Molecular gene mapping of human aldolase A (ALDOA) gene to chromosome 16

1987 ◽  
Vol 76 (1) ◽  
Author(s):  
A. Kukita ◽  
M.C. Yoshida ◽  
S. Fukushige ◽  
M. Sakakibara ◽  
K. Joh ◽  
...  
Keyword(s):  
Gene Mapping ◽  
Chromosome 16 ◽  
Aldolase A

Localization of the active gene of aldolase on chromosome 16, and two aldolase A pseudogenes on chromosomes 3 and 10

1988 ◽  
Vol 78 (2) ◽  
pp. 167-174 ◽  
Author(s):  
S. Serero ◽  
P. Maire ◽  
Nguyen Van Cong ◽  
O. Cohen-Haguenauer ◽  
M. S. Gross ◽  
...  
Keyword(s):  
Chromosome 16 ◽  
Active Gene ◽  
Aldolase A

Abnormalities of 16q in Multiple Myeloma Are Associated with Poor Prognosis: 500K Gene Mapping and Expression Correlations Identify Two Potential Tumor Suppressor Genes, WWOX and CYLD.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 110-110
Author(s):  
Matthew W. Jenner ◽  
Paola E. Leone ◽  
Brian A. Walker ◽  
David C. Johnson ◽  
Laura Chiecchio ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Gene Mapping ◽  
Tumor Suppressor Genes ◽  
Poor Prognosis ◽  
Fragile Site ◽  
Fragile Sites ◽  
Common Fragile Site ◽  
Chromosome 16 ◽  
Common Fragile Sites ◽  
Potential Tumor Suppressor

Abstract Abnormalities of 16q are important recurrent events in multiple myeloma (MM). We performed FISH on CD138 selected plasma cells from 701 newly diagnosed MM patients from the LRF UKMF cytogenetics database. Gene mapping, including paired normal controls, and gene expression analysis was performed on 55 cases using the Affymetrix Human Mapping 500K Array Set and U133 Plus 2.0 Arrays respectively. 16q deletion (del16q) was identified by FISH using probes for cMAF (Abbott Diagnostics) in 131/701 cases (18.7%) and was significantly associated with deletion 17p (16.5% vs. 8.9%, p=0.006), deletion 13 (60.8% vs. 48.5%, p=0.009), deletion of IgH (22.1% vs. 11.1%, p=0.0003) and non-hyperdiploid status (58.3% vs. 42.7%, p=0.006). Del16q showed a trend to poor overall survival, mean survival 43 vs. 61 months (p=0.09), and was associated with significantly worse survival in combination with t(4;14) compared with either t(4;14) or del16q alone, mean survival 15 vs. 26 vs. 45 months respectively (p=0.006). t(14;16) was identified by FISH in 31/701 cases (4.4%) and was associated with poor prognosis, mean survival 29 vs. 54 months (p=0.005). Mapping arrays revealed loss of heterozygosity (LOH) involving all or part of 16q in 20 of 55 cases (36%) in 3 distinct patterns: uniparental disomy (UPD) of chromosome 16 or 16q in 4/55 cases (7%); deletion of chromosome 16 or the whole of 16q in 11/55 cases (20%); and interstitial deletion of small regions of 16q in 5/55 cases (10%), focused on 16q12, the location of CYLD, and 16q23, the location of WWOX. 16q LOH was distributed across translocation groups but was identified in all 4 mapping cases containing 17p deletion, supporting the association identified by FISH. As WWOX is the site of the common fragile site FRA16D and deletions at common fragile sites have been associated with DNA instability in human cancers, we assessed this using gene mapping in these 55 MM cases. Although deletions spanning other common fragile sites were identified, they were not restricted to those with 16q LOH. However, in 2 t(14;16) cases, hemizygous deletions of approximately 100kb could be identified within WWOX at the presumed translocation breakpoint. One of the t(14;16) cases had a similar hemizygous deletion within FHIT, another tumor suppressor gene located within common fragile site FRA3B, consistent with findings in other cancer types. Cases with 16q LOH or t(14;16) all had significantly reduced WWOX expression relative to cases without 16q abnormalities, confirming gene inactivation by either LOH or translocation. Cases with 16q LOH also had significantly reduced expression of two other potential tumor suppressor genes located on 16q, CYLD and RBL2. In summary, our data confirms the adverse prognosis associated with 16q translocation or deletion. Array data reveals 16q LOH occurs due to deletion or UPD with two regions involved, one defined by CYLD and the other by WWOX. WWOX is also inactivated by translocation and is associated with interstitial deletions at this and other common fragile sites. WWOX is a likely candidate gene in MM pathogenesis because of its interaction with TP53 and CYLD via its effects on NF-κB.

Introduction

1978 ◽  
Vol 36 (3) ◽  
pp. 543-544
Author(s):  
W. Bernard
Keyword(s):  
Molecular Weight ◽  
Electron Microscope ◽  
Nucleic Acid ◽  
Gene Mapping ◽  
Molecular Genetics ◽  
Cell Biology ◽  
Gene Activity ◽  
Close Connection ◽  
Basic Information ◽  
Simple Systems

In comparison to many other fields of ultrastructural research in Cell Biology, the successful exploration of genes and gene activity with the electron microscope in higher organisms is a late conquest. Nucleic acid molecules of Prokaryotes could be successfully visualized already since the early sixties, thanks to the Kleinschmidt spreading technique - and much basic information was obtained concerning the shape, length, molecular weight of viral, mitochondrial and chloroplast nucleic acid. Later, additonal methods revealed denaturation profiles, distinction between single and double strandedness and the use of heteroduplexes-led to gene mapping of relatively simple systems carried out in close connection with other methods of molecular genetics.

Diagnosls of α thalassemia in the newborn. cord blood survey utilizing gene mapping

Pathology ◽  
1984 ◽  
Vol 16 (1) ◽  
pp. 16-21 ◽  
Author(s):  
Ronald J. Trent ◽  
P.E. Brock ◽  
J. Yakas ◽  
L.M. Trent ◽  
H. Kronenberg
Keyword(s):  
Gene Mapping ◽  
Cord Blood
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