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

Nosho, Katsuhiko; Yamamoto, Hiroyuki; Adachi, Yasushi; Endo, Takao; Hinoda, Yuji; Imai, Kohzoh

doi:10.1038/sj.bjc.6602442

Cited by 49 publications

(29 citation statements)

References 34 publications

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“…Furthermore, coinciding data was shown in other reports in which fresh samples were used without amplification. For instance, HLA-DQA1 was also reported to be down-regulated in colon adenomas (10). Similarly, genes such as PDCD4, SEPP1, TSNAX and IGLJ3 were also downregulated in our previous expression profiling study of stomach cancer without amplification (11).…”

Section: Discussionmentioning

confidence: 95%

“…It was of interest that down-regulation of HLA-DQA1 has also been described by Nosho et al using fresh tissue samples of colon polyps without signal amplification (10). It has been implicated in Table III.…”

Section: Fcgbp Slc26a2 Eplin Tspan1 Pdcd4 Pex1 Mtus1 Fabp1 Ddmentioning

confidence: 99%

“…Nonetheless, surprisingly little expression profiling data of the adenoma/carcinoma sequence has been reported so far. The available data mostly report the differential expression between whole tissue samples of adenoma and carcinoma from multiple individuals (6)(7)(8)(9)(10). However, DNA microarray data using whole tissue samples of gastrointestinal tracts is particularly difficult to interpret because of considerable data noise from various inflammatory infiltration and reactive stromal changes (11).…”

Section: Introductionmentioning

confidence: 99%

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Differential expression in normal-adenoma-carcinoma sequence suggests complex molecular carcinogenesis in colon

Lee

Bang²,

Song³

et al. 2006

Oncol Rep

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Abstract. The majority of colon cancers develop from preexisting adenomas. We analyzed the expression profiles in the sequence of normal colon crypts, adenomas and earlystage carcinomas using microdissected cells from tubular adenomas with foci of malignant transformation. Differentially expressed genes were detected between normal-adenoma and adenoma-carcinoma, and were grouped according to the patterns of expression changes in the sequence. Down-regulated genes in the sequence included PLA2G2A, TSPAN1, PDCD4, FCGBP, AATK, EPLIN, FABP1, AGR2, MTUS1, TSC1, galectin 4 and MT1F. PLA2G2A has been shown to suppress colon tumorigenesis in mice, but the pathobiological role in humans has been controversial. Our data showed continuous down-regulation of PLA2G2A in the sequence supporting an implication in human colon cancer. Tumor suppressor and/ or proapoptotic activities have also been reported in other genes. Up-regulated genes included ribosomal proteins, IER3 and TPR. TGF-ß2 and matrix metalloproteinase 23B were up-regulated in carcinoma but not in adenoma, supporting the pathobiological roles in malignant transformation. Differentially expressed genes partly coincided with those in the adenoma-carcinoma sequence of the stomach, which was published previously, suggesting a partial overlap between the adenoma-carcinoma sequences of the colon and stomach.

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Section: Discussionmentioning

confidence: 95%

Section: Fcgbp Slc26a2 Eplin Tspan1 Pdcd4 Pex1 Mtus1 Fabp1 Ddmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Differential expression in normal-adenoma-carcinoma sequence suggests complex molecular carcinogenesis in colon

Lee

Bang²,

Song³

et al. 2006

Oncol Rep

View full text Add to dashboard Cite

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“…Adenomatous colorectal polyps are one of the most common human tumors and the most frequent precancerous lesions in the colorectum, but their transcriptome has been only partially analyzed, and the data are generally based on a limited number of cases (17)(18)(19)(20). We attempted to fill this gap by doing a comprehensive whole-genome microarray analysis of a large, highly homogenous set of adenomas that was collected prospectively.…”

Section: Discussionmentioning

confidence: 99%

Transcriptome Profile of Human Colorectal Adenomas

Sabates–Bellver

Flier

Palo

et al. 2007

Molecular Cancer Research

435

389

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Colorectal cancers are believed to arise predominantly from adenomas. Although these precancerous lesions have been subjected to extensive clinical, pathologic, and molecular analyses, little is currently known about the global gene expression changes accompanying their formation. To characterize the molecular processes underlying the transformation of normal colonic epithelium, we compared the transcriptomes of 32 prospectively collected adenomas with those of normal mucosa from the same individuals. Important differences emerged not only between the expression profiles of normal and adenomatous tissues but also between those of small and large adenomas. A key feature of the transformation process was the remodeling of the Wnt pathway reflected in patent overexpression and underexpression of 78 known components of this signaling cascade. The expression of 19 Wnt targets was closely correlated with clear up-regulation of KIAA1199, whose function is currently unknown. In normal mucosa, KIAA1199 expression was confined to cells in the lower portion of intestinal crypts, where Wnt signaling is physiologically active, but it was markedly increased in all adenomas, where it was expressed in most of the epithelial cells, and in colon cancer cell lines, it was markedly reduced by inactivation of the B-catenin/T-cell factor(s) transcription complex, the pivotal mediator of Wnt signaling. Our transcriptomic profiles of normal colonic mucosa and colorectal adenomas shed new light on the early stages of colorectal tumorigenesis and identified KIAA1199 as a novel target of the Wnt signaling pathway and a putative marker of colorectal adenomatous transformation.

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“…Evidence suggests that BMPs are important in tumorigenesis (8)(9)(10). BMPs are members of the transforming growth factor beta (TGFβ) family; thus, BMPs utilize a similar signaling cascade to that of TGFβ.…”

Section: Introductionmentioning

confidence: 99%

Polymorphisms in bone morphogenetic protein 3 and the risk of papillary thyroid cancer

Kim¹,

Hong

Eun

et al. 2012

Oncology Letters

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Abstract. Bone morphogenetic proteins (BMPs) are members of the transforming growth factor beta (TGFβ) superfamily with well-described functions in bone formation. Although disrupted BMP signaling in tumor development has been investigated, a genetic association for BMP3 in papillary thyroid cancer (PTC) has remained largely unexplored. In this study, we investigated whether BMP3 single nucleotide polymorphisms (SNPs) are associated with the development of PTC and its clinicopathological features. A total of 103 PTC patients and 324 control subjects were enrolled. One promoter SNP (rs13138132; -1919C/A) and one missense mutation (rs3733549; Arg192Gln) in BMP3 were genotyped by direct sequencing. SNPStats, SNPAnalyzer, Helixtree and Haploview version 4.2 were used to evaluate the genetic data. Multiple logistic regression models were used to calculate odds ratios (ORs), 95% confidence intervals (CIs) and P-values. The missense SNP (rs3733549) was weakly associated with the development of PTC in a codominant model (AA vs. GG; P=0.017) and a recessive model (AA vs. GG/GA; P=0.023). Additionally, in an analysis according to clinicopathological features, rs13138132 was significantly associated with extrathyroidal invasion in a codominant model (CA vs. CC; P=0.006) and a dominant model (CA/AA vs. CC; P=0.0023). We also identified that the frequency of the A allele in the promoter SNP (rs13138132) was increased in PTC patients with extrathyroidal invasion (P=0.004). Our data suggest that rs3733549 in BMP3 is associated with the development of PTC and that the A allele of rs13138932 in BMP3 is a risk factor for extrathyroidal invasion. IntroductionThyroid cancer is the most common type of endocrine malignancy, accounting for approximately 1% of all cases of cancer. It is the most rapidly increasing cancer among females and the second most rapidly increasing cancer among males. Histologically, thyroid cancer is classified as papillary thyroid cancer (PTC), follicular thyroid cancer, medullary thyroid cancer or undifferentiated or anaplastic thyroid cancer. Of these, PTC is the most common type, and it accounts for 85-90% of all thyroid malignancies (1,2). Although the etiology of PTC is unclear, environmental factors, including radiation, diet, smoking and hormones, have been identified to affect the pathogenesis of thyroid cancer (3,4). Genetic predisposition has also been implicated as a risk factor for thyroid cancer development (5,6).Bone morphogenic proteins (BMPs) have been demonstrated to play an important role during development (particularly during bone formation) and in the regulation of various cellular processes, including cell proliferation, apoptosis and differentiation (7). Evidence suggests that BMPs are important in tumorigenesis (8-10). BMPs are members of the transforming growth factor beta (TGFβ) family; thus, BMPs utilize a similar signaling cascade to that of TGFβ. BMPs have been identified to utilize the SMAD signaling pathway for their growth suppressive effects, and also to affect PTEN and p21 (W...

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

Cited by 49 publications

References 34 publications

Differential expression in normal-adenoma-carcinoma sequence suggests complex molecular carcinogenesis in colon

Differential expression in normal-adenoma-carcinoma sequence suggests complex molecular carcinogenesis in colon

Transcriptome Profile of Human Colorectal Adenomas

Polymorphisms in bone morphogenetic protein 3 and the risk of papillary thyroid cancer

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