c-myc amplification is associated with HER2 amplification and closely linked with cell proliferation in tissue microarray of nonselected breast cancers

Park, Kyeongmee; Kwak, Keumhee; Kim, Jungyeon; Lim, Sung‐Jig; Han, Sehwan

doi:10.1016/j.humpath.2005.04.016

Cited by 52 publications

(40 citation statements)

References 23 publications

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“…We have reported an intimate association between topoisomerase II-· amplification, which is almost always coamplified with HER2 and response to anthracycline-based neoadjuvant chemotherapy (37). We have also observed a close association between the amplification of HER2 and c-myc in breast cancer (38). In the current study, we observed a gain on 17q21 in four patients of the responder group, and topoisomerase II-· amplification by FISH coincided well with aCGH results.…”

Section: Discussionsupporting

confidence: 85%

Genomic change of chromosome 8 predicts the response to taxane-based neoadjuvant chemotherapy in node-positive breast cancer

Han

Park²,

Shin³

et al. 2010

Oncol Rep

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Abstract. This study was performed to investigate whether the response to neoadjuvant chemotherapy in ductal-type breast cancer could be predicted by different genomic alterations. Array-based comparative genomic hybridization (aCGH) was performed on samples from 15 patients who underwent neoadjuvant chemotherapy with epirubicin plus docetaxel (ED). Frozen tissue bank samples were retrospectively selected from 8 patients who demonstrated complete pathologic response (pCR) and from 7 patients resistant to neoadjuvant chemotherapy. We performed aCGH with 4,277 human bacterial artificial chromosome (BAC) clones, scanning the genome for DNA copy number changes. In a cluster dendrogram of aCGH data, responders showed changes clustered in S940, S984, S44, S98, S130, S115, S478, and 1150T, whereas non-responder group changes clustered in S1029, S209, S219, S660, S133, S323, and S670. Compared to responders, non-responders showed more complicated genomic alterations; the most common gains were located at chromosome 8q (71%), 13q (71%), and 20q (57%), with the smallest regions of genomic gain at 8q24. 3, 8q24.22, 8q24.21, 8q22.1, 8q22.2, 8q22.3, 13q21.1, 20q13.2, and 20q13.33. The most frequently deleted regions were observed on chromosome 8p (71%) and 17p (57%), with the smallest regions of deletion at 8p23. 3, 8p23.2, 8p23.1, 8p21.3, 8p21.2, and 17p13.3. The results of the current study suggest that aberrations in chromosome 8 may contribute to the resistance to taxane-based neoadjuvant chemotherapy in ductal-type breast cancer. Results of our study indicate that candidate gene identification through aCGH should be validated by specific gene analysis since the sites of chromosomal aberration are quite different among studies.

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Section: Discussionsupporting

confidence: 85%

Genomic change of chromosome 8 predicts the response to taxane-based neoadjuvant chemotherapy in node-positive breast cancer

Han

Park²,

Shin³

et al. 2010

Oncol Rep

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“…It is well known that c-myc regulates glutamine metabolism by regulating the expression of glutamine transporter (ASCT2) and glutaminase (GLS1) (Wise et al 2008, Gao et al 2009). In addition, c-myc amplification was more common in breast cancers with HER2 amplification than in breast cancers without HER2 amplification (Park et al 2005). Taken together, we postulated that higher glutamine metabolism of molecular subtypes with HER2 amplification could be described by an association with c-myc amplification.…”

Section: Discussionmentioning

confidence: 68%

Expression of glutamine metabolism-related proteins according to molecular subtype of breast cancer

Kim¹,

Kim

Jung

et al. 2013

Endocrine-Related Cancer

126

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The aim of this study was to investigate the expression of glutamine metabolism-related proteins to determine whether glutamine is metabolized differently according to breast cancer molecular subtype. We generated a tissue microarray of 702 breast cancer patients and performed immunohistochemical staining for glutamine metabolism-related proteins, including glutaminase 1 (GLS1 (GLS)), glutamate dehydrogenase (GDH (H6PD)), and amino acid transporter-2 (ASCT2 (SLC1A5)), which were separately evaluated in tumor and stroma compartments and then analyzed by breast cancer molecular subtypes. Breast cancers were classified as follows: 293 luminal A (41.7%), 166 luminal B (23.6%), 67 HER2 type (9.6%), and 176 TNBC (25.1%). HER2 type showed the highest stromal GLS1 (PZ0.001), tumoral GDH (PZ0.001), stromal GDH (P!0.001), and tumoral ASCT (P!0.001) expression. We identified differential expression of glutamine metabolism-related proteins according to molecular subtype of breast cancer. The highest glutamine metabolic activity was seen in HER2-type breast cancer.

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“…Nuclei were counterstained with 4,6-diamino-2-phenylindole. The fluorescence in situ hybridization procedures were done as described previously (19).…”

Section: Methodsmentioning

confidence: 99%

Somatic Mutations of ERBB2 Kinase Domain in Gastric, Colorectal, and Breast Carcinomas

Lee¹,

Soung²,

Seo³

et al. 2006

Clinical Cancer Research

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200

135

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Purpose: Recent reports revealed that the kinase domain of the ERBB2 gene is somatically mutated in lung adenocarcinoma, suggesting the mutated ERBB2 gene as an oncogene in human cancers. However, because previous reports focused the mutational search of ERBB2 primarily on lung cancers, the data on ERBB2 mutations in other types of human cancers have been largely unknown. Experimental Design: Here, we did a mutational analysis of the ERBB2 kinase domain by PCR single-strand conformational polymorphism assay in gastric, colorectal, and breast carcinoma tissues. Results: We detected the ERBB2 kinase domain mutations in 9 of 180 gastric carcinomas (5.0%), in 3 of 104 colorectal carcinomas (2.9%), and in 4 of 94 breast carcinomas (4.3%). All of the detected ERBB2 mutations except for one in-frame deletion mutation were missense mutations. Of the 16 ERBB2 mutations detected, 4 affected Val 777 in the exon 20 site, and 3 affected Leu 755 in the exon 19 site. We simultaneously analyzed the somatic mutations of EGFR, K-RAS, PIK3CA, and BRAF genes in the 16 samples with ERBB2 mutations, and found that all of the 3 colorectal carcinoma samples with ERBB2 mutations harbored K-RAS mutations. Conclusion:This study showed that in addition to lung adenocarcinomas, ERBB2 kinase domain mutation occurs in other common human cancers such as gastric, breast, and colorectal cancers, and suggested that alterations of ERBB2-mediated signaling pathway by ERBB2 mutations alone or together with K-RAS mutations may contribute to the development of human cancers.

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c-myc amplification is associated with HER2 amplification and closely linked with cell proliferation in tissue microarray of nonselected breast cancers

Cited by 52 publications

References 23 publications

Genomic change of chromosome 8 predicts the response to taxane-based neoadjuvant chemotherapy in node-positive breast cancer

Genomic change of chromosome 8 predicts the response to taxane-based neoadjuvant chemotherapy in node-positive breast cancer

Expression of glutamine metabolism-related proteins according to molecular subtype of breast cancer

Somatic Mutations of ERBB2 Kinase Domain in Gastric, Colorectal, and Breast Carcinomas

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