10-(methylthio)decan-1-ol | 855753-25-2

• 分子结构分类: 有机化合物 - 有机硫化合物 - 硫醚类
• 英文名称: 10-(methylthio)decan-1-ol
• 英文别名: 10-methylsulfanyl-decan-1-ol；10-Methylmercapto-decan-1-ol；10-Methylsulfanyldecan-1-ol；10-methylsulfanyldecan-1-ol
• CAS: 855753-25-2
• 化学式: C₁₁H₂₄OS
• 分子量: 204.377
• InChiKey: XTOFHGJGXXLQPJ-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.8
• 重原子数：
  13
• 可旋转键数：
  10
• 环数：
  0.0
• sp3杂化的碳原子比例：
  1.0
• 拓扑面积：
  45.5
• 氢给体数：
  1
• 氢受体数：
  2

反应信息

• 作为反应物：
  描述：

  10-(methylthio)decan-1-ol 在 氯化亚砜 作用下， 生成 1-chloro-10-methylsulfanyl-decane
  参考文献：
  名称：

  Familial Head and Neck Cancer: Molecular Analysis of a New Clinical Entity

  摘要：

  AbstractObjective The tumor suppressor gene p16 encodes a cyclin‐dependent kinase inhibitor that normally inhibits cell proliferation by causing a G1 cell cycle arrest. The p16 gene is frequently mutated in a variety of somatic tumors, as well as in familial melanoma and familial pancreatic carcinoma. We identified a family with a high incidence of head and neck squamous cell carcinoma (HNSCC) and melanoma. Molecular analyses of the p16 gene locus in blood and tumor DNA from this family was performed to determine whether an association between germline p16 gene mutation and HNSCC exists.Study Design Molecular pedigree analyses.Methods Exon 2 of p16 was polymerase chain reaction amplified from blood, tumor, or nontumor DNA isolated from affected and unaffected members, then directly sequenced and compared with consensus p16 sequence. Cell cycle position of cells expressing wild‐type or mutant p16 was determined by flow cytometry.Results Molecular analyses revealed a nonfunctional germline point mutation within exon 2 of the p16 gene that encodes a mutant p16 protein substituting proline at amino acid position 87 for the wild‐type arginine (p16R87P). Relative to wild‐type p16, p16R87P lost ability to cause a growth arrest following ectopic expression. The mutant (p16R87P) allele segregated with cancer predisposition in tested family members, and analyses of HNSCC tumor tissues demonstrated universal loss of wild‐type allele.Conclusions Significance of the mutant p16 (p16R87P) in HNSCC tumorigenesis is strongly suggested by its loss of cell cycle arrest activity and its retention in tumor tissue with simultaneous loss of the wild‐type allele. Further, the germline p16 mutation segregated with cancer predisposition within the family. In aggregate, these data suggest that there is a direct causal relationship between the germline p16 mutation in this family and HNSCC tumorigenesis. Based on our observations, the spectrum of familial cancers associated with p16 mutations should include a new clinical entity, familial HNSCC.

  DOI：

  10.1097/00005537-200209000-00010
• 作为产物：
  描述：

  10-溴-1-癸醇 在 potassium carbonate 、 硫脲 、 potassium iodide 作用下， 以 乙醇 、 N,N-二甲基甲酰胺 为溶剂， 反应 19.0h， 生成 10-(methylthio)decan-1-ol
  参考文献：
  名称：

  离子支持的甲基亚砜和甲基硫化物的高效Swern氧化和Corey-Kim氧化

  摘要：

  在二氯甲烷中，在三乙胺存在下，用两种离子负载的甲基亚砜A-1（C 6）和B-1（C 10）和草酰氯对各种苄基和烯丙基醇，伯醇和仲醇进行Swern氧化，然后简单的乙醚萃取反应混合物，分别以高收率和高纯度分别得到相应的醛和酮。同样，用两种离子支持的甲基硫醚A-2（C 6）和B-2（C 10）对各种苄醇和烯丙基醇，伯醇和仲醇进行Corey-Kim氧化）和N-氯代琥珀酰亚胺在二氯甲烷中的三乙胺存在下，然后简单地用乙醚萃取反应混合物，分别以高收率和高纯度提供相应的醛和酮。两种反应都没有产生任何难闻的气味。在Swern氧化中，以高收率回收了离子负载的甲基硫化物，可以将其重新氧化以生成离子负载的甲基亚砜A-1（C 6）和B-1（C 10），以便在同一氧化中重复使用。在Corey–Kim氧化过程中，离子支撑的甲基硫化物A-2（C 6）和B-2（C 10）以高收率回收，也可用于相同的氧化。

  DOI：

  10.1016/j.tet.2012.06.026

文献信息

• Efficient Swern oxidation and Corey–Kim oxidation with ion-supported methyl sulfoxides and methyl sulfides
  作者：Daisuke Tsuchiya、Masayuki Tabata、Katsuhiko Moriyama、Hideo Togo

  DOI：10.1016/j.tet.2012.06.026

  日期：2012.8

  Swern oxidation of various benzylic and allylic alcohols, primary alcohols, and secondary alcohols with two ion-supported methyl sulfoxides A-1 (C6) and B-1 (C10), and oxalyl chloride in the presence of triethylamine in dichloromethane, followed by simple diethyl ether extraction of the reaction mixture, gave the corresponding aldehydes and ketones, respectively, in good yields with high purity. Similarly

  在二氯甲烷中，在三乙胺存在下，用两种离子负载的甲基亚砜A-1（C 6）和B-1（C 10）和草酰氯对各种苄基和烯丙基醇，伯醇和仲醇进行Swern氧化，然后简单的乙醚萃取反应混合物，分别以高收率和高纯度分别得到相应的醛和酮。同样，用两种离子支持的甲基硫醚A-2（C 6）和B-2（C 10）对各种苄醇和烯丙基醇，伯醇和仲醇进行Corey-Kim氧化）和N-氯代琥珀酰亚胺在二氯甲烷中的三乙胺存在下，然后简单地用乙醚萃取反应混合物，分别以高收率和高纯度提供相应的醛和酮。两种反应都没有产生任何难闻的气味。在Swern氧化中，以高收率回收了离子负载的甲基硫化物，可以将其重新氧化以生成离子负载的甲基亚砜A-1（C 6）和B-1（C 10），以便在同一氧化中重复使用。在Corey–Kim氧化过程中，离子支撑的甲基硫化物A-2（C 6）和B-2（C 10）以高收率回收，也可用于相同的氧化。
• Familial Head and Neck Cancer: Molecular Analysis of a New Clinical Entity
  作者：Kathy K. Yu、Adam M. Zanation、Jonathan R. Moss、Wendell G. Yarbrough

  DOI：10.1097/00005537-200209000-00010

  日期：2002.9

  AbstractObjective The tumor suppressor gene p16 encodes a cyclin‐dependent kinase inhibitor that normally inhibits cell proliferation by causing a G1 cell cycle arrest. The p16 gene is frequently mutated in a variety of somatic tumors, as well as in familial melanoma and familial pancreatic carcinoma. We identified a family with a high incidence of head and neck squamous cell carcinoma (HNSCC) and melanoma. Molecular analyses of the p16 gene locus in blood and tumor DNA from this family was performed to determine whether an association between germline p16 gene mutation and HNSCC exists.Study Design Molecular pedigree analyses.Methods Exon 2 of p16 was polymerase chain reaction amplified from blood, tumor, or nontumor DNA isolated from affected and unaffected members, then directly sequenced and compared with consensus p16 sequence. Cell cycle position of cells expressing wild‐type or mutant p16 was determined by flow cytometry.Results Molecular analyses revealed a nonfunctional germline point mutation within exon 2 of the p16 gene that encodes a mutant p16 protein substituting proline at amino acid position 87 for the wild‐type arginine (p16R87P). Relative to wild‐type p16, p16R87P lost ability to cause a growth arrest following ectopic expression. The mutant (p16R87P) allele segregated with cancer predisposition in tested family members, and analyses of HNSCC tumor tissues demonstrated universal loss of wild‐type allele.Conclusions Significance of the mutant p16 (p16R87P) in HNSCC tumorigenesis is strongly suggested by its loss of cell cycle arrest activity and its retention in tumor tissue with simultaneous loss of the wild‐type allele. Further, the germline p16 mutation segregated with cancer predisposition within the family. In aggregate, these data suggest that there is a direct causal relationship between the germline p16 mutation in this family and HNSCC tumorigenesis. Based on our observations, the spectrum of familial cancers associated with p16 mutations should include a new clinical entity, familial HNSCC.