Elevated Levels of RanBP7 mRNA in Colorectal Carcinoma Are Associated with Increased Proliferation and Are Similar to the Transcription Pattern of the Proto-oncogene c-myc

Li, Shu-Rui; Gyselman, Valerie G.; Dorudi, Sina; Bustin, Stephen A.

doi:10.1006/bbrc.2000.2666

Cited by 27 publications

(21 citation statements)

References 36 publications

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“…It is noteworthy that eIF3 and CDC23, which are the homologues of eIF4 and CDC27, respectively, were identified in our screening. Some of the proteins that we identified have already been reported to be overexpressed in various types of cancer, including ribosomal protein S18 (Chassin et al, 1994), RAN binding protein 7 (Li et al, 2000), and eIF3, p40 subunit (Nupponen et al, 1999). Therefore, given the aberrant expression of these proteins in various malignancies, it is not surprising that they elicit immune responses.…”

Section: Discussionmentioning

confidence: 62%

Identification of heat shock protein 90 and other proteins as tumour antigens by serological screening of an ovarian carcinoma expression library

et al. 2002

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Serological screening of recombinant cDNA expression libraries has been widely used for the identification of tumour antigens in various cancer types. Identification of tumour antigens in ovarian cancer may facilitate the development of vaccine-based therapies and of disease biomarkers. The purpose of our investigation is to identify tumour antigens in ovarian cancer by using the serological analysis of recombinant cDNA expression libraries method. A recombinant ovarian carcinoma cDNA expression library was screened with ascites fluid, pooled from five ovarian cancer patients. Twelve tumour antigens encoded by known genes were isolated, including ribosomal protein S18, heat shock protein 90, JK-recombination signal binding protein, ribonucleoprotein H1, RAN binding protein 7, TG-interacting factor, eukaryotic translation initiation factor p40 subunit, human amyloid precursor protein-binding protein 1, ribosomal protein L8, CDC23, IQ motif containing GTPase activating protein 1, and ribosomal protein L3. Heat shock protein 90 was chosen for further investigation. The prevalence of hsp90 autoantibodies in ovarian cancer was determined with immunoassay. Sera from 22 normal females, 32 from ovarian cancer (22 stage III/IV, 10 stage I/II), 37 colorectal cancer, 13 breast cancer, 10 lung cancer, 20 benign gynaecologic diseases, and 10 benign breast lesions were screened. Seven (32%) stage III/IV ovarian cancer, 1 (10%) stage I/II ovarian cancer, 1 (3%) colorectal cancer, 1 (8%) breast cancer, and 1 (5%) benign gynaecologic disease sera were found to contain hsp90 autoantibodies. These data support the view that hsp90 autoantibodies are frequently found in late stage ovarian cancer. Hsp90 may, therefore, represent a novel biomarker for ovarian cancer and a candidate ovarian cancer vaccine target.

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Section: Discussionmentioning

confidence: 62%

Identification of heat shock protein 90 and other proteins as tumour antigens by serological screening of an ovarian carcinoma expression library

et al. 2002

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“…Similar to our findings, Li et al (23) demonstrated that prostate cancer tissues showed significantly higher expression levels of Ran proteins than benign tissues. In addition, Ran binding proteins such as RanBP7 and Ran-BPM have been reported to be preferentially expressed in cancer tissues and to be associated with the increased proliferation of cancer cells (24,25). In view of the finding that Ran and its associated proteins are strongly and selectively expressed in various cancer tissues, Ran may be one of the ideal target molecules for the treatment of patients with cancer.…”

Section: Discussionmentioning

confidence: 99%

Ran, a Small GTPase Gene, Encodes Cytotoxic T Lymphocyte (CTL) Epitopes Capable of Inducing HLA-A33–restricted and Tumor-Reactive CTLs in Cancer Patients

Azuma

Sasada²,

Takedatsu

et al. 2004

Clinical Cancer Research

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Purpose: The purpose is to identify a gene coding for tumor-associated antigen and peptide capable of inducing CTLs reactive to tumor cells with a HLA-A33-restricted fashion to provide scientific basis for specific immunotherapy to HLA-A33 ؉ cancer patients. Experimental Design: An expression gene-cloning method was used to identify the tumor-associated antigen gene. Northern blot analysis and immunohistochemistry were used to examine the mRNA and protein expression levels in various cells and tissues, respectively. Synthetic peptides were examined for their ability to induce HLA-A33؉ tumor-reactive CTLs in peripheral blood mononuclear cells from cancer patients.Result: A gene of small GTPase, Ran, which controls the cell cycle through the regulation of nucleocytoplasmic transport, mitotic spindle organization, and nuclear envelope formation, was found to encode epitopes recognized by the HLA-A33-restricted CTLs established from T cells infiltrating into gastric adenocarcinoma. The expression of the Ran gene was increased in most cancer cell lines and cancer tissues at both the mRNA and protein levels. However, it was not enhanced in the surrounding normal cells or tissues. It was also undetectable in normal tissues as far as tested. Ran-derived peptides at positions 48 -56 and 87-95 could induce CD8؉ peptide-specific CTLs reactive to tumor cells from HLA-A33؉ epithelial cancer patients in a HLA class I-restricted manner.Conclusions: Because of its increased expression in cancer cells and involvement in malignant transformation and/or the enhanced proliferation of cancer cells, the two Ran-directed peptides could be potent candidates in use for specific immunotherapy against HLA-A33 ؉ epithelial cancers.

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“…We designed 13 primer sets on the basis of sequence data obtained from the NCBI database (http://www.ncbi.nlm.nih.gov/), using Primer Express software (Applied Biosystems); primers for MYC had been described elsewhere. 17 GAPDH (Applied Biosystems) was used as a reference, i.e., each sample was normalized on the basis of its GAPDH content. TATAbinding protein or ␤-actin (Applied Biosystems) was also …”

Section: Methodsmentioning

confidence: 99%

Ptk2 And Eif3s3 Genes May Be Amplification Targets At 8Q23–Q24 and Are Associated With Large Hepatocellular Carcinomas

et al. 2003

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We investigated 39 primary hepatocellular carcinomas (HCCs) for aberrations in DNA copy number, using comparative genomic hybridization (CGH). Gain of DNA at 8q was common in these tumors; high-level gains, indicative of gene amplification, occurred most frequently at 8q23-q24. Gains of 8q correlated with large (>5 cm) tumor size. To identify targets of the amplification events involving 8q, we determined expression levels of 14 candidate genes within that region in a total of 41 HCCs by means of real-time quantitative reverse-transcription polymerase chain reactions (RT-PCR). Significant correlation was found between elevated levels of expression and increases in copy number for PTK2 (located at 8q24.3) and EIF3S3 (at 8q23.3), but for none of the other candidates, which included MYC (8q24.1). Southern blot analyses confirmed that PTK2 and EIF3S3 were amplified, respectively, in 5 (19%) and 7 (26%) of the 27 tumors examined in accordance with expression patterns, an indication that expression of PTK2 and EIF3S3 was probably up-regulated by the amplification mechanism. When we analyzed potential relationships between elevated expression of PTK2 and EIF3S3 and clinicopathologic parameters, high expression of the 2 transcripts was significantly associated with large (>5 cm) tumor size and with hepatitis B virus (HBV) infection. In conclusion, PTK2 and EIF3S3, which, respectively, encode focal adhesion kinase and the p40 subunit of the eukaryotic initiation factor 3, were probable targets within the amplification at 8q23-q24 and may be involved in progression of HCC. Accumulated evidence suggests that multiple genetic alterations occurring sequentially in a cell lineage, at nucleotide as well as chromosome levels, underlie the carcinogenetic process in solid tumors. Amplification of chromosomal DNA is one of the mechanisms capable of activating genes whose over expression contributes to development and progression of cancer in a variety of tissues. We have detected novel regions of amplification in various types of cancer by means of comparative genomic hybridization (CGH) experiments and have identified from such amplicons a number of candidate oncogenes. [1][2][3][4][5][6] Recently we identified TFDP1, CUL4A, and CDC16 as targets of amplification at 13q34 in HCCs. 7 CGH allows a global overview of changes in DNA copy number throughout the genome of a tumor. In the work reported here, we examined 39 primary HCC tumors by CGH to explore genomic alterations that might affect initiation and/or progression of liver tumors. Among losses and gains involving several chromosomal regions, 8q was one of the most frequently amplified seg-

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Elevated Levels of RanBP7 mRNA in Colorectal Carcinoma Are Associated with Increased Proliferation and Are Similar to the Transcription Pattern of the Proto-oncogene c-myc

Cited by 27 publications

References 36 publications

Identification of heat shock protein 90 and other proteins as tumour antigens by serological screening of an ovarian carcinoma expression library

Identification of heat shock protein 90 and other proteins as tumour antigens by serological screening of an ovarian carcinoma expression library

Ran, a Small GTPase Gene, Encodes Cytotoxic T Lymphocyte (CTL) Epitopes Capable of Inducing HLA-A33–restricted and Tumor-Reactive CTLs in Cancer Patients

Ptk2 And Eif3s3 Genes May Be Amplification Targets At 8Q23–Q24 and Are Associated With Large Hepatocellular Carcinomas

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