Oral leukoplakia - To treat or not to treat.
Copenhagen, Denmark. In Oral Dis, Feb 2016
The systemic therapies tested so far include retinoids, extracts of green tea, inhibitors of cyclooxygenase-2 and of epidermal growth factor, and peroxisome proliferator activated receptor-γ agonists (William, 2012), but there is no generally approved standard systemic therapy regimen so far (William, 2012).
Factors affecting platinum sensitivity in cervical cancer.
Tokyo, Japan. In Oncol Lett, Dec 2015
Each specimen was assessed for immunohistochemical expression of Ki-67, p53, B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), cleaved caspase-3, cyclooxygenase-2 (COX-2), and excision repair cross-complementation group 1 (ERCC1).
Pancreatic cancer and thromboembolic disease, 150 years after Trousseau.
Lund, Sweden. In Hepatobiliary Surg Nutr, Oct 2015
The exact pathophysiological mechanisms are still partly understood, but it is known that pancreatic cancer induces a prothrombotic and hypercoagulable state and genetic events involved in neoplastic transformation (e.g., KRAS, c-MET, p53), procoagulant factors [e.g., tissue factor (TF), platelet factor 4 (PF4), plasminogen activator inhibitor type 1 (PAI-1)], mucin production (e.g., through activation of P- and L-selectin) and pro-inflammatory factors [e.g., cytokines, cyclooxygenase-2 (COX-2)] may be implicated.
Blocking PGE2-induced tumour repopulation abrogates bladder cancer chemoresistance.
Houston, United States. In Nature, Feb 2015
In vivo administration of the cyclooxygenase-2 (COX2) inhibitor celecoxib effectively abolishes a PGE2- and COX2-mediated wound response gene signature, and attenuates progressive manifestation of chemoresistance in xenograft tumours, including primary xenografts derived from a patient who was resistant to chemotherapy.
Aspirin use and risk of colorectal cancer according to BRAF mutation status.
Boston, United States. In Jama, 2013
Experimental evidence implicates a role of RAF kinases in up-regulation of prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase 2), suggesting that BRAF-mutant colonic cells might be less sensitive to the antitumor effects of aspirin than BRAF-wild-type neoplastic cells.