B2M Gene Expression Shapes the Immune Landscape of Lung Adenocarcinoma and Determines the Response to Immunotherapy

Scientists performed an integrative analysis of the mutational and transcriptional profiles of large cohorts of non-small-cell lung cancer patients and found that epigenetic downregulation of B2M was common.
[Immunology]
Zhao, Y., Cao, Y., Chen, Y., Wu, L., Hang, H., Jiang, C., & Zhou, X. (n.d.). B2M gene expression shapes the immune landscape of lung adenocarcinoma and determines the response to immunotherapy. Immunology, n/a(n/a). https://doi.org/10.1111/imm.13384 Cite
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Induction of Cell Death in Pancreatic Tumors by Zinc and Its Florescence Chelator TSQ

Upon treatment with N,N,N′,N′-tetrakis(2-pyridinylmethyl)-1,2-ethanediamine, a zinc chelator, organoids degenerated and its negative effect was rescued by co-treatment with zinc, indicating that zinc is necessary for the growth and survival of tumor organoids.
[Biological Trace Element Research]
Asahina, K. (2021). Induction of Cell Death in Pancreatic Tumors by Zinc and Its Fluorescence Chelator TSQ. Biological Trace Element Research. https://doi.org/10.1007/s12011-021-02770-7 Cite
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Macropinocytosis Requires Gal-3 in a Subset of Patient-Derived Glioblastoma Stem Cells

Using glioblastoma patient-derived stem cells, researchers identified and characterized a subset of Gal-3high glioblastoma tumors mainly within the mesenchymal subtype that are addicted to Gal-3-mediated macropinocytosis.
[Communications Biology]
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RAD51AP1 Loss Attenuates Colorectal Cancer Stem Cell Renewal and Sensitizes to Chemotherapy

Researchers provided in vivo evidence that RAD51-Associated Protein 1(RAD51AP1) played a critical role in colorectal cancer (CRC) growth and drug resistance by regulating CRC stem cell self-renewal.
[Molecular Cancer Research]
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Early Detection of Pancreatic Cancer Using DNA-Based Molecular Approaches

Investigators discuss and focus on the pathological and molecular features of precancerous lesions of the pancreas, including pancreatic intraepithelial neoplasia, intraductal papillary mucinous neoplasm and mucinous cystic neoplasm, which are target lesions of early detection approaches.
[Nature Reviews Gastroenterology & Hepatology]
Singhi, A. D., & Wood, L. D. (2021). Early detection of pancreatic cancer using DNA-based molecular approaches. Nature Reviews Gastroenterology & Hepatology, 1–12. https://doi.org/10.1038/s41575-021-00470-0 Cite
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The Pancreatic Cancer Genome Revisited

Given the vast developments within this field, scientists review the wide-ranging and most current information related to pancreatic cancer genomics with the goal of integrating this information into a unifying description of the life history of pancreatic cancer.
[Nature Reviews Gastroenterology & Hepatology]
Hayashi, A., Hong, J., & Iacobuzio-Donahue, C. A. (2021). The pancreatic cancer genome revisited. Nature Reviews Gastroenterology & Hepatology, 1–13. https://doi.org/10.1038/s41575-021-00463-z Cite
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TP53 Missense Mutations in PDAC Are Associated with Enhanced Fibrosis and an Immunosuppressive Microenvironment

Analysis of human pancreatic ductal adenocarcinoma (PDAC) patient data from The Cancer Genome Atlas revealed a negative association between the presence of missense mutp53 and infiltration of CD8+ T cells into the tumor.
[Proceedings of the National Academy of Sciences of the United States of America]
Maddalena, M., Mallel, G., Nataraj, N. B., Shreberk-Shaked, M., Hassin, O., Mukherjee, S., Arandkar, S., Rotkopf, R., Kapsack, A., Lambiase, G., Pellegrino, B., Ben-Isaac, E., Golani, O., Addadi, Y., Hajaj, E., Eilam, R., Straussman, R., Yarden, Y., Lotem, M., & Oren, M. (2021). TP53 missense mutations in PDAC are associated with enhanced fibrosis and an immunosuppressive microenvironment. Proceedings of the National Academy of Sciences, 118(23). https://doi.org/10.1073/pnas.2025631118 Cite
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Tracing Oncogene-Driven Remodelling of the Intestinal Stem Cell Niche

Scientists applied an oncogene-associated, multicolor reporter mouse model to the small intestine to show that oncogene-expressing mutant crypts altered the cellular organization of neighbouring wild-type crypts, thereby driving accelerated clonal drift.
[Nature]
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Suppression of m6A mRNA Modification by DNA Hypermethylated ALKBH5 Aggravates the Oncological Behavior of KRAS Mutation/LKB1 Loss Lung Cancer

ALKBH5 gain- or loss-of function could effectively reverse LKB1 regulated cell proliferation, colony formation, and migration of KRAS-mutated lung cancer cells.
[Cell Death & Disease]
Zhang, D., Ning, J., Okon, I., Zheng, X., Satyanarayana, G., Song, P., Xu, S., & Zou, M.-H. (2021). Suppression of m6A mRNA modification by DNA hypermethylated ALKBH5 aggravates the oncological behavior of KRAS mutation/LKB1 loss lung cancer. Cell Death & Disease, 12(6), 1–14. https://doi.org/10.1038/s41419-021-03793-7 Cite
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Onconova Therapeutics Announces the Initial Dosing of the First Patient in the US Phase I Clinical Trial of ON 123300

Onconova Therapeutics, Inc. announced that the first patient has been dosed in the US Phase I clinical trial of ON 123300, the company’s novel multi-kinase inhibitor, for HR+ HER 2 metastatic breast cancer patients who are refractory to, or progressing on, currently approved CDK 4/6 inhibitors.
[Onconova Therapeutics, Inc. (Globe Newswire, Inc.)]
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Oncogenic KRAS Engages an RSK1/NF1 Pathway to Inhibit Wild-Type RAS Signaling in Pancreatic Cancer

Investigators used proximity labeling to identify protein interactors of active KRAS in pancreatic ductal adenocarcinoma (PDAC) cells. We expressed fusions of wild-type (WT) (BirA-KRAS4B), mutant (BirA-KRAS4BG12D), and nontransforming cytosolic double mutant (BirA-KRAS4BG12D/C185S) KRAS with the BirA biotin ligase in murine PDAC cells.
[Proceedings of the National Academy of Sciences of the United States of America]
Cheng, D. K., Oni, T. E., Thalappillil, J. S., Park, Y., Ting, H.-C., Alagesan, B., Prasad, N. V., Addison, K., Rivera, K. D., Pappin, D. J., Aelst, L. V., & Tuveson, D. A. (2021). Oncogenic KRAS engages an RSK1/NF1 pathway to inhibit wild-type RAS signaling in pancreatic cancer. Proceedings of the National Academy of Sciences, 118(21). https://doi.org/10.1073/pnas.2016904118 Cite
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