Differential gene expression in colon carcinoma cells and tissues detected with a cDNA array

Backert, Steffen; Gelos, Marcos; Kobalz, Ursula; Hanski, Marie‐Luise; Böhm, Christian; Mann, B.; Lövin, Nicole; Gratchev, Alexei; Mansmann, Ulrich; Moyer, Mary Pat; Riecken, Ernst–Otto; Hanski, C.

doi:10.1002/(sici)1097-0215(19990909)82:6<868::aid-ijc16>3.0.co;2-w

Cited by 97 publications

(65 citation statements)

References 34 publications

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“…This ratio is in agreement with other reports (Zhang et al, 1997;Stremmel et al, 2002). Comparison with lists of discriminator genes previously identified in CRC using DNA microarrays (Alon et al, 1999;Backert et al, 1999;Kitahara et al, 2001;Notterman et al, 2001;Agrawal et al, 2002;Birkenkamp-Demtroder et al, 2002;Lin et al, 2002;Zou et al, 2002;Frederiksen et al, 2003;Tureci et al, 2003;Williams et al, 2003) revealed many common genes, further emphasizing the validity of our data. For example, CA4, CHGA, CNN1, MYH11, FCGBP, KCNMB1 and SST were downregulated, whereas CA3, CCT4, EIF3S6 or EEF1A1, IFITM1, CSE1L, NME1 or RAN were upregulated in cancer samples.…”

Section: Comparison Of Normal Versus Cancer Samplessupporting

confidence: 91%

“…Gene expression profiling-based studies of CRC have so far compared normal and tumour tissue samples or different stages of disease (Alon et al, 1999;Backert et al, 1999;Hegde et al, 2001;Kitahara et al, 2001;Notterman et al, 2001;Agrawal et al, 2002;Birkenkamp-Demtroder et al, 2002;Lin et al, 2002;Zou et al, 2002;Frederiksen et al, 2003;Tureci et al, 2003;Williams et al, 2003), but none has directly addressed the issue of prognosis or MSI phenotype. Here we have applied DNA microarray technology to analyse the expression of B8000 genes in 50 cancer and noncancerous colon tissue samples.…”

Section: Introductionmentioning

confidence: 99%

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Gene expression profiling of colon cancer by DNA microarrays and correlation with histoclinical parameters

et al. 2004

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Different diagnostic and prognostic groups of colorectal carcinoma (CRC) have been defined. However, accurate diagnosis and prediction of survival are sometimes difficult. Gene expression profiling might improve these classifications and bring new insights into underlying molecular mechanisms. We profiled 50 cancerous and noncancerous colon tissues using DNA microarrrays consisting of B8000 spotted human cDNA. Global hierarchical clustering was to some extent able to distinguish clinically relevant subgroups, normal versus cancer tissues and metastatic versus nonmetastatic tumours. Supervised analyses improved these segregations by identifying sets of genes that discriminated between normal and tumour tissues, tumours associated or not with lymph node invasion or genetic instability, and tumours from the right or left colon. A similar approach identified a gene set that divided patients with significantly different 5-year survival (100% in one group and 40% in the other group; P ¼ 0.005). Discriminator genes were associated with various cellular processes. An immunohistochemical study on 382 tumour and normal samples deposited onto a tissue microarray subsequently validated the upregulation of NM23 in CRC and a downregulation in poor prognosis tumours. These results suggest that microarrays may provide means to improve the classification of CRC, provide new potential targets against carcinogenesis and new diagnostic and/or prognostic markers and therapeutic targets.

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Section: Comparison Of Normal Versus Cancer Samplessupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Gene expression profiling of colon cancer by DNA microarrays and correlation with histoclinical parameters

et al. 2004

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“…[10][11][12][13][14][15][16][17][18][19][20][21] However, few studies have directly addressed the mechanisms of metastasis formation or sup-FIGURE 2 -Confirmation of microarray data by RT-PCR on 6 RNAs from each group of tumors; 100 ng of each linearly amplified RNA were reversely transcribed and used as PCR templates. While b-actin was expressed at comparable levels in all groups of tumors, GnT-IV and Nup50 were dramatically upregulated in the metastasizing primary tumors and in the correspondent metastases.…”

Section: Discussionmentioning

confidence: 99%

Metastatic transcriptional pattern revealed by gene expression profiling in primary colorectal carcinoma

D’Arrigo

Belluco

Ambrosi

et al. 2005

Intl Journal of Cancer

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Metastatic spread to the liver is the major contributor to mortality in patients with colorectal carcinoma (CRC). In order to seek for gene expression patterns associated with metastatic potential in primary CRC, we compared the transcriptional profiles of 10 radically resected primary CRCs from patients who did not develop distant metastases within a 5-year follow-up period with those of 10 primary/metastatic tumor pairs from patients with synchronous liver metastases. To focus selectively on neoplastic cells, the study was conducted on laser-microdissected bioptic tissues. Arrays of 7,864 human cDNAs were utilized. While a striking transcriptional similarity was observed between the primary tumors and their distant metastases, the nonmetastasizing primary tumors were clearly distinct from the primary/metastatic tumor pairs. Of 37 gene expression differences found between the 2 groups of primary tumors, 29 also distinguished nonmetastasizing tumors from metastases. The gene encoding for mannosyl (a-1,3-)-glycoprotein b-1,4-N-acetyl-glucosaminyl-transferase (GnT-IV) became significantly upregulated in primary/metastatic tumor pairs (p < 0.001). GnT-IV upregulation was confirmed by RT-PCR. These data support the existence of a specific transcriptional signature distinguishing primary colon adenocarcinomas with different metastatic potential, the further pursuit of which may lead to relevant clinical and therapeutic applications. ' 2005 Wiley-Liss, Inc.Key words: DNA microarray; metastasis; colorectal cancer Colorectal carcinoma (CRC) is the second leading cause of cancer deaths in developed countries.1 Metastatic spread, mostly to the liver, is the major cause of mortality in patients with this disease. Yet while the molecular events involved in the CRC adenoma-carcinoma sequence have been largely characterized, 2 little information is available on the mechanisms responsible for the metastatic phenotype. The identification in the primary tumors of molecular factors predictive of metastatic risk may have a relevant clinical impact, allowing for more personalized and effective treatment of CRC patients.Recent evidence based on gene expression profiling has shown that a metastatic fingerprint is detectable in the bulk of primary lung and breast tumors.3,4 On the other hand, no such metastatic signature has been demonstrated in CRC. A general problem related to gene expression studies in the oncologic field is the heterogeneous histology of the bioptic specimens that may contain, in addition to cancer cells, significant fractions of nonneoplastic tissue. Due to this heterogeneity, relevant changes in cancer cell gene expression may be easily overlooked.In order to seek for gene expression patterns specific to metastasis in CRC carcinoma, avoiding interference from nontumoral tissue, we combined laser microdissection of cancer cells and DNA microarray to compare the transcriptional profile of primary colon carcinomas both with that of patient-matched liver metastases and with that of a group of primary tumors of meta...

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“…Mainly advanced cancer has been analysed in gene expression profiling-based studies on colorectal cancer (Alon et al, 1999;Backert et al, 1999;Hegde et al, 2001;Kitahara et al, 2001;Notterman et al, 2001;Takemasa et al, 2001;Agrawal et al, 2002;Birkenkamp-Demtroder et al, 2002;Lin et al, 2002;Zou et al, 2002;Frederiksen et al, 2003;Muro et al, 2003;Tureci et al, 2003;Williams et al, 2003;Bertucci et al, 2004). Only a small number of adenoma and early invasive cancer tissues have been analysed in previous studies, and the issue of flat-and protruded-type adenoma tissues has not been directly addressed (Notterman et al, 2001;Agrawal et al, 2002;Lin et al, 2002;Williams et al, 2003).…”

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confidence: 99%

Gene expression profiling of colorectal adenomas and early invasive carcinomas by cDNA array analysis

et al. 2005

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It is generally accepted that most colorectal carcinomas arise in pre-existing adenomas. Morphologically, colorectal adenomas can be divided into two groups, protruded type and flat type. The aim of this study was to clarify relevant alterations of gene expression associated with the early stage of colorectal carcinogenesis. Using cDNA array, we analysed the expression profiles of 550 cancerrelated genes in 36 colorectal adenomas (18 flat-type and 18 protruded-type adenomas) and 14 early invasive carcinomas. Among the 550 genes, we chose 32 genes the average expression levels of which were at least three-fold up-or downregulated in tumour tissues compared with levels in matched normal tissues. A total of 13 and 19 genes were identified as up-and downregulated genes in tumour tissues, respectively. Among the upregulated genes, the average expression levels of E1AF, bone morphogenic protein (BMP)-4, insulin-like growth factor (IGF)-2, inducible nitric oxide synthase (iNOS), tissue inhibitors of metalloproteinase (TIMP)-1, Smad4, and nm23 in tumour tissues were over five times higher than those in matched normal tissues. Colorectal adenomas and early invasive carcinomas were divided into two major clusters by clustering analysis. Moreover, flat-and protruded-type adenomas were divided into two major clusters by clustering analysis. The expression profiles obtained by the cDNA array clearly indicate that colorectal adenomas and early invasive carcinomas have specific expression profiles. Likewise, the gene expression profiles of flat-and protruded-type adenomas are different. These results indicate that molecular classification of early colorectal tumours by a cDNA array is feasible.

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Differential gene expression in colon carcinoma cells and tissues detected with a cDNA array

Cited by 97 publications

References 34 publications

Gene expression profiling of colon cancer by DNA microarrays and correlation with histoclinical parameters

Gene expression profiling of colon cancer by DNA microarrays and correlation with histoclinical parameters

Metastatic transcriptional pattern revealed by gene expression profiling in primary colorectal carcinoma

Gene expression profiling of colorectal adenomas and early invasive carcinomas by cDNA array analysis

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