A nucleotide insertion in exon 4 is responsible for the absence of expression of an HLA-A*0301 allele in a prostate carcinoma cell line

[1]  R. Blasczyk,et al.  Non-expression of HLA-B*5111N is caused by an insertion into the cytosine island at exon 4 creating a frameshift stop codon. , 2001, Tissue antigens.

[2]  P. Stern,et al.  A mutation determining the loss of HLA-A2 antigen expression in a cervical carcinoma reveals novel splicing of human MHC class I classical transcripts in both tumoral and normal cells , 2000, Immunogenetics.

[3]  John Calvin Reed,et al.  Mutational inactivation of the proapoptotic gene BAX confers selective advantage during tumor clonal evolution. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[4]  P. Stern,et al.  Multiple mechanisms underlie HLA dysregulation in cervical cancer. , 2000, Tissue antigens.

[5]  G. Fleuren,et al.  Human leukocyte antigen class I gene mutations in cervical cancer. , 1999, Journal of the National Cancer Institute.

[6]  F. Marincola,et al.  Selective Histocompatibility Leukocyte Antigen (Hla)-A2 Loss Caused by Aberrant Pre-mRNA Splicing in 624mel28 Melanoma Cells , 1999, The Journal of experimental medicine.

[7]  M. R. Oliva,et al.  A new beta 2 microglobulin mutation found in a melanoma tumor cell line. , 1999, Tissue antigens.

[8]  L. Myeroff,et al.  Mutation of the type II transforming growth factor-beta receptor is coincident with the transformation of human colon adenomas to malignant carcinomas. , 1998, Cancer research.

[9]  J. Cazenave,et al.  A nucleotide insertion in exon 4 is responsible for the absence of expression of an HLA-A*01 allele. , 1997, Tissue antigens.

[10]  E. Weissenstein Filling in the blanks. , 1997, Modern healthcare.

[11]  E. Adams,et al.  Natural inactivation of a common HLA allele (A*2402) has occurred on at least three separate occasions. , 1997, Journal of immunology.

[12]  P. Stern,et al.  Implications for immunosurveillance of altered HLA class I phenotypes in human tumours. , 1997, Immunology today.

[13]  G. Thomas,et al.  BAT-26, an indicator of the replication error phenotype in colorectal cancers and cell lines. , 1997, Cancer research.

[14]  M. Carter,et al.  A splicing‐dependent regulatory mechanism that detects translation signals. , 1996, The EMBO journal.

[15]  J. McCluskey,et al.  Stable inheritance of an HLA-"blank" phenotype associated with a structural mutation in the HLA-A*0301 gene. , 1996, Tissue antigens.

[16]  W. Bodmer,et al.  Immune surveillance in colorectal carcinoma , 1995, Nature Genetics.

[17]  J. Bodmer,et al.  Loss of human leukocyte antigen expression on colorectal tumor cell lines: implications for anti-tumor immunity and immunotherapy. , 1993, Journal of immunotherapy with emphasis on tumor immunology : official journal of the Society for Biological Therapy.

[18]  Darryl Shibata,et al.  Ubiquitous somatic mutations in simple repeated sequences reveal a new mechanism for colonic carcinogenesis , 1993, Nature.

[19]  R. Bontrop,et al.  cis-acting regulatory elements abrogate allele-specific HLA class I gene expression in healthy individuals. , 1992, Journal of immunology.