FDG-PET-positive lower-extremity sebaceous-gland carcinoma in a patient with Muir-Torre syndrome.

Sebaceous-gland carcinoma can occur alone or as one of the defining features of the Muir-Torre syndrome. Cases occurring below the head and neck are extremely rare. Here we describe the case of a 70-year-old male with Muir-Torre syndrome who had a recurrent sebaceous-gland carcinoma in the left lower extremity that demonstrated (18)F-FDG avidity.

Mitochondria and tumor progression in ulcerative colitis.

Background: The role of mitochondria in cancer is poorly understood. Ulcerative colitis (UC) is an inflammatory bowel disease that predisposes to colorectal cancer and is an excellent model to study tumor progression. Our goal was to characterize mitochondrial alterations in UC tumorigenesis.

Combined targeting of MEK and PI3K/mTOR effector pathways is necessary to effectively inhibit NRAS mutant melanoma in vitro and in vivo.

Activating mutations in the neuroblastoma rat sarcoma viral oncogene homolog (NRAS) gene are common genetic events in malignant melanoma being found in 15-25% of cases. NRAS is thought to activate both mitogen activated protein kinase (MAPK) and PI3K signaling in melanoma cells. We studied the influence of different components on the MAP/extracellular signal-regulated (ERK) kinase (MEK) and PI3K/mammalian target of rapamycin (mTOR)-signaling cascade in NRAS mutant melanoma cells.

Ulcerative colitis-associated colorectal cancer arises in a field of short telomeres, senescence, and inflammation.

Inflammation plays a role in the progression to cancer and it is linked to the presence of senescent cells. Ulcerative colitis (UC) is a chronic inflammatory disease that predisposes to colorectal cancer. Tumorigenesis in this setting is associated with telomere shortening that can be observed in the nondysplastic epithelium of UC patients with high-grade dysplasia (HGD) or cancer (UC progressors).