Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P04626 (
erbB-2
)
5,251
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The 17q11-21 chromosomal region is frequently involved in non-random structural rearrangements associated with the M1 and M2 subtypes of acute myeloid leukemias (AML), as well as with the 15;17 translocation typical of the promyelocytic subtype. A number of genes have been localized in this region including the
c-erbA-1
and c-
erbB-2
proto-oncogenes, the genes coding for the granulocyte-colony stimulating factor (G-CSF), the retinoic acid receptor alpha (RAR alpha) and the myeloperoxidase enzyme (MPO). However, the precise location of these genes in relationship to the 17q11-21 breakpoint(s) has not been determined. Using in situ hybridization on metaphase chromosomes, we established the position of the breakpoints in relationship to the
c-erbA-1
, c-
erbB-2
, G-CSF, RAR alpha and MPO loci in a series of AML cases bearing 17q11-21 rearrangements. We report: (i) that the respective position of the five genes is centromere -
c-erbA-1
- G-CSF - c-
erbB-2
- RAR alpha - MPO - telomere; (ii) that the breakpoints of the various AML subtypes are variably located between the centromere and c-
erbB-2
in M1 and M2; (iii) that the breakpoints are consistently located between c-
erbB-2
and RAR alpha/MPO in M3; and (iv) that the breakpoint on chromosome 17 in the 15;17 translocation is located on 17q21 and not on 17q11-12 as previously reported.
...
PMID:Mapping of chromosome 17 breakpoints in acute myeloid leukemias. 170 Dec 31
We studied c-
erbB-2
and
c-erbA-1
(ear-1) gene amplification, and c-
erbB-2
protein expression in 123 primary Japanese breast cancers. c-
erbB-2
amplification was found in 19 of the 123 tumors (15%), and
c-erbA-1
was coamplified in 7 of the 19. The presence or absence of c-
erbB-2
amplification correlated with the grade of cellular atypism (P = 0.008), or that of mitotic index (P = 0.002), but not with the histologic types. The tumor size (P = 0.04) and the lymph node status (P = 0.06) were associated, but the patients' age, the TNM stage, or the presence or absence of estrogen or progesterone receptors was not associated, with c-
erbB-2
amplification. There were no differences in the histologic type, cellular atypism, mitotic index, and other disease parameters between tumors with c-
erbB-2
amplification only and those with coamplification of c-
erbB-2
and
c-erbA-1
. Paraffin sections from all 19 tumors with c-
erbB-2
amplification, and those from only one of 104 tumors without the amplification were positively stained with polyclonal anti-c-
erbB-2
protein antibody. Since the correlation between the amplification and the protein expression was excellent, such immunohistochemical studies may be substituted for the time-consuming DNA studies using Southern blotting.
...
PMID:c-erbB-2 and c-erbA-1 (ear-1) gene amplification and c-erbB-2 protein expression in Japanese breast cancers: their relationship to the histology and other disease parameters. 197 18