1-chloro-14-methylsulfanyl-tetradecane | 856353-42-9

• 分子结构分类: 有机化合物 - 有机硫化合物 - 硫醚类
• 英文名称: 1-chloro-14-methylsulfanyl-tetradecane
• 英文别名: 1-Chlor-14-methylmercapto-tetradecan；Methyl-(14-chlor-tetradecyl)-sulfid
• CAS: 856353-42-9
• 化学式: C₁₅H₃₁ClS
• 分子量: 278.93
• InChiKey: SFXYHJZFXIWRED-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  6.27
• 重原子数：
  17.0
• 可旋转键数：
  14.0
• 环数：
  0.0
• sp3杂化的碳原子比例：
  1.0
• 拓扑面积：
  0.0
• 氢给体数：
  0.0
• 氢受体数：
  1.0

反应信息

• 作为反应物：
  描述：

  1-chloro-14-methylsulfanyl-tetradecane 在 苯乙酮 、 sodium iodide 作用下， 生成 thiacyclopentadecane
  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：

  14-methylsulfanyl-tetradecan-1-ol 在 氯化亚砜 、 苯 作用下， 生成 1-chloro-14-methylsulfanyl-tetradecane
  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