cancer, is the leading cause of cancer- related deaths in the U.S. While chemotherapy and targeted therapy are the main treatment modalities in the clinic, many patients do not respond to these treatments. Strikingly, the median age for lung cancer diagnosis is 71. Yet, preclinical and clinical research have largely been skewed towards young mice and patients. Here, we address this gap in knowledge and evaluate if old age affects the response to standard of care NSCLC therapies in KRAS-driven NSCLC. Using human sera from young an

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Lankadasari, Manendra B., Yuan Liu, Di He, et al. "Abstract 3142: BRMS1 alters the tumor inflammatory signature and immune infiltration in lung adenocarcinoma." Cancer Research 82, no. 12_Supplement (2022): 3142. http://dx.doi.org/10.1158/1538-7445.am2022-3142.

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Abstract Background: Lung adenocarcinoma (LUAD) is the leading cause of cancer-related deaths. Metastatic cancer is highly fatal which contributes to at least 90% of cancer-associated morbidities and mortalities. During metastasis, tumor cells alter their signaling cascade and interact with the immune cells in the tumor microenvironment Therefore, it is necessary to characterize and understand how these cancer cells influence tumor-infiltrating immune cells to facilitate and even enhance their ability to metastasize. BRMS1 is a metastasis suppressor gene which is frequently downregulated in LU

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Lankadasari, Manendra B., Yuan Liu, Brooke Mastrogiacomo, et al. "Abstract 6596: BRMS1 downregulation alters the tumor microenvironment and induces immunotherapy resistance in lung adenocarcinoma." Cancer Research 84, no. 6_Supplement (2024): 6596. http://dx.doi.org/10.1158/1538-7445.am2024-6596.

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Abstract Background: Lung cancer is the leading cause of cancer-related deaths globally. During cancer progression, tumor cells interact with tumor-infiltrating immune cells (TIICs) creating an immunosuppressive microenvironment. Therefore, it is essential to delineate the communication dynamics between cancer cells and TIICs to identify novel pathways for therapeutic targeting. BRMS1 is a metastasis suppressor gene that is frequently downregulated in lung adenocarcinoma (LUAD). We, and others, have shown that loss of BRMS1 results in increased distant metastatic disease. Given the strong corr

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Yang, Xiaojie, Mohamad Zoabi, Simone Hausmann, et al. "Abstract A080: METTL21A inhibits pancreatic ductal adenocarcinoma tumorigenesis through methylation of HSPA1/8." Cancer Research 82, no. 22_Supplement (2022): A080. http://dx.doi.org/10.1158/1538-7445.panca22-a080.

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Abstract Background: Our work focuses on the role of METTL21A, a member of the little studied seven β-strand family of candidate lysine methyltransferases (KMTs), and its role in the regulation of pancreatic ductal adenocarcinoma (PDAC) development. Using a meta-analysis of publicly available gene expression datasets, we found that METTL21A is significantly downregulated in PDAC versus normal tissue and the reduced expression predicts poor patient survival. Thus, there are intriguing correlations connecting METTL21A to PDAC pathogenesis; however, to date, there are no data on the role of METTL

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Jeevanandam, Advait, Kelli Connolly, and Nikhil Joshi. "Abstract B032: Spatial study of tertiary lymphoid structures in lung adenocarcinoma using 3D lightsheet whole-organ Imaging and machine learning-based quantification." Cancer Research 84, no. 22_Supplement (2024): B032. http://dx.doi.org/10.1158/1538-7445.tumbody-b032.

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Abstract Lung Adenocarcinoma (LUAD) leads in cancer deaths worldwide. Immune Checkpoint blockade (ICB) therapy has improved patient survival of some subtypes (like Kras oncogene-driven; loss of tumor-suppressor p53– “KP”), but not others (Kras oncogene-driven; loss of LKB1– “KL”). Some studies suggest the poorly inflamed KL tumor environment reduces T cell infiltration. However, the impact of other immune mechanisms/cell types on overall ICB-responsiveness remains understudied. Tertiary lymphoid structures (TLSs) are T/B cell aggregates organized by various cell types that form within inflamed

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Nutt, W. Sam, Takahiro Miyazaki, Mario Marcondes, Stanley R. Riddell, and Shivani Srivastava. "Abstract 1152: NKTR-255, a polymer-conjugated IL-15, dramatically improves ROR1 CAR-T cell persistence and anti-tumor efficacy in an autochthonous model of ROR1+ lung cancer." Cancer Research 83, no. 7_Supplement (2023): 1152. http://dx.doi.org/10.1158/1538-7445.am2023-1152.

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Abstract CAR-T cells have mediated remarkable clinical responses against hematological malignancies, but this success has yet to extend to solid tumors, where many factors in the tumor microenvironment (TME) inhibit their persistence and function. In a phase 1 trial at our Center, CAR-T cells targeting the tumor-associated antigen ROR1 in patients with non-small cell lung cancer (NSCLC) and triple negative breast cancer rapidly became dysfunctional and persisted poorly at tumor sites, ultimately failing to mediate objective responses. To evaluate strategies to improve ROR1 CAR-T efficacy, we a

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McAndrews, Kyle L., Pinaki Mondal, Dulce Maroni, Dongdong Wang, Michael A. Hollingsworth, and Sarah P. Thayer. "Abstract C055: Activation of oncogenes within Tff2 expressing cells of the pancreatic ductal glands results in increased lineage stemness preceding tumorigenesis: Insights from an inducible mouse model and derived organoids." Cancer Research 84, no. 2_Supplement (2024): C055. http://dx.doi.org/10.1158/1538-7445.panca2023-c055.

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Abstract Introduction: Adult stem cell dysregulation can initiate cancer. Pancreatic ductal glands (PDGs) act as a stem cell niche for the pancreatic main duct epithelium (MD). Previous studies have shown that Tff2+ cells within the PDGs give rise to progeny that migrate to the MD epithelium during inflammation. In human IPMN, the PDGs have been shown to comprise the basal proliferative compartment of these neoplasms. Here we investigate the effect of oncogenic activation and tumor suppressor deletion within Tff2+ PDG cells. Methods: We utilized Tff2CreERT2;Rosa26mT/mG;KrasLSL-G12D;P53fl/fl mi

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Miyamoto, Ryo, Jiyeon Park, Benigno Aquino, and David Kirsch. "Abstract 3822: Development and characterization of mouse models of epithelioid sarcoma." Cancer Research 85, no. 8_Supplement_1 (2025): 3822. https://doi.org/10.1158/1538-7445.am2025-3822.

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Abstract Epithelioid sarcoma (EPS) is a soft-tissue tumor that arises in the extremities (classical type) or the trunk (proximal type). Genetically, EPS is characterized by the loss of SMARCB1, a core subunit of the SWI/SNF (BAF) chromatin remodeling complex. Although rare, EPS predominantly affects young adults and is considered one of the most aggressive types of sarcomas due to its highly metastatic nature and few effective treatment options. Research on EPS has been hindered by limited patient samples and models that allow investigation of mechanisms of tumor initiation, inter-patient hete

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Kalantzakos, Thomas, Anusha Soni, Cameron Durfee, et al. "Abstract P1-02-25: New Murine Mammary Tumor Cell Lines for Syngeneic Studies Including Immunotherapy." Clinical Cancer Research 31, no. 12_Supplement (2025): P1–02–25—P1–02–25. https://doi.org/10.1158/1557-3265.sabcs24-p1-02-25.

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Abstract Breast cancer (BC) is the most common cancer diagnosis in women globally, accounting for more than 1 in 10 new cancer diagnoses. While BC has historically been a poor candidate for immune checkpoint blockade (ICB), recent studies in triple-negative BC (TNBC) have demonstrated anti-PD-1 treatment efficacy when employed in conjunction with chemotherapy1. APOBEC3 (A3) enzymes, such as A3A and A3B, catalyze cytosine-to-uracil deamination in single-stranded DNA, leading to signature single base substitution mutations (SBS2 and SBS13). A3 expression and mutagenesis have been associated with

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Maldonado, Ana M., Natalia de la Fuente, and Francisco Portillo. "Characterization of an Allele-Nonspecific Intragenic Suppressor in the Yeast Plasma Membrane H+-ATPase Gene (PMA1)." Genetics 150, no. 1 (1998): 11–19. http://dx.doi.org/10.1093/genetics/150.1.11.

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Abstract We have analyzed the ability of A165V, V169I/D170N, and P536L mutations to suppress pma1 dominant lethal alleles and found that the P536L mutation is able to suppress the dominant lethality of the pma1-R271T, -D378N, -D378E, and -K474R mutant alleles. Genetic and biochemical analyses of site-directed mutants at Pro-536 suggest that this amino acid may not be essential for function but is important for biogenesis of the ATPase. Proteins encoded by dominant lethal pma1 alleles are retained in the endoplasmic reticulum, thus interfering with transport of wild-type Pma1. Immunofluorescenc

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Melissourgou-Syka, Lydia, Michael A. Gillespie, Lily V. S. Hillson, et al. "Abstract P022: Investigating the role of the tumor microenvironment in the rectal cancer response to preclinical radio-immunotherapy combinations." Clinical Cancer Research 31, no. 2_Supplement (2025): P022. https://doi.org/10.1158/1557-3265.targetedtherap-p022.

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Abstract Background: Locally-advanced rectal cancer (LARC) is traditionally treated with neoadjuvant chemoradiotherapy before surgery, however, response heterogeneity necessitates the development of novel treatment combinations. Immune checkpoint blockade (ICB) with or without radiotherapy (RT) elicits clinical benefit in various solid tumors, yet ICB’s effectiveness so far is limited to colorectal tumors with microsatellite instability and the role of the tumor microenvironment (TME) is unclear. We present a novel orthotopic immunocompetent mouse model of LARC, where combinations of RT and IC

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Sinha, Nikita, Shuning Chen, Jennifer Haag, et al. "Abstract 5909: Sulindac exhibits anti-proliferative effects in pre-clinical models of ovarian cancer." Cancer Research 84, no. 6_Supplement (2024): 5909. http://dx.doi.org/10.1158/1538-7445.am2024-5909.

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Abstract Objectives: Given the intricate relationship between inflammation and ovarian cancer (OC) development and progression, anti-inflammatory drugs may have potential in the prevention and treatment of OC. Sulindac exhibits potent anti-inflammatory effects through inhibition of COX1/COX2 pathways and promising anti-tumor activity in pre-clinical models of colorectal and endometrial cancer. Thus, we investigated the efficacy of sulindac as an anti-tumorigenic agent in OC pre-clinical cell and mouse models. Methods: The human OC cell lines, MES and OVCAR5, and the K18-gT121+/-;p53fl/fl;Brca1

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Shingu, Takashi, and Jian Hu. "CBMT-17. DEFECTIVE QKI-DEPENDENT LIPID METABOLISM INDUCES GENOMIC INSTABILITY AND SENSITIZES GLIOBLASTOMA TO IMMUNOTHERAPY." Neuro-Oncology 21, Supplement_6 (2019): vi36. http://dx.doi.org/10.1093/neuonc/noz175.139.

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Abstract Despite transformative effects on the therapy of cancers such as melanoma and lung adenocarcinoma, blockade of the T cell immune checkpoints has generated limited impact on glioblastoma. Identifying genetic/genomic alterations that could potentially sensitize the patients to immunotherapy will significantly improve the efficacy of immunotherapy on glioblastoma patients. As part of our effort to identify novel glioma suppressors that affect the interaction of GSCs with their microenvironment, we discovered that the RNA-binding protein Quaking (QKI) is a key regulator of cellular endocy

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Nakeesathit, Supatchara, Naowarat Saralamba, Sasithon Pukrittayakamee, et al. "Limited Polymorphism of the Kelch Propeller Domain in Plasmodium malariae and P. ovale Isolates from Thailand." Antimicrobial Agents and Chemotherapy 60, no. 7 (2016): 4055–62. http://dx.doi.org/10.1128/aac.00138-16.

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ABSTRACTArtemisinin resistance inPlasmodium falciparum, the agent of severe malaria, is currently a major obstacle to malaria control in Southeast Asia. A gene named “kelch13” has been associated with artemisinin resistance inP. falciparum. The orthologue of thekelchgene inP. vivaxwas identified and a small number of mutations were found in previous studies. Thekelchorthologues in the other two human malaria parasites,P. malariaeandP. ovale, have not yet been studied. Therefore, in this study, the orthologouskelchgenes ofP. malariae,P. ovale wallikeri, andP. ovale curtisiwere isolated and anal

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Meloni, Alessandra, Roberto Perniola, Valeria Faà, Enrico Corvaglia, Antonio Cao, and Maria Cristina Rosatelli. "Delineation of the Molecular Defects in the AIRE Gene in Autoimmune Polyendocrinopathy-Candidiasis-Ectodermal Dystrophy Patients from Southern Italy." Journal of Clinical Endocrinology & Metabolism 87, no. 2 (2002): 841–46. http://dx.doi.org/10.1210/jcem.87.2.8209.

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In this study, we have carried out molecular analysis of the AIRE (autoimmune regulator) gene in 11 patients (from 8 families) affected by autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy, originating from a restricted area of Southern Italy (the Salento peninsula in Puglia). Of the 16 mutant AIRE alleles from the 8 probands studied, 12 carried a missense mutation (W78R in 9, P539L in 2, and P252L in 1), 2 carried the Q358X nonsense mutation, and 2 carried the 1058delT frameshift mutation. All these mutations except the 1058delT are novel. Each of the detected mutations either pr

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Wei, Yongkun, Minghui Liu, Er-Yen Yen, et al. "Abstract 3921: Development of a KRAS-G12C-driven pancreatic cancer mouse model." Cancer Research 85, no. 8_Supplement_1 (2025): 3921. https://doi.org/10.1158/1538-7445.am2025-3921.

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Abstract KRASG12C inhibitor (G12Ci) has produced encouraging, albeit mild clinical benefit in pancreatic ductal adenocarcinoma (PDAC). Identifying and targeting resistance mechanisms to G12Ci treatment remains the major challenge due to the lack of faithful preclinical models. To better understand the tumor biology of the KRASG12C allele, we established a mouse model engineered with the LSL-KrasG12C, conditional p53 knockout (p53L), and pancreatic-specific p48-Cre alleles. The resulting p48-Cre LSL-KrasG12C p53L/+ (KCPC) mice exhibit decreased number and area of PanIN/ADM lesions compared to a

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Ghevaert, Cedric, Alexandre Salsmann, Nicholas A. Watkins та ін. "A nonsynonymous SNP in the ITGB3 gene disrupts the conserved membrane-proximal cytoplasmic salt bridge in the αIIbβ3 integrin and cosegregates dominantly with abnormal proplatelet formation and macrothrombocytopenia". Blood 111, № 7 (2008): 3407–14. http://dx.doi.org/10.1182/blood-2007-09-112615.

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AbstractWe report a 3-generation pedigree with 5 individuals affected with a dominantly inherited macrothrombocytopenia. All 5 carry 2 nonsynonymous mutations resulting in a D723H mutation in the β3 integrin and a P53L mutation in glycoprotein (GP) Ibα. We show that GPIbα-L53 is phenotypically silent, being also present in 3 unaffected pedigree members and in 7 of 1639 healthy controls. The β3-H723 causes constitutive, albeit partial, activation of the αIIbβ3 complex by disruption of the highly conserved cytoplasmic salt bridge with arginine 995 in the αIIb integrin as evidenced by increased P

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Wei, Yongkun, Minghui Liu, Phuoc T. Nguyen, Dean N. Pan, Wantong Yao, and Haoqiang Ying. "Abstract C097: KRASG12C exhibits allele-specific biology in pancreatic cancer and targeting CD24 sensitizes KRASG12C-driven tumors to sotorasib treatment." Cancer Research 84, no. 2_Supplement (2024): C097. http://dx.doi.org/10.1158/1538-7445.panca2023-c097.

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Abstract Pancreatic adenocarcinoma (PDAC) is predominantly driven by KRAS oncogene. While all oncogenic KRAS mutations result in its hyperactivation, the allele-specific biology of KRAS mutations remain poorly understood. Addressing such issues has become particularly important with the recent advancements in the development of allele-specific and pan-KRAS inhibitors. Among the KRAS inhibitors, KRASG12C inhibitors (G12Ci), Sotorasib and Adagrasib, have been approved for treating KRASG12C-mutant lung cancer. Sotorasib also exhibited promising anticancer activity in human PDAC, with 21% response

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ROMERO, Irma, Ana M. MALDONADO, and Pilar ERASO. "Glucose-independent inhibition of yeast plasma-membrane H+-ATPase by calmodulin antagonists." Biochemical Journal 322, no. 3 (1997): 823–28. http://dx.doi.org/10.1042/bj3220823.

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Glucose metabolism causes activation of the yeast plasma-membrane H+-ATPase. The molecular mechanism of this regulation is not known, but it is probably mediated by phosphorylation of the enzyme. The involvement in this process of several kinases has been suggested but their actual role has not been proved. The physiological role of a calmodulin-dependent protein kinase in glucose-induced activation was investigated by studying the effect of specific calmodulin antagonists on the glucose-induced ATPase kinetic changes in wild-type and two mutant strains affected in the glucose regulation of th

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Montoya, Rafael Heinz, Rasoul Pourebrahim, Zoe Alaniz, Lauren B. Ostermann, Jared K. Burks, and Michael Andreeff. "Osterix Marks a Distinct Population of Circulatory Bone Marrow Mesenchymal Stem Cells That Is Increased upon Oncogenic Stress." Blood 136, Supplement 1 (2020): 1. http://dx.doi.org/10.1182/blood-2020-142713.

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Bone marrow mesenchymal stem cells (BM-MSCs) are multipotent stromal cells that can differentiate into a variety of lineages and play a critical role in tissue homeostasis upon injury and repair. Previous studies using Osx-Cre transgenic mice have demonstrated that the expression of Sp7 (Osterix) marks a population of mesenchymal progenitor cells that can differentiate to osteoblasts as well as bone marrow stromal cells (Mizoguchi et al., 2014). Using a lineage-tracing system, we show that in addition to marking mesenchymal progenitor cells in the bone marrow, Osx-Cre also marks a population o

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Padariya, Monikaben, Robin Fahraeus, Ted Hupp, and Umesh Kalathiya. "Molecular Determinants and Specificity of mRNA with Alternatively-Spliced UPF1 Isoforms, Influenced by an Insertion in the ‘Regulatory Loop’." International Journal of Molecular Sciences 22, no. 23 (2021): 12744. http://dx.doi.org/10.3390/ijms222312744.

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The nonsense-mediated mRNA decay (NMD) pathway rapidly detects and degrades mRNA containing premature termination codons (PTCs). UP-frameshift 1 (UPF1), the master regulator of the NMD process, has two alternatively-spliced isoforms; one carries 353-GNEDLVIIWLR-363 insertion in the ‘regulatory loop (involved in mRNA binding)’. Such insertion can induce catalytic and/or ATPase activity, as determined experimentally; however, the kinetics and molecular level information are not fully understood. Herein, applying all-atom molecular dynamics, we probe the binding specificity of UPF1 with different

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Tien, Jean Ching-Yi, Seema Chugh, Andrew E. Goodrum, et al. "AGO2 promotes tumor progression in KRAS-driven mouse models of non–small cell lung cancer." Proceedings of the National Academy of Sciences 118, no. 20 (2021): e2026104118. http://dx.doi.org/10.1073/pnas.2026104118.

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Lung cancer is the deadliest malignancy in the United States. Non–small cell lung cancer (NSCLC) accounts for 85% of cases and is frequently driven by activating mutations in the gene encoding the KRAS GTPase (e.g., KRASG12D). Our previous work demonstrated that Argonaute 2 (AGO2)—a component of the RNA-induced silencing complex (RISC)—physically interacts with RAS and promotes its downstream signaling. We therefore hypothesized that AGO2 could promote KRASG12D-dependent NSCLC in vivo. To test the hypothesis, we evaluated the impact of Ago2 knockout in the KPC (LSL-KrasG12D/+;p53f/f;Cre) mouse

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Shen, Jieli, Dat P. Ha, Genyuan Zhu, et al. "GRP78 haploinsufficiency suppresses acinar-to-ductal metaplasia, signaling, and mutant Kras-driven pancreatic tumorigenesis in mice." Proceedings of the National Academy of Sciences 114, no. 20 (2017): E4020—E4029. http://dx.doi.org/10.1073/pnas.1616060114.

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Pancreatic ductal adenocarcinoma (PDAC) remains a highly lethal disease in critical need of new therapeutic strategies. Here, we report that the stress-inducible 78-kDa glucose-regulated protein (GRP78/HSPA5), a key regulator of endoplasmic reticulum homeostasis and PI3K/AKT signaling, is overexpressed in the acini and PDAC of Pdx1-Cre;KrasG12D/+;p53f/+ (PKC) mice as early as 2 mo, suggesting that GRP78 could exert a protective effect on acinar cells under stress, as during PDAC development. The PKC pancreata bearing wild-type Grp78 showed detectable PDAC by 3 mo and rapid subsequent tumor gro

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Bui, Khac Cuong, Mai Ly Thi Nguyen, Samarpita Barat, et al. "Effect of AdipoR agonist in cholangiocarcinoma." Journal of Clinical Oncology 36, no. 4_suppl (2018): 323. http://dx.doi.org/10.1200/jco.2018.36.4_suppl.323.

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323 Background: Adiponectin is the key adipokine, which plays an important role in health and disease such as obesity, diabetes, and cancer. Adiponectin is reduced in different tumor types, especially in obesity-related cancer, and recent studies showed that Adiponectin had a potential anti-cancer effect. Obesity is a risk factor for various tumor diseases including cholangiocarcinoma (CC), the second most common primary hepatic cancer. The aim of this study is to investigate for the first time the anti-cancer effect of AdipoR agonist in CC cell lines and a CC engineered mouse model. Methods:

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Zamler, Daniel, Er-Yen Yen, Takashi Shingu, et al. "IMMU-10. ESTABLISHING EFFECTIVE MODELS FOR IMMUNOTHERAPY IN GBM." Neuro-Oncology 21, Supplement_6 (2019): vi121. http://dx.doi.org/10.1093/neuonc/noz175.504.

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Abstract The introduction of immunotherapies has been paradigm shifting for cancers that were previously a death sentence. However, preclinical/clinical studies on glioblastoma (GBM) have generated mixed outcomes in patients, likely due to its great heterogeneity of immune microenvironment, particularly the myeloid cell populations. Primary patient studies have been limited by a difficulty in performing longitudinal studies, uncontrolled environmental conditions, and genetic variability. There is also, unfortunately, a paucity of mouse models that effectively re-capitulate the immune microenvi

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Duong, Loan, and Xin Lu. "Abstract 5132: DNMT1-associated EMT promotes KRAS escape in pancreatic cancer." Cancer Research 85, no. 8_Supplement_1 (2025): 5132. https://doi.org/10.1158/1538-7445.am2025-5132.

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Abstract Pancreatic adenocarcinoma (PDAC) is presently the 3rd leading cause of cancer death in the United States and is further projected to overcome colorectal cancer to become the 2nd leading cause by 2030. The genetic landscape of PDAC is characterized by pervasive oncogenic mutations in KRAS, observed in over 90% of PDAC tumors. KRAS is considered essential for maintaining tumor progression and so targeting it has long been considered crucial to improving outcomes for PDAC patients. For preclinical studies of KRAS in our lab, we are using an inducible KRAS (iKRAS) model to model KRAS acti

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Mehta, Anita, Madeline Townsend, Madisson Oliwa, et al. "614 Investigating immune mediated mechanisms of PARPi resistance in BRCA1-associated triple negative breast cancer (TNBC)." Journal for ImmunoTherapy of Cancer 9, Suppl 2 (2021): A644. http://dx.doi.org/10.1136/jitc-2021-sitc2021.614.

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BackgroundPoly(ADP-ribose) polymerase inhibitors (PARPi) have improved the outcomes of BRCA-associated breast cancer; however, treatment responses are often not durable. Our preclinical studies demonstrated that PARPi activates the cGAS/STING pathway and recruitment of anti-tumor CD8+ T-cells that are required for tumor clearance [1]. These studies contributed to development of clinical trials testing PARPi plus immune checkpoint blockade (ICB). Unfortunately, early phase trials of PARPi + ICB have not yet suggested efficacy will be superior to PARPi monotherapy. Lack of demonstrated clinical

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Nirala, Bikesh Kumar, Lyazat Kurenbekova, Tajhal Patel, et al. "Abstract 6713: Myc-regulated miR17, 20a modulate RANK expression in osteosarcoma." Cancer Research 83, no. 7_Supplement (2023): 6713. http://dx.doi.org/10.1158/1538-7445.am2023-6713.

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Abstract Osteosarcoma (OS) is the most common primary bone tumor in children and adolescents. Approximately 25-30% of these tumors carry amplification of chromosome 8q24, which harbors the oncogene c-Myc, and correlates with a poor prognosis in patients with OS. To understand the mechanisms that underlie the ability of Myc to alter both the tumor and its surrounding tumor immune microenvironment (TiME), we generated and molecularly characterized an osteoblast-specific Cre-Lox-Stop-Lox;(LSL)-c-MycT58A;p53f/+ knockin genetically engineered mouse model (GEMM). Phenotypically, the Myc knockin-GEMM

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Barade, Aruna, Arun Kumar Arunachalam, Deborah Arul, et al. "Germline Variants Contribute Significantly to the Pathogenesis of Aplastic Anemia in India." Blood 138, Supplement 1 (2021): 1105. http://dx.doi.org/10.1182/blood-2021-148348.

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Abstract Introduction Aplastic anemia (AA) is characterized by a hypoplastic marrow and bone marrow failure (BMF), leading to peripheral pancytopenia. The treatment for AA currently consists of either hematopoietic stem cell transplant (HSCT) or immunosuppressive therapy (IST) with anti-thymocyte globulin and cyclosporine. We have previously reported poor responses to IST in Indian children with AA while adults (&gt;15 years) show responses of 60%. Therefore, we wanted to study if we could identify constitutional variants in children and young adults with AA. Methods We included 102 young

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Nanni, Jacopo, Jayakumar Vadakekolathu, Lorenza Bandini, et al. "T Cell/Natural Killer (NK) Cell Transcriptional Profiles Are Associated with Response to Gilteritinib in FLT3-Mutated Acute Myeloid Leukemia." Blood 142, Supplement 1 (2023): 2947. http://dx.doi.org/10.1182/blood-2023-184741.

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S.R. & A.C. equally contributed Background: Despite significative improvements in the management of FLT3-mutated AML and its prognosis since FLT3 inhibitors ( FLT3i) adoption, a significant proportion of patients results refractory or ultimately relapses after this targeted treatment. Gilteritinib is an oral and selective FLT3i with single-agent activity as salvage therapy in Relapsed/Refractory patients (R/R). The investigation of resistance mechanism to Gilteritinib is crucial to guide next therapeutic choices and improve drug effectiveness. Thus far, correlative studies have elucidated

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