scholarly journals Identification of novel cancer fusion genes using chromosome breakpoint screening

2017 ◽  
Vol 37 (4) ◽  
pp. 2101-2108 ◽  
Author(s):  
Kate Hua ◽  
Chin-Hui Lin ◽  
Ya-Lun Chen ◽  
Chi-Hung Lin ◽  
Yueh-Hsin Ping ◽  
...  
Keyword(s):  
Fusion Genes ◽  
Chromosome Breakpoint

Using the sleeping beauty system to investigate different MLL fusion genes

2012 ◽  
Vol 224 (03) ◽  
Author(s):  
K Karl ◽  
E Kowarz ◽  
T Dingermann ◽  
R Marschalek
Keyword(s):  
Sleeping Beauty ◽  
Fusion Genes

Investigation of BRAF fusion genes as a therapeutic target in pilocytic astrocytoma

2012 ◽  
Vol 224 (06) ◽  
Author(s):  
H Cin ◽  
J Gronych ◽  
A Korshunov ◽  
DTW Jones ◽  
D Milford ◽  
...  
Keyword(s):  
Pilocytic Astrocytoma ◽  
Therapeutic Target ◽  
Fusion Genes ◽  
Braf Fusion

Genomic structure and nucleotide sequence of AML1-ETO fusion genes in children with acute myeloid leukemia

2004 ◽  
Vol 216 (03) ◽  
Author(s):  
C Gall ◽  
T Langer ◽  
M Metzler ◽  
S Viehmann ◽  
J Harbott ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Nucleotide Sequence ◽  
Myeloid Leukemia ◽  
Genomic Structure ◽  
Fusion Genes ◽  
Acute Myeloid

Simultaneous detection of 45 fusion genes in leukemia by dual-color fluorescence real-time PCR

2017 ◽  
Vol 39 (2) ◽  
pp. 175-184
Author(s):  
Z. Zheng ◽  
P. Zhang ◽  
G. He ◽  
K. Liao ◽  
Z. Wang ◽  
...  
Keyword(s):  
Real Time ◽  
Real Time Pcr ◽  
Simultaneous Detection ◽  
Fusion Genes ◽  
Dual Color

The impact of fusion genes on cancer stem cells and drug resistance

2021 ◽  
Author(s):  
Saurav Panicker ◽  
Sivaramakrishnan Venkatabalasubramanian ◽  
Surajit Pathak ◽  
Satish Ramalingam
Keyword(s):  
Stem Cells ◽  
Drug Resistance ◽  
Cancer Stem Cells ◽  
Fusion Genes ◽  
The Impact

scholarly journals Fusion genes in gynecologic tumors: the occurrence, molecular mechanism and prospect for therapy

2021 ◽  
Vol 12 (8) ◽  
Author(s):  
Bingfeng Lu ◽  
Ruqi Jiang ◽  
Bumin Xie ◽  
Wu Wu ◽  
Yang Zhao
Keyword(s):  
Tumor Progression ◽  
Massively Parallel Sequencing ◽  
Gynecologic Cancer ◽  
Endometrial Stromal Sarcoma ◽  
Driver Mutations ◽  
Fusion Genes ◽  
Stromal Sarcoma ◽  
Uterine Tumors ◽  
Rearrangement Mechanism ◽  
Gynecologic Tumors

AbstractGene fusions are thought to be driver mutations in multiple cancers and are an important factor for poor patient prognosis. Most of them appear in specific cancers, thus satisfactory strategies can be developed for the precise treatment of these types of cancer. Currently, there are few targeted drugs to treat gynecologic tumors, and patients with gynecologic cancer often have a poor prognosis because of tumor progression or recurrence. With the application of massively parallel sequencing, a large number of fusion genes have been discovered in gynecologic tumors, and some fusions have been confirmed to be involved in the biological process of tumor progression. To this end, the present article reviews the current research status of all confirmed fusion genes in gynecologic tumors, including their rearrangement mechanism and frequency in ovarian cancer, endometrial cancer, endometrial stromal sarcoma, and other types of uterine tumors. We also describe the mechanisms by which fusion genes are generated and their oncogenic mechanism. Finally, we discuss the prospect of fusion genes as therapeutic targets in gynecologic tumors.

scholarly journals A NOTE ON THE MATERNAL EFFECT MUTANTS DAUGHTERLESS AND ABNORMAL OOCYTE IN DROSOPHILA MELANOGASTER

Genetics ◽  
1973 ◽  
Vol 73 (1) ◽  
pp. 73-86
Author(s):  
Arthur P Mange ◽  
L Sandler
Keyword(s):  
Drosophila Melanogaster ◽  
Maternal Effect ◽  
Sex Chromosome ◽  
Chromosome 2 ◽  
Dominant Marker ◽  
Enhancing Effect ◽  
X Irradiation ◽  
The Right ◽  
Chromosome Breakpoint ◽  
Special Region

ABSTRACT Two deficiencies for, and a dominant enhancer of, the second chromosome maternal effect mutant, "daughterless" (da), were induced with X-irradiation. Their properties were studied with respect to both da and the linked maternal effect mutant, "abnormal oocyte" (abo), with the following conclusions. (1) The most probable map positions of da and abo are: J–½–da–2½–abo, where J is a dominant marker located at 41 on the standard map. (2) The da locus is in bands 31CD-F on the polytene chromosome map; abo is to the right of 32A. (3) Because homozygous da individuals survive while individuals carrying da and a deficiency for da are lethal, it is concluded that da is hypomorphic. (4) From a weak da-like maternal effect in heterozygous da females induced by an "Enhancer of da," we have confirmed a previous report that (a) the amount of sex chromosome heterochromatin contributed by the father can influence the severity of the da maternal effect, and (b) the sex chromosome heterochromatin which influences the da effect is different from that which influences the abo effect. (5) The possibility that da and abo are in a special region of chromosome 2 concerned with the regulation of sex chromosome heterochromatin is strengthened by the observation that the Enhancer of da appears to rescue abnormal eggs produced by homozygous abo mothers. (6) The Enhancer of da is a translocation between chromosomes 2 and 3 with the second chromosome breakpoint in the basal heterochromatin; because the enhancing effect maps in this region of chromosome 2, it is possible that autosomal, as well as sex chromosomal, heterochromatin interacts with da and abo.

scholarly journals MA27.01 Establishment of PDX From Tumors Characterized by EGFR Mutations or ALK Fusion Genes from Resections, Biopsies and Pleural Fluids

2018 ◽  
Vol 13 (10) ◽  
pp. S454-S455
Author(s):  
S. Martins-Filho ◽  
M. Cabanero ◽  
N. Pham ◽  
E. Stewart ◽  
D. Ravi ◽  
...  
Keyword(s):  
Egfr Mutations ◽  
Fusion Genes

Expression of the angiotensinogen gene is synergistically stimulated by 8-BrcAMP and Dex in opossum kidney cells

1995 ◽  
Vol 268 (1) ◽  
pp. R105-R111 ◽  
Author(s):  
M. Ming ◽  
T. T. Wang ◽  
S. Lachance ◽  
A. Delalandre ◽  
S. Carriere ◽  
...  
Keyword(s):  
Fusion Gene ◽  
Dependent Manner ◽  
Fusion Genes ◽  
Opossum Kidney ◽  
Ok Cells ◽  
Angiotensinogen Gene ◽  
Opossum Kidney Cells ◽  
Dependent Protein ◽  
Flanking Region ◽  
Responsive Element

We transiently transfected fusion genes with the 5'-flanking region of the angiotensinogen gene linked to a bacterial chloramphenicol acetyltransferase (CAT) coding sequence as a reporter into opossum kidney (OK) cells. The addition of 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) (10(-3)-10(-7) M) or forskolin (10(-9)-10(-5) M) stimulated the expression of the plasmid pOCAT [angiotensinogen nucleotide (N) -1498/+18] fusion gene in OK cells in a dose-dependent manner. The addition of dexamethasone (Dex) (10(-6) M) further enhanced the stimulatory effect of 8-BrcAMP or forskolin, whereas the addition of (R)-p-adenosine 3',5'-cyclic monophosphorothioate [(Rp)-cAMP[S], an inhibitor of cAMP-dependent protein kinase A, I and II] blocked the stimulatory effect of 8-BrcAMP. Furthermore, the addition of 8-BrcAMP (10(-3) M) or Dex (10(-6) M) or a combination of both stimulated the expression of pOCAT (angiotensinogen N -1138/+18), pOCAT (angiotensinogen N -960/+18), pOCAT (angiotensinogen N -814/+18), and pOCAT (angiotensinogen N -688/+18), but had no effect on the expression of pOCAT (angiotensinogen N -280/+18), pOCAT (angiotensinogen N -198/+18), pOCAT (angiotensinogen N -110/+18), pOCAT (angiotensinogen N -53/+18), and pOCAT (angiotensinogen N -35/+18). To further localize the putative cAMP-responsive element (CRE) in the angiotensinogen gene, we constructed fusion genes by inserting the DNA fragments angiotensinogen N -814 to N -689, angiotensinogen N -814 to N -761, and angiotensinogen N -760 to N -689 of the 5'-flanking region of the angiotensinogen gene upstream of the thymidine kinase (TK) promoter fused to a CAT gene and introduced them into OK cells.(ABSTRACT TRUNCATED AT 250 WORDS)

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