Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04626 (erbB-2)
 5,251 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have shown that the nontransformed AKR-2B cells when arrested in the G1 phase of the cell cycle due to low-molecule-weight nutrient (amino acid) deficiency exhibit a 5- to 10-fold lower level of epidermal growth factor (EGF) receptor activity than do the same cells in the rapidly growing state or arrested in G1 due to growth factor deficiency. The chemically transformed AKR-MCA and C3H/MCA-58 cell lines spontaneously arrest growth in G1 due to nutrient deficiency when grown to saturation density in medium with 10% fetal bovine serum. An examination of 125I-labeled EGF binding in rapidly growing and G1-arrested AKR-MCA and C3H/MCA-58 cells showed that the G1-arrested chemically transformed cells also have a 10- to 20-fold reduction in the amount of 125I-labeled EGF binding relative to the same cells in the rapidly growing state. Stimulation of DNA synthesis in the arrested cells by the addition of serum-free medium caused a 6- to 10-fold increase in 125I-labeled EGF binding. This recovery of receptor activity was inhibited by actinomycin D and cycloheximide, suggesting that new messenger RNA synthesis as well as increased protein synthesis is necessary for the recovery of EGF binding. A comparison of EGF binding in C3H/MCA-58 cells and the nontransformed parent line (C3H/10T 1/2) in the rapidly growing state showed the same approximate level of receptor activity. However, the rapidly growing AKR-MCA cells had approximately one-tenth the amount of EGF binding as did the rapidly growing nontransformed parent line (AKR-2B). Scatchard analysis of binding data showed a 10-fold greater number of receptors in the AKR-2B cells relative to the AKR-MCA cells with a lesser difference in apparent receptor affinity. The chemically transformed BP-3T3, like the other two chemically transformed lines, was also demonstrated to arrest growth spontaneously due to nutrient deficiency with an associated 100-fold decrease in EGF binding. Rapidly growing BP-3T3 cells had only slightly less 125I-labeled EGF binding than did the nontransformed parent line (BALB-3T3) in the rapidly growing state. The data indicate that one mechanism for reduction of EGF binding in chemically transformed cells is the propensity of these cells to arrest growth in G1 at saturation density due to low-molecular-weight nutrient deficiency, a state associated with decreased EGF binding.
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PMID:Cell cycle variation in 125I-labeled epidermal growth factor binding in chemically transformed cells. 697 83

Two human cancer cell lines (MA 2 and MA 3) were established from pleural effusions of infiltrating ductal carcinomas of the breast. The lines were maintained in continuous monolayer culture with doubling times of 70 (MA 2) and 78 (MA 3) hr for more than two years and possessed extensively rearranged abnormal karyo-types with modal chromosome number of 83 (MA 2) and 81 (MA 3) and DNA index values of 1.65 and 1.77, respectively. No amplifications or rearrangements were evident in the c-myc, int-2, c-erb B2, c-Ha-ras, or hst 1 genes in MA 2 and MA 3 cell lines. The clinical histories of the patients from whom the cell lines were derived are reported and compared with the results observed in the cell lines in vitro. The presence of CEA, CA 15-3, and MCA tumor markers observed in the primary tumor tissues was retained by the established cell lines. While the primary tumor tissues were ER+/PgR borderline+ (MA 2) and ER-/PgR+ (MA 3), the MA 2 line was ER+/PgR- and the MA 3 line remained ER-/PgR+. The MDR P-glycoprotein was not expressed either in primary tumor tissues or in the respective cell lines. High expression of cytokeratins 7, 18, and 19 was evident by immunohistochemical analysis in each cell line. whereas cytokeratins 8 and 17 were poorly or not at all expressed. The treatment history of the patients from whom the cell lines were derived involved CMF followed six months later by novantrone and cisplatin plus VP 16 (MA 2) and FEC followed four years later by CMF (MA 3). The chemosensitivity pattern assay of the cell lines indicated that the MA 2 line was sensitive to doxorubicin, cisplatin, and vinblastine, whereas the MA 3 line was sensitive to doxorubicin and cisplatin. The characteristics of these cell lines indicate them to be a good experimental model to investigate breast cancer biology and anticancer drug response.
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PMID:Establishment and characterization of two new cell lines derived from human metastatic breast carcinomas. 913 Dec 70

A multi-aminolinked oligodeoxynucleotide (ODN) was synthesized by substitution of dT with aminolinked dU in the sequence, following conjugation with isothiocyanobenzyl-EDTA (IBE) for 111In labeling. As a model target gene, the c-erbB-2 protooncogene was used. The probability of the number of aminolinked dU in the 20mer ODN was 5, but there were actually 3 and 4 in the selected antisense and sense ODNs, respectively. The IBE/ODN conjugation levels of probes with multi-chelating sites (MCS-probe) were 1.6 (antisense) and 2.4 (sense), more than 50 times higher than those of our previous studies using 5'-end aminolinked ODNs (IBE/ODN = 0.03). Labeling studies using the MCS-probe and 111In indicated that specific radioactivity as high as 48 MBq/nmol could be obtained with a labeling efficiency of over 90%. The 111In-antisense-MCS-probe could bound to sense ODN under physiological conditions, but the 111In-sense-MCA-probe could not. Thus, side-chain modification of ODN for metal labeling is considered to be useful for antisense techniques.
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PMID:A novel 111In-labeled antisense DNA probe with multi-chelating sites (MCS-probe) showing high specific radioactivity and labeling efficiency. 1009 96