scholarly journals Multistep tumorigenesis and the microenvironment

2004 ◽  
Vol 6 (2) ◽  
Author(s):  
Pepper Schedin ◽  
Anthony Elias
Keyword(s):  
Multistep Tumorigenesis

Mouse models for multistep tumorigenesis

2001 ◽  
Vol 11 (11) ◽  
pp. S2-S9 ◽  
Author(s):  
Xuemei Wu ◽  
Pier Paolo Pandolfi
Keyword(s):  
Mouse Models ◽  
Multistep Tumorigenesis

Mouse models for multistep tumorigenesis

2001 ◽  
Vol 11 ◽  
pp. S2-S9 ◽  
Author(s):  
Xuemei Wu ◽  
Pier Paolo Pandolfi
Keyword(s):  
Mouse Models ◽  
Multistep Tumorigenesis

Familial meningioma: analysis of expression of neurofibromatosis 2 protein Merlin

1998 ◽  
Vol 88 (3) ◽  
pp. 562-569 ◽  
Author(s):  
Marius Maxwell ◽  
Sarah D. Shih ◽  
Theofanis Galanopoulos ◽  
E. Tessa Hedley-Whyte ◽  
G. Rees Cosgrove
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Suppressor Gene ◽  
Protein Product ◽  
Neurofibromatosis 2 ◽  
Content Type ◽  
Spinal Meningiomas ◽  
Almost All ◽  
Second Tumor ◽  
Multistep Tumorigenesis

✓ Meningiomas are primarily benign brain tumors thought to arise through multistep tumorigenesis, involving both the activation of oncogenes and the loss of tumor suppressor genes. The recently isolated neurofibromatosis 2 (NF2) tumor suppressor gene has been found to be mutated in a large proportion of meningiomas. Almost all cases of familial meningioma occur in association with NF2. Familial meningioma in isolation from NF2 (sporadic) is exceedingly rare, with only 14 reports since 1959. The authors report the existence of a family lacking any stigmata of NF2, in which two members had spinal meningiomas. Tumor specimens were subjected to immunocytochemical analysis for the NF2 protein product Merlin, which has been implicated in the tumorigenesis of meningioma. Merlin immunoreactivity was present in both tumor specimens, implying that the NF2 tumor suppressor gene was not deleted in these tumors. This supports the hypothesis that a second tumor suppressor gene locus, other than NF2, acts in the formation of familial sporadic meningioma. The results are discussed in the context of putative oncogenic mechanisms of familial meningiomas.

scholarly journals An Alternative Route for Multistep Tumorigenesis in a Novel Case of Hereditary Renal Cell Cancer and a t(2;3)(q35;q21) Chromosome Translocation

1998 ◽  
Vol 62 (6) ◽  
pp. 1475-1483 ◽  
Author(s):  
Daniëlle Bodmer ◽  
Marc J. Eleveld ◽  
Marjolijn J.L. Ligtenberg ◽  
Marian A.J. Weterman ◽  
Bert A.P. Janssen ◽  
...  
Keyword(s):  
Renal Cell Cancer ◽  
Renal Cell ◽  
Cell Cancer ◽  
Chromosome Translocation ◽  
Alternative Route ◽  
Multistep Tumorigenesis

scholarly journals Expression of the Apoptosis-Suppressing Gene BCL-2 in Pheochromocytoma is Associated with the Expression of C-MYC

1997 ◽  
Vol 82 (6) ◽  
pp. 1949-1952 ◽  
Author(s):  
Da-Gong Wang ◽  
Colin F. Johnston ◽  
John J. Marley ◽  
Kerry V. Phenix ◽  
A. Brew Atkinson ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Blot Analysis ◽  
Messenger Rna ◽  
Malignant Tumors ◽  
Immunoperoxidase Staining ◽  
Critical Component ◽  
Molecular Events ◽  
Familial Tumors ◽  
Multistep Tumorigenesis

Abstract It has become increasingly clear that deregulation of programmed cell death is a critical component in multistep tumorigenesis. Previous studies have demonstrated a high frequency of Bcl-2 expression in tumors arising from cells derived from the neural crest and in tumor cell lines of neural origin. The present investigation was undertaken to determine whether similar molecular events occur in human pheochromocytoma. With the aim of determining the potential role of apoptosis in the pathogenesis of this tumor, we assessed proto-oncogene Bcl-2 and c-myc protein products as well as Bcl-2 messenger RNA levels in a collection of such tumors. Western blot analysis revealed that such tumors expressed the 26 kDa Bcl-2 (5 of 8 cases) and the 64 kDa c-Myc (7 of 8 cases) proteins. Northern blot analysis detected the Bcl-2 transcripts in 6 of 8 tumors. Immunoperoxidase staining, using a monoclonal anti-Bcl-2 antibody, was positive in 18 (82%), including 5 malignant tumors, of the 22 specimens examined. This Bcl-2 immunoreactivity was seen in 14 of 18 (78%) sporadic tumors, including 2 that were extra-adrenal, and all familial tumors. Of the 22 tumor samples examined for c-Myc protein, 20 (91%) tumors were positive. Our results suggest that deregulation of programmed cell death may be a critical component in the multistep tumorigenesis of human pheochromocytoma. The genetic complementation of simultaneously deregulated Bcl-2 and c-myc may be implicated in this process.

scholarly journals How Does Multistep Tumorigenesis Really Proceed?

2015 ◽  
Vol 5 (1) ◽  
pp. 22-24 ◽  
Author(s):  
Christine L. Chaffer ◽  
Robert A. Weinberg
Keyword(s):  
Multistep Tumorigenesis
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