|1.||Wilson, Samuel H: 7 articles (09/2013 - 01/2003)|
|2.||Horton, Julie K: 6 articles (09/2013 - 01/2003)|
|3.||Prasad, Rajendra: 3 articles (09/2013 - 10/2003)|
|4.||Lutz, Werner K: 3 articles (08/2009 - 08/2005)|
|5.||Narayan, Satya: 3 articles (10/2007 - 03/2002)|
|6.||Jaiswal, Aruna S: 3 articles (10/2007 - 03/2002)|
|7.||Stefanick, Donna F: 2 articles (09/2013 - 09/2005)|
|8.||Lutz, Roman W: 2 articles (08/2009 - 08/2005)|
|9.||Takeda, Shunichi: 2 articles (06/2008 - 01/2002)|
|10.||Brem, Reto: 2 articles (06/2008 - 01/2005)|
|2.||Prostatic Neoplasms (Prostate Cancer)
02/01/2008 - "Previous studies of yeast trf4Delta mutants revealed hypersensitivity to methylmethane sulfonate (MMS) but not UV light, a characteristic of BER mutants in other organisms. "
04/01/2012 - "Also, we found that ectopic expression of the region from residue 166-436 partially rescued the methyl methanesulfonate (MMS) hypersensitivity of XRCC1-deficient EM9 cells, suggesting a key role for this region in mediating DNA repair. "
06/27/2008 - "Loss of ASCIZ led to mild sensitivity to the base damaging agent methylmethane sulfonate (MMS), yet remarkably, suppressed the dramatic MMS hypersensitivity of polbeta-deficient cells. "
06/01/2008 - "XRCC1-deficient human cells show hypersensitivity to cell killing, increased genetic instability and a significant delay in S-phase progression after exposure to the alkylating agent methyl methanesulfonate (MMS). "
05/01/2004 - "Mutations altering all the favored ATM/ATR phosphorylation sites of Sae2 not only abolish its in vivo phosphorylation after DNA damage but also cause hypersensitivity to methyl methanesulfonate treatment, synthetic lethality with RAD27 deletion, and decreased rates of mitotic recombination between inverted Alu repeats, suggesting that checkpoint-mediated phosphorylation of Sae2 is important to support its repair and recombination functions."
07/06/2012 - "Tumors harboring variants with reduced enzyme activity may have compromised base excision repair function, as evidenced by our methylmethane sulfonate sensitivity studies. "
11/12/2009 - "This estimate was based on a lifetime cancer study with methyl methanesulfonate (MMS; as insufficient data were available for EMS) in rodents and default linear back extrapolation. "
06/01/2012 - "p53-Independent expression of wild-type p53-induced phosphatase 1 (Wip1) in methylmethane sulfonate-treated cancer cell lines and human tumors."
08/24/2007 - "Alkylating agent methyl methanesulfonate (MMS) induces a wave of global protein hyperacetylation: implications in cancer cell death."
10/01/2004 - "Compound 2 was capable of potentiating the action of the monofunctional methylating agent methyl methanesulfonate in cultured human cancer cells, consistent with the possible utility of inhibitors of this type in vivo."
|5.||Hepatocellular Carcinoma (Hepatoma)
09/01/1991 - "N-Methyl-N-nitrosourea, methyl methanesulfonate, N-hydroxyethyl-N-chloroethylnitrosourea, UV light, and X rays caused a similar accumulation of MGMT mRNA in rat hepatoma cells. "
01/01/1987 - "The O6-methylguanine-DNA-methyltransferase activity was measured in rat hepatoma cells (H4 cells) at different times after N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), methylmethane sulfonate (MMS) or ethylmethane sulfonate (EMS) treatment. "
03/01/1985 - "Pretreatment of H4 (rat hepatoma) cells for 48 h with non toxic doses of alkylating agents methylmethane sulfonate, (MMS), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) renders the cells more resistant to the toxic and mutagenic effects of these compounds. "
12/01/2009 - "In this study, we evaluated the ability of AN to protect human hepatoma cells (HepG2) from micronucleus (MN) induction against three different mutagens: benzo(a)pyrene (B(a)P), doxorubicin (DXR), and methyl methanesulfonate (MMS). "
02/01/1982 - "The purpose of this study was to test for a possible synergism in the antitumor action of the antimetabolite pyrazofurin (PF) and the alkylating agent lycurim (LY) [1,4-di(2'-mesyloxy-ethylamino)-1,4-dideoxy-m-erythritol dimethylsulfonate] on proliferating and resting rat hepatoma 3924A cells in tissue culture. "
|2.||DNA (Deoxyribonucleic Acid)
|4.||Hydrogen Peroxide (Hydroperoxide)
|1.||Drug Therapy (Chemotherapy)