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1.  Aberrant cytological localization of p16 and CDK4 in colorectal epithelia in the normal adenoma carcinoma sequence 
AIM: To study the correlation between the patterns of subcellular expression of p16 and CDK4 in colorectal epithelia in the normal-adenoma-carcinoma sequence.
METHODS: Paraffin sections of 43 cases of normal colorectal epithelia and corresponding adenomas as well as carcinomas were analysed immunocytochemically for subcellular expression of p16 and CDK4 proteins.
RESULTS: Most carcinomas showed more cytoplasmic overexpression for p16 and CDK4 than the adenomas from which they arised or the adjacent normal mucosa. Most normal or non-neoplastic epithelia showed more p16 and CDK4 expression in the nucleus than their adjacent adenomas and carcinomas. There was a significant difference between the subcellular expression pattern of p16 and CDK4 in normal-adenoma-carcinoma sequence epithelia (P < 0.001). Neither p16 nor CDK4 subcellular patterns correlated with histological grade or Dukes' stage.
CONCLUSION: Interaction of expression of p16 and CDK4 plays an important role in the Rb/p16 pathway. Overexpression of p16 and CDK4 in the cytoplasm, as well as loss expression of p16 in the nucleus might be important in the evolution of colorectal carcinoma from adenoma and, of adenoma from normal epithelia.
doi:10.3748/wjg.v12.i39.6391
PMCID: PMC4088153  PMID: 17072968
Colorectal neoplasm; p16; CDK4; Immuno-cytochemistry
2.  Sexual dimorphism in immune response genes as a function of puberty 
BMC Immunology  2006;7:2.
Background
Autoimmune diseases are more prevalent in females than in males, whereas males have higher mortality associated with infectious diseases. To increase our understanding of this sexual dimorphism in the immune system, we sought to identify and characterize inherent differences in immune response programs in the spleens of male and female mice before, during and after puberty.
Results
After the onset of puberty, female mice showed a higher expression of adaptive immune response genes, while males had a higher expression of innate immune genes. This result suggested a requirement for sex hormones. Using in vivo and in vitro assays in normal and mutant mouse strains, we found that reverse signaling through FasL was directly influenced by estrogen, with downstream consequences of increased CD8+ T cell-derived B cell help (via cytokines) and enhanced immunoglobulin production.
Conclusion
These results demonstrate that sexual dimorphism in innate and adaptive immune genes is dependent on puberty. This study also revealed that estrogen influences immunoglobulin levels in post-pubertal female mice via the Fas-FasL pathway.
doi:10.1186/1471-2172-7-2
PMCID: PMC1402325  PMID: 16504066
3.  Loss of heterozygosity of Kras2 gene on 12p12-13 in Chinese colon carcinoma patients 
AIM: To study the loss of heterozygosity (LOH) on 12p12-13 in Chinese colon carcinoma patients.
METHODS: DNA was extracted from 10 specimens of cancer tissue, 10 specimens of adjacent tissue and 10 specimens of normal tissue, respectively. LOH of Kras2 gene was analyzed by polymerase chain reaction (PCR) and denaturing polyacrylamide gel electrophoresis using 11 microsatellite markers on 12p-12-13.
RESULTS: LOH of Kras gene was detected at least on one marker of 12p-12-13 in 30% (3/10) of adjacent tissue specimens. The highest frequency of LOH was identified on D12S1034 in 28.57% (2/7) of adjacent tissue specimens. LOH was detected at least on one marker of 12p12-13 in 60% (6/10) of carcinoma tissue specimens, the most frequent LOH was found on D12S1034 and D12S1591 in 42.86% (3/7) of carcinoma tissue specimens. LOH was detected in 30% (3/10) of carcinoma tissue specimens, 30% (3/10) of adjacent tissue specimens, and no signal in 1% (1/0) carcinoma tissue specimen. The occurrence of LOH did not correlate with sex, age, tumor size and lymph node metastasis.
CONCLUSION: Genomic instability may occur on 12p-12-13 of Kras2 gene in the development and progression of colon carcinoma. The high LOH of Kras2 gene may directly influence the transcription and translation of wild type Kras2 gene.
doi:10.3748/wjg.v12.i7.1037
PMCID: PMC4087893  PMID: 16534842
Colon carcinoma; Loss of heterozygosity; Kras2

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