Neuroblastoma (NB) is a malignant neoplasm originating from the primary cells of the sympathetic nervous system. Patients with NB are risk-stratified using a number of features including age at diagnosis, disease stage, tumor histology and genetic profile (status of genes regions 1p and 11q). The interpretation of the results of genetic studies can become a source of problems because neuroblastoma has a heterogeneous histological pattern. The article describes 2 cases with classical for NB chromosomal aberrations in the stromal component of the tumor.
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http://dx.doi.org/10.17116/patol20238504147 | DOI Listing |
Int J Mol Sci
December 2024
Department of Clinical Gene Therapy, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan.
Pancreatic ductal adenocarcinoma (PDAC) characterized by an abundant cancer stroma is an aggressive malignancy with a poor prognosis. Periostin (Pn) is a key extracellular matrix (ECM) protein in various tumor progression. Previously, we described the role of Pn alternative splicing variants (ASVs) with specific functional features in breast cancer.
View Article and Find Full Text PDFACS Appl Mater Interfaces
November 2024
College of Biotechnology and Bioengineering, Zhejiang University of Technology, Hangzhou 310032, China.
Pancreatic ductal adenocarcinoma (PDAC) is a clinically challenging cancer and is often characterized with rich stroma and mutated KRAS, which determines the tumor microenvironment (TME) and therapy response. Turning immunologically "cold" PDAC into "hot" is an unmet need to improve the therapeutic outcome. Herein, we propose a programmable strategy by sequential delivery of pirfenidone (PFD) and nanoengineered KRAS specific inhibitor (AMG510) and gemcitabine (GEM) liposomes.
View Article and Find Full Text PDFACS Appl Mater Interfaces
October 2024
Department of Chemistry, CICECO─Aveiro Institute of Materials, University of Aveiro, Campus Universitário de Santiago, Aveiro 3810-193, Portugal.
The establishment of organotypic preclinical models that accurately resemble the native tumor microenvironment at an anatomic human scale is highly desirable to level up platforms potential for screening candidate therapies. The bioengineering of anatomic-scaled three-dimensional (3D) models that emulate native tumor scale while recapitulating their cellular and matrix components remains, however, to be fully realized. In this focus, herein, we leveraged embedded 3D bioprinting for biofabricating pancreatic ductal adenocarcinoma (PDAC) models combining gelatin-methacryloyl and hyaluronic acid methacrylate extracellular matrix (ECM)-mimetic biomaterials with human pancreatic cancer cells and cancer-associated fibroblasts to generate models capable of emulating native tumor size (∼6 mm) and stromal elements.
View Article and Find Full Text PDFAm J Physiol Cell Physiol
November 2024
Laboratory for Cell Biology, Department of Physiology, Croatian Institute for Brain Research, University of Zagreb School of Medicine, Zagreb, Croatia.
Acute myeloid leukemia (AML) is a heterogeneous group of hematological malignancies characterized by differentiation arrest, high relapse rates, and poor survival. The bone marrow (BM) microenvironment is recognized as a critical mediator of drug resistance and a primary site responsible for AML relapse. Our previous study reported that 5-aminoimidazole-4-carboxamide ribonucleoside (AICAr) induces AML cell differentiation by inhibiting pyrimidine synthesis and activating Checkpoint kinase 1.
View Article and Find Full Text PDFInt J Mol Sci
August 2024
Pancreas Cancer Research Lab, Department of Clinical Science, Intervention and Technology (CLINTEC), Karolinska Institutet, SE 141 86 Huddinge, Sweden.
Pancreatic ductal adenocarcinoma (PDAC) is a deadly disease that is almost entirely resistant to conventional chemotherapy and radiation therapy. A significant factor in this resistance appears to be the dense desmoplastic stroma, which contains various cancer-associated fibroblast (CAF) populations. However, our understanding of the communication between tumor cells and CAFs that contributes to this aggressive malignancy is still developing.
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