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Age-associated loss of mitochondrial complex I and IV in human colonic crypts induces metabolic remodelling, including upregulation of PHGDH, resulting in favorable metabolic conditions for tumor growth.
Postdoctoral researchers face substantial challenges and stresses that have been exacerbated by the COVID-19 pandemic. Positive action is needed from research institutions, funders and individual investigators to support postdocs and fortify the research endeavor.
Effective methods for treating retinoblastoma while preserving vision are an unmet clinical need. Subretinal delivery of a hydrogel containing T cells that secrete the cytokine IL-15 and express a chimeric antigen receptor directed at the ganglioside protein GD2 completely controls retinoblastoma in immunocompromised mice, with no obvious damage to the surrounding retina.
Mitochondrial DNA damage, metabolic disruption and aging have all been associated with cancer. These three threads are now woven together to show that aging-associated somatic mutations to mitochondrial DNA alter mitochondrial serine metabolism to support cell transformation and colon-cancer development.
Cancer has found a formidable foil in COVID-19, and this has brought to the fore the early concerns that COVID-19 could have a deeper impact on oncology patients. Two studies now provide insights into the enigma surrounding the determinants of the worsening of COVID-19 symptoms in patients with cancer.
Smith et al. report that age-associated mutations in mitochondrial DNA cause defects in oxidative phosphorylation. This results in metabolic rewiring, which subsequently contributes to accelerated development of colorectal cancer.
Han and colleagues develop a CAR T cell directed at GD2, a molecule overexpressed in retinoblastoma, which showed efficacy against murine retinoblastoma when combined with IL-15 in a hydrogel delivery system.
Gottlieb and colleagues show that stearoyl-CoA desaturase promotes metabolic adaptation of acute lymphoblastic leukemia cells to the central nervous system microenvironment, revealing a potential site-specific metabolic vulnerability of this disease.