Relevant bibliographies by topics / P53FL

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  2. Dissertations / Theses
  3. Books
  4. Conference papers

Academic literature on the topic 'P53FL'

Author: Grafiati
Published: 6 September 2023
Last updated: 31 July 2025

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Journal articles on the topic "P53FL"

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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<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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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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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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Dissertations / Theses on the topic "P53FL"

1

Katoch, Aanchal. "Regulation of Expression of p53 and its Isoform Δ40p53 : Consequences on Cellular Gene Expression". Thesis, 2018. http://etd.iisc.ac.in/handle/2005/4178.

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The TP53 tumour suppressor gene encodes for p53 protein which is the frequently altered gene in most of the cancers. p53 protein is activated in response to different stresses and plays major role in maintaining genome integrity by regulating cell cycle and cell survival. It is known that p53 has twelve isoforms generated using alternate splicing, alternate promoters and translation initiation sites. Out of these isoforms ∆40p53 (also known as ∆N-p53/p47) is the only translational isoform of p53, produced from the same mRNA by using an ‘internal ribosome entry site’ (IRES). From our laboratory
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Books on the topic "P53FL"

1

Creating an Inviting Classroom Environment. Phi Delta Kappa Educational Foundation, 1998.

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Conference papers on the topic "P53FL"

1

Johnson, Neil, Yu-Chen Li, Zandra Walton, et al. "Abstract 2979: Combined cdk1 and PARP inhibition results in tumor regression in a KrasG12D p53L/L murine lung adenocarcinoma model." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2979.

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