Tumour cells surviving in vivo cisplatin chemotherapy display elevated c-myc expression

Walker, Todd; White, Jason D.; Esdale, Warren; Burton, Mark; Decruz, Exmond E.

doi:10.1038/bjc.1996.105

Cited by 36 publications

(30 citation statements)

References 38 publications

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“…20,21 However, to our knowledge the high levels of c-myc expression in AML demonstrated in our study have not been reported previously. One reason that this area has not been intensively studied might be that translocations involving c-myc and overexpression of c-myc by extrachromosomal copies (double minute) in AML are rare.…”

Section: Figurecontrasting

confidence: 50%

Expression of the p14ARF tumor suppressor predicts survival in acute myeloid leukemia

Müller‐Tidow

Buerger

et al. 2004

Leukemia

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Cell cycle aberrations are associated with therapy outcome in many types of cancer. We analyzed mRNA expression levels of 18 cell cycle-related genes in bone marrow samples from 78 acute myeloid leukemia (AML) patients and six controls using high-throughput quantitative RT-PCR. Samples of AML patients contained significantly increased mRNA expression levels of the mdm2 and c-myc oncogenes. Also, the average expression levels of p14 ARF and p16 INK4A were higher in patient samples compared to controls. Leukemic blasts and control bone marrow samples did not differ significantly in the expression levels of proliferation-associated genes such as cyclin A2 and pcna. When single genes were analyzed for prognostic significance in Kaplan-Meier and Cox regression analyses, a low p14 ARF level emerged as a strong and independent predictor for poor survival (P ¼ 0.04 and 0.029). Subsequently, p14 ARF mRNA levels were analyzed in a second, independent patient population (n ¼ 57). Again, low p14 ARF levels were associated with a worse outcome. Finally, immunohistochemistry analysis of AML tissue arrays confirmed the widespread expression of c-myc and p14 ARF in AML on the protein level. Taken together, the expression of the p53 regulators mdm2 and p14 ARF are altered in AML, and low p14 ARF levels indicate a poor prognosis.

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Section: Figurecontrasting

confidence: 50%

Expression of the p14ARF tumor suppressor predicts survival in acute myeloid leukemia

Müller‐Tidow

Buerger

et al. 2004

Leukemia

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“…New predictive factors are needed, because conventional histopathologic factors do not accurately predict the likelihood that an individual patient will respond to cytotoxic chemotherapy. This is a possible area for future investigation, as some studies have implicated expression of c-myc in resistance to cisplatin-based chemotherapy in multiple tumour types (Walker et al, 1996), in MDR1 expression in rhabdomyosarcoma cell lines (Prados et al, 1996), and in resistance to 5-fluorouracil and cisplatin in squamous cell carcinomas of the head and neck (Riva-Lavielle, 1994). A rigorous study, designed specifically to address the relationship between c-myc amplification and drug and hormone resistance in breast cancer, may provide valuable insight into more effective treatment strategies.…”

Section: Amplification Of C-myc: Role As An Independent Prognostic Famentioning

confidence: 99%

C-myc amplification in breast cancer: a meta-analysis of its occurrence and prognostic relevance

et al. 2000

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Data from basic research suggests that amplification of the proto-oncogene c-myc is important in breast cancer pathogenesis, but its frequency of amplification and prognostic relevance in human studies have been inconsistent. In an effort to clarify the clinical significance of c-myc amplification in breast cancer, we conducted a comprehensive literature search and a meta-analysis in which 29 studies were evaluated. The weighted average frequency of c-myc amplification in breast tumours was 15.7% (95% CI = 12.5–18.8%), although estimates in individual studies exhibited significant heterogeneity, P < 0.0001. C-myc amplification exhibited significant but weak associations with tumour grade (RR = 1.61), lymph-node metastasis (RR = 1.24), negative progesterone receptor status (RR = 1.27), and postmenopausal status (RR = 0.82). Amplification was significantly associated with risk of relapse and death, with pooled estimates RR = 2.05 (95% CI = 1.51–2.78) and RR = 1.74 (95% CI = 1.27–2.39), respectively. This effect did not appear to be merely a surrogate for other prognostic factors. These results suggest that c-myc amplification is relatively common in breast cancer and may provide independent prognostic information. More rigorous studies with consistent methodology are required to validate this association, and to investigate its potential as a molecular predictor of specific therapy response. © 2000 Cancer Research Campaign http://www.bjcancer.com

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“…Furthermore, c‐MYC has been found to be involved in drug resistance. Tumour cells resistant to cisplatin chemotherapy in vivo display elevated c‐myc expression , and c‐myc antisense oligonucleotides sensitize human colorectal cancer cells to chemotherapeutic drugs . Recent study has been shown that c‐MYC overexpression decreased the expression level of the bridging integrator 1, leading to increased poly (ADP‐ribose) polymerase 1 (PARP1) activity and resistance to cisplatin .…”

Section: Introductionmentioning

confidence: 99%

The c‐MYC‐ABCB5 axis plays a pivotal role in 5‐fluorouracil resistance in human colon cancer cells

Kugimiya

Nishimoto

Hosoyama

et al. 2015

J Cellular Molecular Medi

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c-MYC overexpression is frequently observed in various cancers including colon cancer and regulates many biological activities such as aberrant cell proliferation, apoptosis, genomic instability, immortalization and drug resistance. However, the mechanism by which c-MYC confers drug resistance remains to be fully elucidated. In this study, we found that the c-MYC expression level in primary colorectal cancer tissues correlated with the recurrence rate following 5-fluorouracil (5-FU)-based adjuvant chemotherapy. Supporting this finding, overexpression of exogenous c-MYC increased the survival rate following 5-FU treatment in human colon cancer cells, and knockdown of endogenous c-MYC decreased it. Furthermore, c-MYC knockdown decreased the expression level of ABCB5, which is involved in 5-FU resistance. Using a chromatin immunoprecipitation assay, we found that c-MYC bound to the ABCB5 promoter region. c-MYC inhibitor (10058-F4) treatment inhibited c-MYC binding to the ABCB5 promoter, leading to a decrease in ABCB5 expression level. ABCB5 knockdown decreased the survival rate following 5-FU treatment as expected, and the ABCB5 expression level was increased in 5-FU-resistant human colon cancer cells. Finally, using a human colon cancer xenograft murine model, we found that the combined 5-FU and 10058-F4 treatment significantly decreased tumorigenicity in nude mice compared with 5-FU or 10058-F4 treatment alone. 10058-F4 treatment decreased the ABCB5 expression level in the presence or absence of 5-FU. In contrast, 5-FU treatment alone increased the ABCB5 expression level. Taken together, these results suggest that c-MYC confers resistance to 5-FU through regulating ABCB5 expression in human colon cancer cells.

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Tumour cells surviving in vivo cisplatin chemotherapy display elevated c-myc expression

Cited by 36 publications

References 38 publications

Expression of the p14ARF tumor suppressor predicts survival in acute myeloid leukemia

Expression of the p14ARF tumor suppressor predicts survival in acute myeloid leukemia

C-myc amplification in breast cancer: a meta-analysis of its occurrence and prognostic relevance

The c‐MYC‐ABCB5 axis plays a pivotal role in 5‐fluorouracil resistance in human colon cancer cells

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