Disease relevance of KIAA0194

• A pilot study of mixed beam radiotherapy (fast neutrons alternating with photons) followed by combination chemotherapy with SMF (streptozotocin, 5-fluorouracil, mitomycin C) in localized pancreatic cancer was performed [1].
• 153 women with advanced breast cancer were randomly allocated for treatment with SMF [prednimustine (Sterecyt) + methotrexate + 5-fluorouracil, 83 patients] or CMF (cyclophosphamide+methotrexate+5-fluorouracil, 70 patients) [2].
• Patients with primary myelofibrosis (PMF) and myelofibrosis secondary to carcinoma (SMF) were compared with regard to circulating granulocyte macrophage progenitor cells (CFU-GM) using in vitro tissue culture techniques [3].
• Toxicity was moderate for both regimens, with SMF having greater gastrointestinal and renal toxicity [4].
• Ten of 23 patients with advanced measureable adenocarcinoma of the pancreas achieved an objective response after treatment with a regimen consisting of streptozotocin, mitomycin-C and 5-fluorouracil (SMF) [5].

High impact information on KIAA0194

• Pulse-chase studies combined with subcellular fractionation indicated that LpB 100 (i.e. the apoprotein B (apoB) 100 containing lipoproteins) was released to the lumen of the secretory pathway in a subcellular fraction enriched in smooth vesicles, and referred to as SMF (the smooth membrane fraction) [6].
• The migration of SMF during gradient ultracentrifugation as well as kinetic studies indicated that the fraction was derived from a pre-Golgi compartment, probably the smooth endoplasmic reticulum (ER) [6].
• These programs led us to identify a novel gene, designated SMF, immediately downstream of FMS, in the opposite orientation [7].
• The intrinsic mutagenicity of SMF was enhanced by addition of extra chloride ion to the assay medium [8].
• Plasmapheresis was run with cellulose diacetate membranes in single (SMF) and double (DMF) membrane filtration and with a new polycarbonate membrane in SMF [9].

Chemical compound and disease context of KIAA0194

• These results suggest that the SMF may enhance nicardipine-induced hypotension by more effectively antagonizing the Ca2+ influx through the Ca2+ channels compared with the nicardipine treatment alone [10].

Biological context of KIAA0194

• In addition, the enhanced antihypertensive effects of the SMF on the nicardipine-treated rats might be, at least in part, related to the increased NO(x), primarily due to the upregulation of inducible nitric oxide synthase [10].

Anatomical context of KIAA0194

• Continuous application of a static magnetic field (SMF; a maximum magnetic flux density of 180 millitesla, a peak magnetic gradient of 133 millitesla/mm) to the left carotid sinus baroreceptors of rats was carried out for 6 weeks using a disc-shaped magnetic implant (4.4 mm in diameter, 2.2 mm in height) [10].

Associations of KIAA0194 with chemical compounds

• The 5-FU and streptozotocin were repeated on days 60, 81, and 88, and the stretozotocin and mitomycin (SMF) cycles were repeated every 8 weeks until progression [11].
• The SMF did not significantly induce any changes in the SBF and SBV in nicardipine-treated nor untreated rats [10].

Analytical, diagnostic and therapeutic context of KIAA0194

• In conclusion, SMF seems to be as efficient as CMF with regard to response rate, time to treatment failure and survival [2].

References