The LKB1 (also called STK11) tumor suppressor is mutationally inactivated in ∼20% of non-small cell lung cancers (NSCLC). LKB1 is the major upstream kinase activating the energy-sensing kinase AMPK, making LKB1-deficient cells unable to appropriately sense metabolic stress. We tested the therapeutic potential of metabolic drugs in NSCLC and identified phenformin, a mitochondrial inhibitor and a...

Celiac disease stands out as a major health problem with a frequent association with many other disorders. Studies show an increased risk of developing pancreatitis and after that pancreatic cancer in patients with celiac disease. A frequent occurrence and a remarkably close association with the HLA-DQ2 and/or DQ8 gene loci represent main genetic characteristic of celiac disease. A particular a...

Lung cancer is the major cancer killer worldwide, and 5-yr survival is extremely poor (<or=15%), accentuating the need for more effective therapeutic strategies. Significant advances in lung cancer biology may lead to customised therapy based on targeting specific genes and pathways. The main signalling pathways that could provide roadmaps for therapy include the following: growth promoting pat...

Germ-line mutations of LKB1 (STK11) lead to Peutz-Jeghers syndrome characterized by gastrointestinal polyps and cancer of different organ systems. The mutations lead to loss or severe impairment of Lkb1 serine/threonine kinase activity. Therefore LKB1 has been implicated as a tumor suppressor gene, but only a few mutations in the coding exons of LKB1 have been detected in sporadic tumors. Here,...

Mammalian target of rapamycin (mTOR) is aberrantly activated in many cancer types, and two rapamycin derivatives are currently approved by the Food and Drug Administration (FDA) of the United States for treating renal cell carcinoma. Mechanistically, mTOR is hyperactivated in human cancers either due to the genetic activation of its upstream activating signaling pathways or the genetic inactiva...

А im: to reveal the rate of large rearrangements in genes responsible for familial adenomatous polyposis, MUTYH -associated polyposis and Peutz–Jeghers syndrome. Materials methods. The MLPA method was used identification rearrangements. A total number 135 patients included study: 83 with a clinical diagnosis “familial polyposis”, 18 — suspected 34 “Peutz–Jeghers syndrome”. Results. Seven deleti...