Cancer cells expand through mutations – but not just through mutations. They also change their behavior in the absence of underlying genetic alterations. Such plasticity helps the cells both adapt to the cellular stress fueled by out-of-control growth and resist targeted and chemotherapies alike. Investigators from Memorial Sloan Kettering Cancer Center and Huazhong Agricultural University have gained new insights into the underlying mechanisms of plasticity.
Cancer cells expand through mutations – but not just through mutations. They also change their behavior in the absence of underlying genetic alterations. Such plasticity helps the cells both adapt to the cellular stress fueled by out-of-control growth and resist targeted and chemotherapies alike. Investigators from Memorial Sloan Kettering Cancer Center and Huazhong Agricultural University have gained new insights into the underlying mechanisms of plasticity.
Cancer cells expand through mutations – but not just through mutations. They also change their behavior in the absence of underlying genetic alterations. Such plasticity helps the cells both adapt to the cellular stress fueled by out-of-control growth and resist targeted and chemotherapies alike. Investigators from Memorial Sloan Kettering Cancer Center and Huazhong Agricultural University have gained new insights into the underlying mechanisms of plasticity.
Long noncoding RNAs (lncRNAs) have emerged as potential markers of disease, since they associate with proteins that regulate gene expression, translation or stability, among others, and where hypoxia might play a role in this scenario. In recently published work, researchers analyzed clinical data from patients with lung adenocarcinoma to identify hypoxia-modulated lncRNAs in vivo and in vitro, and which could correlate with prognosis.
Long noncoding RNAs (lncRNAs) have emerged as potential markers of disease, since they associate with proteins that regulate gene expression, translation or stability, among others, and where hypoxia might play a role in this scenario. In recently published work, researchers analyzed clinical data from patients with lung adenocarcinoma to identify hypoxia-modulated lncRNAs in vivo and in vitro, and which could correlate with prognosis.
Lung cancer, which often occurs as lung adenocarcinoma, is the leading cause of cancer-related death worldwide. At least 70% of lung adenocarcinoma patients fail to show long-term benefit from immune checkpoint inhibitors, highlighting the need to identify in advance those more likely to benefit.
Splicing is a process necessary for the correct synthesis of proteins and an essential step in gene expression. An impaired minor splicing may lead to aberrant pre-mRNA transcripts and exon skipping, leading to premature stop codons and truncated synthesized proteins, resulting in severe consequences.
The polarization of macrophages is crucial in modulating the tumor microenvironment and impacting cancer development. Long noncoding RNAs (lncRNAs) have been identified as key regulators in this process.
Researchers at Jilin University and collaborators combed through data in the public Cancer Genome Atlas and identified a potential target for lung adenocarcinoma.
Researchers from Guilin Medical University and collaborators investigated the potential role of ubiquitin-specific protease 4 (USP4) in the occurrence and development of lung adenocarcinoma.