Instability of chromosome 8 as an indicator of aggressive tumor phenotype in pancreatic cancer

Sato, Norihiro; Mizumoto, Kazuhiro; Maehara, Naoki; Shono, Masaki; Nagai, Eishi; Tanaka, Masao

doi:10.1002/jso.1032

Cited by 5 publications

(3 citation statements)

References 22 publications

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“…Furthermore, numerical imbalances for chromosome 8 are found more frequently in metastatic pancreatic carcinomas than in primary tumors [21]. Similar results were reported by Sato et al [22] who found that the majority of pancreatic cancer cell lines show numerical aberrations in chromosome 8 and these abnormalities are associated with malignant tumor growth. These findings suggest a possible involvement of gene(s) on chromosome 8 in the acquisition of aggressive phenotypes.…”

Section: Discussionsupporting

confidence: 76%

Establishment and Characterization of a Pancreatic Carcinoma Cell Line Derived from Malignant Pleural Effusion

Starr

Vexler²,

Marmor³

et al. 2005

Oncology

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Background/Aims:A novel cell line, designated p34, was developed from the malignant pleural effusion of a patient with carcinoma of pancreas. The objective of this work was to characterize this cell line. Method: The in vitrostudies included karyotype analysis, immunohistochemistry, XTT cell proliferation assay, analysis of the cell cycle by FACS and cell sensitivity to chemotherapeutic drugs and irradiation. Subcutaneous and intraspleen inoculations into nude mice were carried out to study the tumorigenicity and the metastatic tendency of this cell line. Results: The p34 cell line showed typical morphological characteristics of epithelial pancreatic tumor cells. The cells were hyperdiploid with a modal number of 48, and had two markers, deletion in the short arm of chromosome 2 and duplication of the short arm of chromosome 8. The doubling time was 16 h. Subcutaneous inoculation of the cells into nude mice yielded 100% tumorigenicity, and intraspleen inoculation resulted in extensive intra-abdominal spread. The antiproliferative effect of chemotherapy (gemcitabine, cisplatin, taxol and vinorelbine), chemopreventive agents (celecoxib and curcumin) and radiotherapy showed dose-dependent cytotoxicity. Conclusions: This p34 cell line can be used as a new model for studying various aspects of the biology of human pancreatic cancer and potential treatment approaches for the disease.

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Section: Discussionsupporting

confidence: 76%

Establishment and Characterization of a Pancreatic Carcinoma Cell Line Derived from Malignant Pleural Effusion

Starr

Vexler²,

Marmor³

et al. 2005

Oncology

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“…Furthermore, its overexpression-induced cell cycle arrest at the G1- to S-phase transition to inhibit human pancreatic cancer SW1990 cell proliferation [ 77 ]. KLF10 is located on chromosome 8q22, where mutations are quite frequent in pancreatic cancers [ 90 ]; however, mutational screening of a panel of the twenty-two human pancreatic cell lines showed no alteration in KLF10 expression [ 78 ].…”

Section: Role Of Klf10 As a Tumor Suppressor In Various Cancersmentioning

confidence: 99%

KLF10 as a Tumor Suppressor Gene and Its TGF-β Signaling

Memon

Lee

2018

Cancers

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Krüppel-like factor 10 (KLF10), originally named TGF-β (Transforming growth factor beta) inducible early gene 1 (TIEG1), is a DNA-binding transcriptional regulator containing a triple C2H2 zinc finger domain. By binding to Sp1 (specificity protein 1) sites on the DNA and interactions with other regulatory transcription factors, KLF10 encourages and suppresses the expression of multiple genes in many cell types. Many studies have investigated its signaling cascade, but other than the TGF-β/Smad signaling pathway, these are still not clear. KLF10 plays a role in proliferation, differentiation as well as apoptosis, just like other members of the SP (specificity proteins)/KLF (Krüppel-like Factors). Recently, several studies reported that KLF10 KO (Knock out) is associated with defects in cell and organs such as osteopenia, abnormal tendon or cardiac hypertrophy. Since KLF10 was first discovered, several studies have defined its role in cancer as a tumor suppressor. KLF10 demonstrate anti-proliferative effects and induce apoptosis in various carcinoma cells including pancreatic cancer, leukemia, and osteoporosis. Collectively, these data indicate that KLF10 plays a significant role in various biological processes and diseases, but its role in cancer is still unclear. Therefore, this review was conducted to describe and discuss the role and function of KLF10 in diseases, including cancer, with a special emphasis on its signaling with TGF-β.

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“…69 In contrast, instability of chromosome 8 and gains or amplifications of chromosome 8q24 have been previously associated with a poorer prognosis and a more aggressive tumor phenotype among PDAC patients as also found among our patients. 33,34,70 Despite this, the exact role of specific cancer-associated genes coded in this chromosomal region (eg, MYC ) in PDAC remains unclear. 71e74 Upregulation of MYC represents a hallmark of several different types of cancer 75 ; however, expression data from half of our cases revealed down-regulation of MYC in tumor versus inflammatory tissues, particularly among the patients harboring 8q24 gains.…”

Section: Figurementioning

confidence: 99%

Altered Interphase Fluorescence in Situ Hybridization Profiles of Chromosomes 4, 8q24, and 9q34 in Pancreatic Ductal Adenocarcinoma Are Associated with a Poorer Patient Outcome

Gutiérrez

Muñoz-Bellvis

Sarasquete

et al. 2014

The Journal of Molecular Diagnostics

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Most patients with pancreatic ductal adenocarcinoma (PDAC) die within 6 months of diagnosis. However, 20% to 25% patients undergoing total tumor resection remain alive and disease-free 5 years after diagnostic surgery. Few studies on tumor markers have predicted patient prognosis and/or survival. We evaluated the effect of tumor cytogenetic copy number changes detected by interphase fluorescence in situ hybridization on overall survival (OS) of 55 PDAC patients. The prognostic value of copy number changes showing an effect on OS was validated in an external cohort of 44 surgically resected PDAC patients by comparative genomic hybridization arrays, and the genes coded in altered chromosomes with prognostic value were identified by high-density single-nucleotide polymorphism arrays in 20 cases. Copy number changes of chromosomes 4 and 9q34 with gains of 8q24 were independently associated with shorter OS. On the basis of these three chromosomal alterations, a score is proposed that identifies patients with significantly different (P < 0.001) 5-year OS rates: 60% ± 20%, 16% ± 8%, and 0% ± 0%, respectively. Our results show an association between tumor cytogenetics and OS of PDAC patients and provide the basis for further prognostic stratification of patients undergoing complete tumor resection. Further studies to identify specific genes coded in these chromosomes and their functional consequences are necessary to understand the clinical effect of these changes.

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Instability of chromosome 8 as an indicator of aggressive tumor phenotype in pancreatic cancer

Abstract: These results suggest that the increased level of chromosomal instability may play a critical role in the development of aggressive tumor phenotype during pancreatic cancer progression. J. Surg. Oncol. 2001;76:181-187.

Cited by 5 publications

References 22 publications

Establishment and Characterization of a Pancreatic Carcinoma Cell Line Derived from Malignant Pleural Effusion

Establishment and Characterization of a Pancreatic Carcinoma Cell Line Derived from Malignant Pleural Effusion

KLF10 as a Tumor Suppressor Gene and Its TGF-β Signaling

Altered Interphase Fluorescence in Situ Hybridization Profiles of Chromosomes 4, 8q24, and 9q34 in Pancreatic Ductal Adenocarcinoma Are Associated with a Poorer Patient Outcome

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