Results 201 to 210 of about 72,863 (253)

Role of SoxE transcription factors in development and disease

open access: yesDevelopmental Dynamics, EarlyView.
Abstract Sox8, Sox9, and Sox10 arose by multiple rounds of genome duplications from a single SoxE gene in ancestral vertebrates. In this review, we will briefly discuss the molecular structure and function of SoxE transcription factors and their evolutionary origin. We will then discuss their expression, function, and developmental disorders.
Merin Lawrence, Gerhard Schlosser
wiley   +1 more source

Genomic insights into red squirrels in Scotland reveals loss of heterozygosity associated with extreme founder effects

open access: yes
Marr MM   +11 more
europepmc   +1 more source
Some of the next articles are maybe not open access.

Related searches:

Loss of Constitutional Heterozygosity in Human Cancer

Annual Review of Genetics, 1991
INTRODUCTION 282 CANCER AS A GENETIC DISEASE 282 Visible Chromosomal Rearrangements in Tumor Cells. . . . . . . . . . . . . . .. . . . . .. . . . . . . . . . . . . . . 282 Inherited Syndromes Predisposing to Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Webster K Cavenee, Magnus Nordenskjold
exaly   +3 more sources

Loss of heterozygosity by SCRaMbLEing

Science China Life Sciences, 2019
Genetic variation drives phenotypic evolution within populations. Genetic variation can be divided into different forms according to the size of genomic changes. However, study of large-scale genomic variation such as structural variation and aneuploidy is still limited and mainly based on the static, predetermined feature of individual genomes.
Yunxiang, Li   +5 more
openaire   +2 more sources

Loss of Heterozygosity

2009
The most common molecular alteration observed in human cancers,1 loss of heterozygosity (LOH), is a significant mecha-nism by which critical genes involved in growth regulation and homeostasis become inactivated, or silenced, during disease evolution. This chapter provides a review of LOH and its implications in various cancers as well as a review of ...
Belinda J. Wagner, Sharon C. Presnell
openaire   +2 more sources

Loss of Heterozygosity in Endometrial Carcinoma

International Journal of Gynecological Pathology, 2008
Inactivation of a tumor suppressor gene typically occurs in two steps, thus fulfilling Knudson hypothesis. One "hit" is frequently a point mutation or a small deletion. The other alteration is usually a large genomic loss of part of a gene, or even part of a chromosome, or the whole chromosome.
Ana, Velasco   +9 more
openaire   +2 more sources

Loss of heterozygosity in liver tumours

Journal of Hepatology, 1995
ARCINOGENESIS is a multifactorial and multistep C process. In the process genetic factors play a pivotal role. There is a wealth of evidence that cancer is a set of fundamentally genetic diseases (1,2). While about 1% of total cancer patients inherit their tumours (3), genetic abnormalities have been demonstrated in all types of cancers, either ...
S F, Ding, N A, Habib
openaire   +2 more sources

Loss of heterozygosity in Neuroblastomas—an Overview

European Journal of Cancer, 1997
Although previous studies have demonstrated a relatively high incidence of loss of heterozygosity (LOH) on chromosomes 1p, 11q and 14q in neuroblastoma, it is unclear whether LOH occurs specifically on these chromosomes or not. It might be due to the lack of allelotyping of neuroblastoma. When we assessed all 22 autosomes and chromosome X for LOH in 81
J, Takita, Y, Hayashi, J, Yokota
openaire   +2 more sources

Mechanisms of loss of heterozygosity in retinoblastoma

Cytogenetics and Cell Genetics, 2008
Retinoblastoma (RB) tumors arise when both alleles of the RBI gene are inactivated by two mutational events (Ml and M2). Ml can be an initial germline or somatic mutation; M2 is frequently loss of heterozygosity (LOH), which makes the cell homozygous or hemizygous for the original mutation. LOH is the major mechanism by which many cancers are initiated.
X, Zhu   +6 more
openaire   +2 more sources

Home - About - Disclaimer - Privacy