Amplification of the proto-oncogenes int-2, c-erbB-2 and c-myc in human breast cancer

Machotka, S. V.; Garrett, Carleton T.; Schwartz, Arnold M.; Callahan, Robert

doi:10.1016/0009-8981(89)90053-3

Cited by 41 publications

(16 citation statements)

References 38 publications

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“…Two previous studies noted an association between 11q13 ampli®cation and younger patient age i.e. 450 years (Machotka et al, 1989;Tsuda et al, 1989a), but the sample sizes in both studies were relatively small. Berns et al (1994), with a series of 661 patients and ®ve other smaller studies (Lidereau et al, 1988;Fantl et al, 1990;Borg et al, 1991;Schuuring et al, 1992b;Gaey et al, 1993) did not ®nd a relationship between 11q13 ampli®cation and patient age.…”

mentioning

confidence: 84%

EMS1 amplification can occur independently of CCND1 or INT-2 amplification at 11q13 and may identify different phenotypes in primary breast cancer

et al. 1997

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mentioning

confidence: 84%

EMS1 amplification can occur independently of CCND1 or INT-2 amplification at 11q13 and may identify different phenotypes in primary breast cancer

et al. 1997

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“…The amplification of the chromosomal region that contains the c-myc gene has also been reported to contain, apparently through translocation events, the p40 subunit of eukaryotic translation initiation factor 3 (eIF3) and the Her2 gene (Nupponen et al 1999), although the frequency of co-localization of these two genes in a common amplicon has not been established (Deming et al 2000). Her2 (also termed erbb2) is a gene in Locker et al (1989) IHC Not related to any clinicopathologic parameters Machotka et al (1989) SB More frequently in patients with node metastases Spandidos et al (1989a) ELISA Not correlated with survival Spandidos et al (1989b) IHC Not correlated with node metastasis Tauchi et al (1989) IHC Not correlated with ER, tumor histology or sizes Tavassoli et al (1989) SB,Slot-B Correlated with tumour grade, but not with metastasis Tsuda et al (1989) Slot-B Correlated with poor prognosis Walker et al (1989) ISH Spaventi et al (1994) IHC Not related to clinicopathologic parameters Pechoux et al (1994) SB,ISHS,IHC Also overexpressed in benign lesions Soini et al (1994) SB Mimori et al (1998) RT-PCR Correlated with ODC expression Stanta et al (1998) RT-PCR No clinicopathologic parameters mentioned Bieche et al (1999) RT-PCR Correlated with tumor size but inversely with survival Le et al (1999) NB Related to positive nodes Nupponen et al (1999) SSH Associated with eIF 3-amplification Schraml et al (1999) FISH Amplification detected in tissue-microarray Scorilas et al (1999) SB,NB Related to survival and local recurrence Sierra et al (1999) IHC Related to metastasis when Bcl-2 also increased Vos et al (1999) SB , WB Not related to Beta-catenin Rao et al (2000) PCR Up to 94% biopsies with amplification Sierra et al (2000) IHC Not related to clinicopathologic parameters CGH, comparative genomic hybridization; Dot-B, dot blot; FISH, fluorescence in situ hybridization; IHC, immunohistochemistry; ISH, in situ hybridization; NB, northern blot; RT-PCR, reverse transcription and PCR; SB, southern blot; Slot-B, slot blot; SSCP, single-strand conformation polymorphism; SSH, suppression substractive hybridization; WB; western blot; IGF1R, insulin-like growth factor-1; DCIS, ductal carcinoma in situ.…”

Section: The C-myc Gene In Human Breast Cancermentioning

confidence: 99%

c-Myc in breast cancer.

Liao¹,

Dickson²

2000

Endocrine-Related Cancer

316

265

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Ever since Bishop and his co-workers discovered the c-myc gene in the late 1970s (Bishop 1982), voluminous literature has documented its central role in proliferation and malignant transformation of human and animal cells (Amati et al. 1998, Bouchard et al. 1998, Dang et al. 1999). Most, if not all, types of human malignancy have been reported to have amplification and/or overexpression of this gene, although the frequency of these alterations varies greatly among different reports (Nesbit et al. 1999). In 1992, researchers started to realize that aberrant expression of c-myc could cause apoptosis (Evan et al. 1992, Shi et al. 1992), although the phenomenon had actually been observed much earlier (Wurm et al. 1986). Studies in recent years have further shown that the c-myc gene regulates growth, both in the sense of cell size and in the context of tissue differentiation (Gandarillas & Watt 1997, Iritani & Eisenman 1999, Johnston et al. 1999, Schmidt 1999, Schuhmacher et al. 1999). Thus, it is now known that the c-myc gene participates in most aspects of cellular function, including replication, growth, metabolism, differentiation, and apoptosis (Packham & Cleveland 1995, Hoffman & Liebermann 1998, Dang 1999, Dang et al. 1999, Elend & Eilers 1999, Prendergast 1999). How the c-Myc protein may be specifically directed to perform one, but not the others, of these functions is still obscure, despite the fact that the relevant literature has been accumulating at a fast pace in the past two decades. This review focuses on the profound roles of c-Myc in breast cancer and in the actions of the hormones that are eitologically related to breast cancer.

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“…For example, homogeneously stained regions have been found in 60% of primary breast carcinomas (7). Although genetic analysis has found amplification of oncogenes, such as ERBB2 (17q12), MYC (8q24), PRADII CYCLIN D (11q13), FLG (8p12), BEK (10q24), and IGFR-1/FES (15q24-q25) (8)(9)(10)(11)(12), in most cases these do not explain the presence of large homogeneously stained regions (13). Thus, amplification of currently unknown genes may often occur in breast cancer.…”

mentioning

confidence: 99%

Detection and mapping of amplified DNA sequences in breast cancer by comparative genomic hybridization.

Kallioniemi

Piper

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

649

433

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Comparative genomic hybridization was applied to 5 breast cancer cell lHes and 33 primary tumors to discover and map regions of the genome with increased DNAsequence copy-number. Two-thirds of primary tumors and almost all cell lines showed increased DNA-sequence copynumber affecting a total of 26 chromosomal subregions. Most of these loci were distinct from those of currently known amplified genes in breast cancer, with sequences originating from 17q22-q24 and 20q13 showing the highest frequency of amplification. The results indicate that these chromosomal regions may contain previously unknown genes whose increased expression contributes to breast cancer progression.Chromosomal regions with increased copy-number often spanned tens of Mb, suggesting involvement of more than one gene in each region.Increased expression of specific genes plays an important role in the pathogenesis of solid tumors (1-3). Gene amplification, characterized by distinct cytogenetic structures, such as homogeneously stained regions, double-minute chromosomes (1-7), is commonly found in tumor cells and is considered an important mechanism by which tumor cells gain increased levels of expression of critical genes. Increased copy-numbers also occur as a result of extensive chromosomal rearrangements, such as duplications, isochromosomes, extra marker chromosomes, and acentric chromosomal fragments that may affect the gene dosage of numerous genes simultaneously. In breast cancer, cytogenetic evidence of increased DNA-sequence copy-number is common (4-7). For example, homogeneously stained regions have been found in 60% of primary breast carcinomas (7). Although genetic analysis has found amplification of oncogenes, such as ERBB2 (17q12), MYC (8q24), PRADII CYCLIN D (11q13), FLG (8p12), BEK (10q24), and IGFR-1/FES (15q24-q25) (8-12), in most cases these do not explain the presence of large homogeneously stained regions (13). Thus, amplification of currently unknown genes may often occur in breast cancer.We have recently developed a method, comparative genomic hybridization (CGH), for surveying entire genomes for DNA-sequence copy-number variation (14, 15). In CGH, the relative intensities of tumor DNA (detected using green fluorescence) and normal reference DNA (detected with red fluorescence) after hybridization to normal metaphase chromosomes is used to reveal and map regions of increased DNA-sequence copy number (14-16). These loci are visualized as chromosomal region(s) with predominantly green fluorescence ( Fig. 1) and quantified by digital image analysis as an increased green-to-red fluorescence intensity ratio (Fig. 2). As no specific probes or previous knowledge of aberrations is required, CGH is especially suitable for identification and mapping of previously unknown DNA copy-number changes that may highlight locations of important genes. In the present study, we have used CGH to identify and map increases in DNA-sequence copy number in 15 breast cancer cell lines and 33 uncultured primary breast tumors. MATERIALS AND ME...

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Amplification of the proto-oncogenes int-2, c-erbB-2 and c-myc in human breast cancer

Cited by 41 publications

References 38 publications

EMS1 amplification can occur independently of CCND1 or INT-2 amplification at 11q13 and may identify different phenotypes in primary breast cancer

EMS1 amplification can occur independently of CCND1 or INT-2 amplification at 11q13 and may identify different phenotypes in primary breast cancer

c-Myc in breast cancer.

Detection and mapping of amplified DNA sequences in breast cancer by comparative genomic hybridization.

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