Combination treatment with Grb7 peptide and Doxorubicin or Trastuzumab (Herceptin) results in cooperative cell growth inhibition in breast cancer cells

Pero, Stephanie C.; Shukla, Girja S.; Cookson, Michelle; Flemer, Stevenson; Krag, David N.

doi:10.1038/sj.bjc.6603732

Cited by 66 publications

(81 citation statements)

References 24 publications

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“…This is further corroborated by preclinical models, which have shown that a Grb7 peptide inhibitor in combination with Herceptin treatment enhances the inhibitory effect on the proliferation of SKBR3 cells and inhibit the proliferation of MDA-MB-361 cells. 32 Taken together, these findings suggest that HER2 may not be the sole oncogene in this amplicon.…”

Section: Discussionmentioning

confidence: 73%

Genomic analysis of the HER2/TOP2A amplicon in breast cancer and breast cancer cell lines

Arriola

Marchiò

Tan

et al. 2008

Laboratory Investigation

140

150

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HER2 and TOP2A are targets for the therapeutic agents trastuzumab and anthracyclines and are frequently amplified in breast cancers. The aims of this study were to provide a detailed molecular genetic analysis of the 17q12-q21 amplicon in breast cancers harbouring HER2/TOP2A co-amplification and to investigate additional recurrent co-amplifications in HER2/ TOP2A-co-amplified cancers. In total, 15 breast cancers with HER2 amplification, 10 of which also harboured TOP2A amplification, as defined by chromogenic in situ hybridisation, and 6 breast cancer cell lines known to be amplified for HER2 were subjected to high-resolution microarray-based comparative genomic hybridisation analysis. This revealed that the genomes of 12 cases were characterised by at least one localised region of clustered, relatively narrow peaks of amplification, with each cluster confined to a single chromosome arm (ie 'firestorm' pattern) and 3 cases displayed many narrow segments of duplication and deletion affecting the vast majority of chromosomes (ie 'sawtooth' pattern). The smallest region of amplification (SRA) on 17q12 in the whole series extended from 34.73 to 35.48 Mb, and encompassed HER2 but not TOP2A. In HER2/TOP2A-co-amplified samples, the SRA extended from 34.73 to 36.54 Mb, spanning a region of B1.8 Mb. Apart from HER2 and TOP2A, this region encompassed four additional genes whose expression levels as defined by quantitative real-time PCR are significantly higher in HER2/TOP2A-co-amplified vs HER2-amplified breast cancers: CASC3, CDC6, RARA and SMARCE1. Of the cell lines studied, SKBR3 and UACC812 showed HER2/TOP2A co-amplification. In conclusion, this is the first detailed genome-wide characterisation of HER2/TOP2A-amplified breast cancers; cell lines were identified that can be used to model these cancers in vitro. The 17q12 amplicon is complex and harbours multiple genes that may be associated with breast cancer development and progression, and potentially exploitable as therapeutic targets.

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Section: Discussionmentioning

confidence: 73%

Genomic analysis of the HER2/TOP2A amplicon in breast cancer and breast cancer cell lines

Arriola

Marchiò

Tan

et al. 2008

Laboratory Investigation

140

150

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“…Pero et al (46) identified a novel peptide that binds to the SH2 domain of Grb7 and inhibits its association with receptor tyrosine kinases. The proliferation of various breast cancer cell lines was impaired by treatment with Grb inhibitors, including an inhibitor of Grb10.…”

Section: Discussionmentioning

confidence: 99%

Immunity to Growth Factor Receptor–Bound Protein 10, a Signal Transduction Molecule, Inhibits the Growth of Breast Cancer in Mice

et al. 2008

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This study describes the application of a unique strategy to identify breast cancer antigens [tumor-associated antigen (TAA)]. In a mouse model, the strategy led to the identification of growth factor receptor-bound protein 10 (Grb10) as a newly identified TAA. Grb10 is a signal transduction molecule associated with multiple transmembrane tyrosine kinase receptors. It was discovered by comparing microarrays of cellular breast cancer vaccines highly enriched for cells that induced breast cancer immunity in tumor-bearing mice with nonenriched vaccines. The vaccines were prepared by transferring a cDNA expression library derived from SB5b cells, a breast cancer cell line C3H/He origin (H-2 k

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“…RTKs are among the most critical targets for tumor therapy, and studies have been employed to inactivate RTKs as an effective strategy to enhance the chemosensitivity (19,20). Met overexpression and subsequent activation is correlated with tumor invasive growth, so it was tested that whether the sensitivity of Met-expressing tumor cells toward chemotherapeutic drugs could be modulated by the Met inhibition.…”

Section: Tctpmentioning

confidence: 99%

“…Various studies have shown that inactivation of RTKs such as ErbB2 (19) or other important functioning proteins such as Grb7 (20) can significantly enhance the chemosensitivity. Here, a novel peptide-based sensitizer specifically targeting the Met inactivation was supposed to be investigated.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of the met receptor tyrosine kinase signaling enhances the chemosensitivity of glioma cell lines to CDDP through activation of p38 MAPK pathway

Lou

Zhou

Yin

et al. 2009

Molecular Cancer Therapeutics

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The Met receptor tyrosine kinase is known to be overexpressed in many solid tumors and plays a crucial role in tumor invasive growth and metastasis. In this study, we showed that hepatocyte growth factor-induced Met activation as well as Met-dependent downstream signaling of AKT and p44/42 mitogen-activated protein kinase (MAPK) could be efficiently blocked by TAT-coupled carboxyl-terminal tail peptide of Met receptor (TCTP), and inactivation of Met signaling significantly enhanced the sensitivity of T98G and U251 glioma cells to cisdiaminedichloroplatinum (CDDP, cisplatin). However, neither phosphoinositide 3-kinase/AKT inhibitor LY294002 nor p44/42 MAPK inhibitor PD98059 alone or combined could imitate the effect of TCTP on chemosensitivity enhancement of T98G cells to CDDP, indicating that Met-dependent inactivation of AKT and p44/42 MAPK signaling was not the main cause for the increased chemosensitivity to CDDP. Further studies revealed that TCTP significantly activated p38 MAPK in T98G and U251 cell lines. Activation of p38 MAPK by sorbitol pretreatment resembled the sensitization effects, whereas inhibition of p38 MAPK activation by its inhibitor SB202190 counteracted the sensitization effects induced by TCTP. Therefore, p38 MAPK activation was one of the major causes for the increased chemosensitivity to CDDP induced by Met inactivation. Taken together, the study indicated that Met receptor played an important role in regulating cell response to chemotherapy and suggested that inhibition of Met signaling could be used in combination with other chemotherapeutic regimens in treatment of tumor patients.

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Combination treatment with Grb7 peptide and Doxorubicin or Trastuzumab (Herceptin) results in cooperative cell growth inhibition in breast cancer cells

Cited by 66 publications

References 24 publications

Genomic analysis of the HER2/TOP2A amplicon in breast cancer and breast cancer cell lines

Genomic analysis of the HER2/TOP2A amplicon in breast cancer and breast cancer cell lines

Immunity to Growth Factor Receptor–Bound Protein 10, a Signal Transduction Molecule, Inhibits the Growth of Breast Cancer in Mice

Inhibition of the met receptor tyrosine kinase signaling enhances the chemosensitivity of glioma cell lines to CDDP through activation of p38 MAPK pathway

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