We have isolated the proto-oncogene c-myb from Drosophila melanogaster. This gene is represented by a single locus at position 13E-F on the X chromosome, and is expressed in early embryos by transcription into two polyadenylated RNAs with lengths of approximately 3.0 and 3.8 kb. The gene may encode a protein with a molecular weight of at least 55,000 that shares a domain with c-myb (chicken) in...

1. Studies of cells transfected with specific expression vectors allow functions of specific gene products to be investigated. We first established optimum conditions for transfection of neonatal cardiac myocytes in primary culture. Increased proto-oncogene expression has been implicated in the development of cardiac hypertrophy; we therefore wished to examine the effects of overexpression of t...

INTRODUCTION Amplification of the HER-2/neu (HER-2) proto-oncogene occurs in 10%-15% of primary breast cancer, leading to an activated HER-2 receptor, augmenting growth of cancer cells. Tumor classification is determined in primary tumor tissue and metastatic biopsies. However, malignant cells tend to alter their phenotype during disease progression. Circulating tumor cell (CTC) analysis may se...

The HER-2 oncogene, a member of the erythroblastosis oncogene B (ERBB)-like oncogene family, has been shown to be amplified in many types of cancer, including breast cancer. However, the molecular mechanism of HER-2 overexpression is not completely understood. The phosphorylation of proteins on the serine or threonine residues that immediately precede proline (pSer/Thr-Pro) is specifically cata...

Proto-oncogenes are the genes that have potential to transform normal cells into cancer as a result of mutations. They usually contain encoding proteins whose function is inhibit cell differentiation, stimulate division, and prevent death cells. While prognosis regarding proto-oncogene may occur at varying phases cancer, accuracy identification method always questionable. The standard procedure...

The reciprocal translocation between the long arms of chromosomes 9 and 22, t(9 : 22), results in the Philadelphia (Ph1) chromosome, the karyotypic hallmark of chronic myeloid leukaemia (CML) [1]. The molecular consequences of this translocation have been well characterized, although their contribution to the disease process is less clear. The translocation creates a hybrid transcription unit c...