𝔖 Bobbio Scriptorium
✦   LIBER   ✦

Analysis of p53 gene mutations in acute myeloid leukemia

✍ Scribed by Dino Trecca; Letizia Longo; Andrea Biondi; Lilla Cro; Rossella Calori; Fausto Grignani; Anna Teresa Maiolo; Pier Giuseppe Pelicci; Dr. Antonino Neri


Publisher
John Wiley and Sons
Year
1994
Tongue
English
Weight
676 KB
Volume
46
Category
Article
ISSN
0361-8609

No coin nor oath required. For personal study only.


πŸ“œ SIMILAR VOLUMES


Analysis of N-ras gene mutations in acut
✍ A. V. Todd; C. M. Ireland; T. J. Radloff; H. Kronenberg; Dr. H. J. Iland πŸ“‚ Article πŸ“… 1991 πŸ› John Wiley and Sons 🌐 English βš– 645 KB

## Abstract N‐ras gene activation occurs via single base substitutions in codons 12, 13, and 61. We have developed a rapid screening method, termed allele specific restriction analysis (ASRA), for detection of N‐ras mutations at these three critical codons in acute myeloid leukemia (AML). Patient D

Mutation analysis of PTEN/MMAC1 in acute
✍ Liu, Ta-Chih; Lin, Pai-Mei; Chang, Jan-Gowth; Lee, Jing-Ping; Chen, Tyen-Po; Lin πŸ“‚ Article πŸ“… 2000 πŸ› John Wiley and Sons 🌐 English βš– 285 KB πŸ‘ 2 views

Recently, a putative tumor suppressor gene, PTEN/MMAC1, has been identified at chromosome 10q23.3, which encodes a 403 amino acid dual-specificity phosphatase containing a region of homology to tensin and auxillin. Somatic mutations of the PTEN/MMAC1 gene have been identified in a number of cancer c

Amplification of ribosomal RNA genes in
✍ Christa Fonatsch; Hadwiga Nowotny; Elisabeth Pittermann-HΓΆcker; Berthold Streube πŸ“‚ Article πŸ“… 2001 πŸ› John Wiley and Sons 🌐 English βš– 412 KB πŸ‘ 3 views

## Abstract Gene amplification is a relatively rare event in acute myeloid leukemia (AML). Double minutes (dmin) and homogeneously staining regions are well established phenomena as cytogenetic correlates of gene amplification. Recently, however, two additional mechanisms leading to gene amplificat

RAS gene mutations in childhood acute my
✍ Dr. Bert Vogelstein; Dr. Curt I. Civin; Antonette C. Preisinger; Jeffrey P. Kris πŸ“‚ Article πŸ“… 1990 πŸ› John Wiley and Sons 🌐 English βš– 336 KB

Mutations at codon I 2, I 3, and 6 I of the HRAS, KRAS, and NRASgenes were evaluated in 99 cases of pediatric acute myeloid leukemia (AML) using oligonucleotide hybridization to polymerase chain reacted derived products. Twenty-four mutations were identified in the NRAS gene, I 3 in the KRAS gene, a

Mutations of the AML1 gene in acute myel
✍ Stephen E. Langabeer; Rosemary E. Gale; Sara J. Rollinson; Gareth J. Morgan; Dav πŸ“‚ Article πŸ“… 2002 πŸ› John Wiley and Sons 🌐 English βš– 260 KB

## Abstract The __AML1__ gene encodes a transcription factor that, together with its heterodimeric partner CBFB, regulates a number of target genes that are essential for normal hemopoiesis. In acute myeloid leukemia (AML), __AML1__ is disrupted not only by chromosomal translocations but also by mu

Aberrant methylation of multiple tumor s
✍ Cumhur G. Ekmekci; Marina I. GutiΓ©rrez; Abdul K. Siraj; Ugur Ozbek; Kishor Bhati πŸ“‚ Article πŸ“… 2004 πŸ› John Wiley and Sons 🌐 English βš– 261 KB πŸ‘ 3 views

## Abstract Hypermethylator phenotype, a propensity of tumors to incur nonrandom concurrent methylation, has been described in several tumors, including acute myeloid leukemia (AML). More recent studies identified methylation of other tumor suppressor genes, DAP‐kinase and SOCS1, singly in AML. We