Somatic mutations of the CD95 gene in Hodgkin and Reed-Sternberg cells

Cancer Research

Volumn 60, Issue 20, 2000, Pages 5640-5643

  Muschen, M ^a   Re, D ^a   Brauninger, A ^a   Wolf, J ^a   Hansmann, M L ^a   Diehl, V ^a   Kuppers, R ^a   Rajewsky, K ^a  

^a UNIVERSITY OF COLOGNE   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

FAS ANTIGEN; INHIBITOR PROTEIN;

ADOLESCENT; ADULT; AGED; ALLELE; APOPTOSIS; ARTICLE; B LYMPHOCYTE; CONTROLLED STUDY; FEMALE; GENE MUTATION; GERMINAL CENTER; HODGKIN DISEASE; HUMAN; HUMAN CELL; MALE; MICROMANIPULATION; NUCLEOTIDE SEQUENCE; PRIORITY JOURNAL; REED STERNBERG CELL; SCHOOL CHILD; SOMATIC MUTATION;

ADULT; AGED; ANTIGENS, CD95; APOPTOSIS; CHILD; FEMALE; GENE AMPLIFICATION; HODGKIN DISEASE; HUMANS; MALE; MIDDLE AGED; MUTATION; POLYMERASE CHAIN REACTION; REED-STERNBERG CELLS;

EID: 0034667371     PISSN: 00085472     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (27)

1. The origin of Hodgkin and Reed-Stenaberg cells in Hodgkin's disease
2. Hodgkin disease: Hodgkin and Reed-Sternberg cells picked from histological sections show clonal immunoglobulin gene rearrangements and appear to be derived from B cells at various stages of development
3. Hodgkin and Reed-Sternberg cells in Hodgkin's disease represent the outgrowth of a dominant tumor clone derived from (crippled) germinal center B cells
4. Rare occurrence of classical Hodgkin's disease as a T cell lymphoma
5. Clonal selection and learning in the antibody system
6. Human germinal center B cells express the apoptosis-inducing genes Fas, c-myc, p53 and Bax but not the survival gene bcl-2
7. Mechanisms of selection and differentiation in germinal centers
8. Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis
9. Spontaneous development of plasmacytoid tumors in mice with defective Fas-Fas ligand interactions
10. Dominant interfering Fas gene mutations impair apoptosis in a human autoimmune lymphoproliferative syndrome
11. Defective apoptosis due to a point mutation in the death domain of CD95 associated with autoimmune lymphoproliferative syndrome, T-cell lymphoma, and Hodgkin's disease
12. Pathological findings in human autoimmune lympho-proliferative syndrome
13. Mutations in the Fas antigen in patients with multiple myeloma
14. Somatic Fas mutations in non-Hodgkin's lymphoma: Association with extranodal disease and autoimmunity
15. CD95 (Apo-1/Fas) mutations in childhood T-lineage acute lymphoblastic leukemia
16. Alterations of Fas (Apo-I/CD95) gene in transitional cell carcinomas of urinary bladder
17. Alterations of Fas (Apo-1/CD95) gene in non-small cell lung cancer
18. Defining CD95 as a tumor suppressor gene
19. Fas/Apo-1 (CD95) receptor lacking the intracytoplasmic signaling domain protects tumor cells from Fas-mediated apoptosis
20. Cultivated H/RS cells are resistant to CD95L-mediated apoptosis despite expression of wild-type CD95
21. Clonal deleterious mutations in the IκBα gene in the malignant cells in Hodgkin's lymphoma
22. Whole genome amplification of a single cell: Implication for genetic analysis
23. p53 Activates the CD95 (Apo-I/Fas) gene in response to DNA damage by anticancer drugs
24. Mutation of the p53 gene is not a typical feature of Hodgkin and Reed-Sternberg cells in Hodgkin's disease
25. Single cell analysis of the t(14, 18) (q31, q21) chromosomal translocation in Hodgkin's disease demonstrates the absence of this rearrangement in neoplastic Hodgkin and Reed-Sternberg cells
26. Expression of Fas and Fas ligand in Hodgkin's disease
27. A genetic model for colorectal tumorigenesis