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Autophagy, inflammation, and immune dysfunction in the pathogenesis of pancreatitis

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The mutations driving the growth of benign Spitz naevi, considered initiating alterations, include Harvey Rat Sarcoma Viral Oncogene Homolog ( HRAS) mutations, most frequently Q61K/R in exon 3, BRAF V600E , as well as larger genomic rearrangements involving the Anaplastic Lymphoma Receptor Tyrosine Kinase ( ALK ), Neurotrophic Receptor Tyrosine Kinase 1 ( NTRK1 ), Ret Proto-Oncogene ( RET ), ROS Proto-Oncogene 1, Receptor Tyrosine Kinase ( ROS1 ), Met receptor tyrosine kinases ( MET RTK s), and BRAF genes