Previous studies have demonstrated that increased expression of the granulocyte-macrophage colony-stimulating factor (GM-CSF) correlated with poor prognosis in patients with cholangiocarcinoma (CCA) and pancreatic ductal adenocarcinoma (PDAC). In the current study, a research team at the University of Rochester Medical Center aimed to assess the impact of blocking GM-CSFR signaling in CCA and PDAC.

While fecal immunochemical tests (FIT) are common strategies for colorectal cancer (CRC) screening, the potential use of blood-based biomarkers could provide an alternative method to increase compliance in population-based screening programs for early detection of CRC. Researchers from EDP Biotech Corp. aimed to identify novel blood-based biomarker candidates for use in CRC screening.

Cholangiocarcinoma (CCA) is a lethal cancer affecting the bile ducts and still has limited therapeutic options.

Recently, it has been found that loss-of-function of TPC2 alkalized melanosomes promoted pigmentation, while gain-of-function of TPC2 acidified melanosomes and inhibited melanin synthesis.

During metastasis, the mechanical properties of the nucleus make translocation of this organelle the rate-limiting step during constrained migration, and these properties are regulated through interactions between the cytoskeleton, integral nuclear envelope (NE) proteins, the nuclear lamina and chromatin.

Malformations of cortical development (MCD) are a group of neurodevelopmental disorders characterized by malformation of cortical structures, which often lead to epilepsy, and include cortical dysplasia (FCD), hemimegalencephaly (HME) and tuberous sclerosis complex (TSC).

Lung cancer associated transcript 1 (LUCAT1) is a long noncoding RNA and has been identified as a negative feedback regulator of interferon I and inflammatory cytokine expression in myeloid cells; the anti-inflammatory protein nuclear receptor 4A2 (NR4A2) was identified as a LUCAT1-binding protein involved in regulating splicing and processing of mRNAs. NR4A2 inhibits the inflammatory process driven by NF-κB. It was observed that cells lacking LUCAT1 expression had their splicing of immune genes altered, with reduced expression of NR4A2 (altered splicing on exon 7) in those cells lacking LUCAT1, as shown by ChIRP-MS assay in THP-1 cells.

Trastuzumab-based chemotherapy has demonstrated clinical benefits in the treatment of HER2+ breast cancer. There is a percentage of patients who do not respond to therapy and have a poorer prognosis than those who respond. To better understand the mechanisms behind trastuzumab resistance, researchers in China studied the role of transcription elongation factor A protein-like 9 (TCEAL9) in resistance to trastuzumab-based chemotherapy in HER+ breast cancer.