Gene Pair Information
Gene Pair: ERBB2, TP53
Related Sentences
| # | PMID | Sentence |
| 1 | 8007694 | Perturbations of oncogenes in breast carcinoma include amplifications of the HER-2/neu and PRAD1 genes, as well as p53 mutations. |
| 2 | 8007694 | Such germline abnormalities may occur at the BRCA1, H-RAS VNTR, and p53 loci. |
| 3 | 8117599 | Of the available markers, those with the greatest promise in 1993 include the yet-to-be-cloned BrCa1, the p53 tumor suppressor gene, tissue-associated prognostic factors such as HER-2/neu, cathepsin-D, and indicators of angiogenesis, and circulating tumor markers that provide an indication of clinical course, such as CA15-3 and CEA. |
| 4 | 8605112 | The major types of genetic abnormalities that are frequently observed in breast tumors are amplification of protooncogenes (MYC, ERBB2) and DNA from chromosome band 11q13; mutation of TP53; and loss of heterozygosity from chromosomes and chromosome arms 1, 3p, 6q, 7q, 8p, 11, 13q, 16q, 17, 18q, and 22q. |
| 5 | 8605112 | Recently, linkage analyses of large families with a predisposition to breast cancer have been performed in order to map breast cancer susceptibility genes (TP53, BRCA1, BRCA2). |
| 6 | 8707769 | Of the available markers, those with the greatest promise in 1994 include the yet-to-be-cloned BrCa1, the p53 tumor suppressor gene, tissue-associated prognostic factors such as HER-2/neu, cathepsin-D, and indicators of angiogenesis, and circulating tumor markers that provide an indication of clinical course, such as CA15-3 and CEA. |
| 7 | 8709940 | The major types of genetic alterations that are frequently observed in breast cancer are amplification of protooncogenes (MYC, ERBB2); mutation of TP53; and loss of heterozygosity on chromosomes 1, 3p, 8p, 11p, 13q, 17q, 17, and 22q. |
| 8 | 8709940 | Recently, two major distinct breast susptibility genes were isolated, namely BRCA1 and BRCA2. |
| 9 | 8718525 | Many oncogenes and tumour suppressor genes have been implicated, encoding proteins that are important at many levels of cell regulation, from cell surface molecules responding to external signals (eg ERBB2) to nuclear factors controlling gene transcription (eg TP53, MYC). |
| 10 | 8787054 | Of the available markers, those with the greatest promise include circulating tumor markers that provide an indication of clinical course, such as CA15-3 and CEA, and novel markers such as BrCa1, antibodies to p53, antibodies to HER-2/neu, indicators of angiogenesis, and the extracellular domain of HER-2/neu. |
| 11 | 8976125 | The major types of genetic alterations in breast cancer are amplification of protooncogenes (ERBB2 and MYC) and DNA from chromosome band 11q13; mutation of p53; and loss of heterozygosity on 1p, 3p, 8p, 11p, 13q, 16q, 17p, 17q, 18q. |
| 12 | 8976125 | Recently, two distinct familial breast cancer susceptibility genes, BRCA1 and BRCA2, have been isolated. |
| 13 | 9155518 | Prior to BRCA1 analysis, 79 breast and 19 ovarian tumours from 57 breast and breast-ovarian cancer families, and 170 tumours from a comparison group of stage II breast cancers were studied with regard to histopathological features; immunohistochemistry [c-erbB-2, p53, oestrogen receptor (ER) and progesterone receptor (PR)], DNA flow cytometry and S-phase fraction. |
| 14 | 9155518 | Additionally, as compared to BRCA1 negative tumours, the BRCA1 positive tumours were significantly more often ER, PgR and c-erbB-2 negative. |
| 15 | 9178910 | At least four genes implicated in breast cancer reside on chromosome 17 (p53, 17p13; Her-2/neu/ERBB2, 17q12; BRCA1, 17q21; and nm23, 17q22). |
| 16 | 9378159 | Highly expressed oncogenes such as bcl-2, HER2/neu and others or mutated suppressor genes such as p53 or BRCA1 have been characterised as hereditary susceptibility genes leading to syndromes such as breast/ovarian cancer syndrome, Li-Fraumeni and others. |
| 17 | 9378159 | Furthermore efflux-genes such as MDR-1 or MRP can be circumvented, suicide-genes can be employed which can facilitate sensitivity by encoding enzymes capable of converting inactive forms of a drug into toxic antimetabolites and immunotherapy can be achieved, by transfection of tumour cells with adenoviral vectors encoding immunomodulators such as IL-2 or MHC molecules. |
| 18 | 9408751 | Chromosome 17 contains at least four genes implicated in breast cancer (TP53, ERBB2 (Her2/neu), BRCA1, and NM23), as well as other putative tumor suppressor genes and oncogenes implicated in loss of heterozygosity or allelic imbalance studies. |
| 19 | 9500773 | We compared molecular alterations in histologically homologous ovarian and uterine carcinomas, including the prevalence of allelic loss of markers on 17q (within and distal to the familial breast-ovarian cancer gene BRCA1), mutations of codon 12 of Ki-ras and immunohistochemical expression of the p53 and c-erbB2 gene products in endometrioid and papillary serous carcinomas occurring in the uterus and ovary. |
| 20 | 9500773 | Immunohistochemical expression of c-erbB2 and mutations of codon 12 of Ki-ras were present in a minority of carcinomas. |
| 21 | 9618944 | They also express the BRCA-1, erbB2, and EGF receptor genes and possess the H-ras, K-ras, and p53 genes. |
| 22 | 9833771 | Cell lines included those from patients with germline BRCA1 and FHIT gene mutations and others with possible genetic predisposition. |
| 23 | 9833771 | Analysis of the breast tumor cell lines indicated that most of the cell lines had the following features: they were derived from large tumors with or without axillary node metastases; were aneuploid and exhibited a moderate to poorly differentiated phenotype; were estrogen receptor (ER)- and progesterone receptor (PR)-negative; and overexpressed p53 and HER2/neu proteins. |