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PubMedDate not supplied

Gene expression profiling during erythroid differentiation of K562 cells.

We studied the temporal changes in gene expression in K562 cells at intervals from 2 to 48 h following induction using differential display polymerase chain reaction and gene expression arrays. More than 110 cDNA fragments representing 86 unique mRNAs were either up- or downregulated during erythroid differentiation. Sixty-one of the differentially expressed cDNA fragments had more than 95% homology to known GenBank sequences; 21 represented cDNA sequences with only dbEST or high-throughput gene-screening database matches. Four fragments had no database matches. Using gene expression arrays, 73 differentially expressed genes were observed. Unique expressed sequence tags (ESTs) were used to "clone" two novel genes from available databases and their tissue expression was examined. Erythroid maturation in induced K562 cells is associated with differential expression of many genes. Some differentially expressed clones were transcription factors and 25 expressed fragments with open reading frames were found whose function remains unknown.

Base Sequence↗
PubMed2001

Gene expression profiling of cultured human bronchial epithelial and lung carcinoma cells.

Lung cancer is a complex collection of diseases that is thought to begin with single mutated progenitor cells and culminates in any of several clinically described pathologies. Our knowledge of the molecular events that lead to different lung cancer types--small cell carcinoma, squamous cell carcinoma, adenocarcinoma, and large cell carcinoma--is incomplete. Nonetheless, it is evident that genetic changes that impact multiple molecular networks are involved in the generation of each specific phenotype. Due to the obvious complexity of these processes, the simultaneous quantitative monitoring of changes in the expression of genes that define these networks can provide mechanistic information to increase our understanding of the molecular basis for human pulmonary carcinogenesis. To this end, we have employed a commercially available human cDNA array (Atlas Human Array, Clontech Laboratories) to systematically screen for alterations in the expression of 600 genes in normal human bronchial epithelial (NHBE) cells as well as in several lung carcinoma lines. Studies on the reproducibility and variability of array results indicate that a 2-fold or greater difference in the expression of a particular gene could be considered a real difference in transcript abundance. Accuracy of gene expression as measured in the array was verified by comparing mRNA levels of the proto-oncogene c-myc in the array with results obtained by traditional Northern blot analysis and by quantitative RT-PCR. Gene expression profiles were compared within and among cell types. The differential expression of 17 genes, including downregulation of MRP8 and MRP14 and upregulation of CYP1B1, was observed in all four carcinoma lines compared to NHBE cells. The direction of all 17 gene expression differences, either upregulation or downregulation relative to NHBE cells, was the same for all four carcinoma lines, underscoring their common molecular features. Each lung tumor line also exhibited a number of unique differences compared to both normal cells and the other tumor cell lines. These differences may be due to differences in the cellular origin and/or pathology of the cell lines studied.

Adenocarcinoma↗
PubMed2001

Cancer-related gene expression profiles in NF1-associated pilocytic astrocytomas.

BACKGROUND: Individuals affected with neurofibromatosis 1 (NF1) develop juvenile pilocytic astrocytomas (JPA) at an increased frequency, suggesting that the NF1 gene product, neurofibromin, functions as a negative growth regulator for astrocytes. Previously, the authors demonstrated that NF1-associated astrocytomas exhibit deletions and loss of NF1 gene expression on the DNA and protein levels. However, little is known about additional genetic events in clinically and radiographically progressive NF1-associated pilocytic astrocytomas. OBJECTIVE/METHODS: To understand the potential role of cooperating genetic events in the development of these low-grade tumors, the authors used immunohistochemistry and selected confirmatory Western blots to examine nine symptomatic NF1-associated pilocytic astrocytomas for gene products whose expression patterns are altered in fibrillary astrocytomas. RESULTS: The authors demonstrate that p53, p16, retinoblastoma (RB), epidermal growth factor receptor (EGFR), cyclin-dependent kinase 4 (CDK4), platelet-derived growth factor A (PDGF-A) and PDGF receptor alpha (PDGF-Ralpha) protein expression profiles are not altered in NF1-associated pilocytic astrocytomas. Similar to their sporadic counterparts, NF1-associated JPA also strongly expressed PEN5, a marker of post-O2A stage oligodendroglial precursor cells. CONCLUSIONS: These results suggest that NF1-associated pilocytic astrocytomas lack the genetic changes typically associated with the more clinically aggressive fibrillary astrocytomas and lay the foundation for future studies to identify NF1 JPA-specific alterations.

Adolescent↗
PubMed2000

Hunting the subset-specific genes of neuroblastoma: expression profiling and differential screening of the full-length-enriched oligo-capping cDNA libraries.

BACKGROUND: Neuroblastoma (NBL) has a distinct nature in different prognostic subgroups. PROCEDURE: To understand the molecular mechanism of NBL's genesis and biology as well as that of the neural crest development, we constructed full-length-enriched cDNA libraries by an oligo-capping method from two different subsets of primary NBL, one with favorable biology and the other with MYCN amplification. RESULTS: Sequencing analysis of these libraries revealed that the expression profile was markedly different between both subsets. To identify the genes differentially expressed between the subsets, semi-quantitative RT-PCR analyses are proceeding. CONCLUSION: So far, 54 transcripts have been found to be expressed at high levels in favorable NBLs, and significantly at low levels in unfavorable NBLs.

Gene Expression Regulation, Neoplastic↗
PubMed2001

Expression profiles of betaTRCP1 and betaTRCP2, and mutation analysis of betaTRCP2 in gastric cancer.

betaTRCP1 and betaTRCP2, components of the beta-catenin-ubiquitin ligase complex, are negative regulators of the WNT signaling pathway. We have previously isolated the betaTRCP2 gene, and detected betaTRCP2 in all gastric cancer cell lines examined. Here, expression profiles of betaTRCP1 and betaTRCP2 in various normal tissues and in primary gastric cancer were investigated. betaTRCP1 was predominant in small intestine, while betaTRCP2 was predominant in stomach. betaTRCP1 was expressed in gastric cancer cell lines MKN28, MKN45, MKN74, and KATO-III, but not in any cases of primary gastric cancer. betaTRCP2 was expressed in most cases of primary gastric cancer at almost the equal level in tumor and in non-cancerous portion of gastric mucosa. As betaTRCP2 was found to be the major betaTRCP expressed in gastric cancer, genetic alterations of betaTRCP2 in 7 gastric cancer cell lines and 12 cases of primary gastric cancer were investigated. A nucleotide substitution (Tright curved arrow C) at the nucleotide position 1486 of betaTRCP2 was identified in OKAJIMA cells, which lead to F462S amino acid substitution in the seventh WD-repeat domain. F462 was conserved among betaTRCPs derived from human, mouse, Xenopus laevis, and Drosophila melanogaster. As WD-repeats of betaTRCPs are the substrate-recognition motif of the beta-catenin-ubiquitin ligase, F462S amino-acid substitution might lead to beta-catenin stabilization, and might be implicated in carcinogenesis through activation of the WNT signaling pathway. This is the first report on comprehensive expression analyses of betaTRCP1 and betaTRCP2, and also on mutation analysis of betaTRCP2.

Blotting, Northern↗
PubMedDate not supplied

Tyrosine kinase expression profile in bladder cancer.

The expression pattern of tyrosine kinase in bladder cancer cells was evaluated by PCR amplification with degenerate primers derived from conserved catalytic domain in tyrosine kinase. The results indicated that TRK-E and Arg kinases were more abundantly expressed than several other kinases in bladder cancer. In addition, we identified a novel clone whose sequence could not be matched in GeneBank. This clone may represent a serine/threonine kinase based on sequence similarity.

Amino Acid Sequence↗
PubMed2000

mRNA expression profile of a human cancer cell line in response to Ginkgo biloba extract: induction of antioxidant response and the Golgi system.

Supplementation of diets with plant extracts for health and prevention of degenerative diseases is popular. However the molecular basis of their therapeutic potentials are poorly defined. We hypothesized that in vitro assays that enable quantitative analysis of the gene expression profiles combined with targeted biochemical analysis can identify the potential effects of phytochemicals. The hypothesis was tested by application of GeneChips to define mRNA expressions of a human bladder cancer cell line incubated with a flavonoid containing extract of Ginkgo biloba leaves. The analysis of the transcriptional response revealed a net activation of transcription. Functional classification of the affected mRNAs showed the largest changes in the abundance of mRNAs for intracellular vesicular transport, mitochondria, transcription and antioxidants. The transcripts for hemeoxygenase-1, mitochondrial superoxide dismutase and the regulatory subunit of gamma-glutamyl-cysteinyl synthetase and their encoded proteins were elevated. The extract also increased intracellular glutathione, the transcripts for DNA repair and synthesis, and decreased 3H-thymidine incorporation. These results demonstrate that a flavonoid containing extract initiates an adaptive transcriptional response that augments the "antioxidant status" of the cells and inhibits DNA damage. These in vitro studies using GeneChips demonstrated a promising strategy for identifying nutritional supplement induced cellular responses that may have a role in counteracting chronic human diseases.

Antioxidants↗
PubMed1997

Expression profiles of transcripts from 126 open reading frames in the entire chromosome VI of Saccharomyces cerevisiae by systematic northern analyses.

Chromosome VI of Saccharomyces cerevisiae contains 126 open reading frames (ORFs), and the functions of proteins encoded by 80 ORFs are still unknown. In this report, we have systematically examined the expression profiles of all 126 ORFs on chromosome VI under five kinds of growth conditions by quantitative Northern hybridization. A series of Northern analyses and reverse transcription polymerase chain reactions have revealed that more than 64 novel ORFs are transcribed. Two ORFs (YFL059w and YFR011c) are specifically expressed in the presence of galactose. Two ORFs (YFL012w and YFR032c) are specifically transcribed in sporulation. Six ORFs (YFL049w, YFL035c, YFL010c, YFR006w, YFR010w and YFR017c) are abundantly expressed in many growth conditions.

Blotting, Northern↗
PubMed1997

Analysis of an expression profile of genes in the human adipose tissue.

Increasing evidence suggests that in addition to storing excess energy as fat, adipose tissue acts as an endocrine organ secreting various factors into the blood stream. Every time a new factor is found in adipose tissue, however, its implication is discussed independently, and a systematic analyses based upon a global view of gene expression of this tissue has not been performed. To describe the function of this tissue in terms of gene expression, and to find new factors, we performed random complementary DNA (cDNA) sequencing using a 3'-directed cDNA library that faithfully represents the composition of the messenger RNA (mRNA). Various well-known but unexpected genes, including those for gelsolin, plasma glutathione peroxidase (GPX-3) and carboxypeptidase E (CPE) were shown to be very active. By comparing the expression profile of active genes in the adipose with those of other tissues and with data in dbEST, we identified seven new genes that are specifically expressed in adipose tissue. Among these, one encoded a protein with collagen-like repeats and a putative secretion signal. These data can be used as new tools for analyses of the physiology of this tissue, as well as the etiology and complications of obesity.

Adipose Tissue↗
PubMed1998

Comparative gene expression profiling by oligonucleotide fingerprinting.

The use of hybridisation of synthetic oligonucleotides to cDNAs under high stringency to characterise gene sequences has been demonstrated by a number of groups. We have used two cDNA libraries of 9 and 12 day mouse embryos (24 133 and 34 783 clones respectively) in a pilot study to characterise expressed genes by hybridisation with 110 hybridisation probes. We have identified 33 369 clusters of cDNA clones, that ranged in representation from 1 to 487 copies (0.7%). 737 were assigned to known rodent genes, and a further 13 845 showed significant homologies. A total of 404 clusters were identified as significantly differentially represented (P < 0.01) between the two cDNA libraries. This study demonstrates the utility of the fingerprinting approach for the generation of comparative gene expression profiles through the analysis of cDNAs derived from different biological materials.

Animals↗
PubMed1999

Reduced expression of the CDK inhibitor p27(KIP1) in rat two-stage bladder carcinogenesis and its association with expression profiles of p21(WAF1/Cip1) and p53.

The cyclin-dependent kinase (CDK) inhibitor p27(KIP1) exerts its growth suppressive effects by targeting the cyclin-CDK complexes. Reduced protein levels of p27(KIP1) have been reported in numerous human cancers and this has been attributed to increased degradation. However, few reports have addressed the significance of p27(KIP1) expression in chemical carcinogenesis of rodents. In a rat two-stage urinary bladder carcinogenesis model, with N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) initiation followed by promotion with sodium L-ascorbate (Na-AsA), we evaluated the expression of p27(KIP1) protein using immunohistochemistry during various stages of urinary bladder carcinogenesis. In addition, we evaluated the mRNA expression profiles for p27(KIP1), p21(WAF1/Cip1) and p53 in tumors. Fisher 344 rats were initiated with 0.05% BBN in the drinking water for 4 weeks and then administered 5% Na-AsA in the diet. Immunohistochemical examination revealed p27(KIP1) protein to be constitutively expressed in normal urothelium, simple hyperplasia and in most papillary and nodular (PN) hyperplasias and small papillomas, but diminished or absent in large papillomas and in transitional cell carcinomas. An inverse correlation between expression of p27(KIP1) and cell proliferation was generally observed. Quantitation of mRNA by multiplex reverse transcription-PCR showed a significant downregulaton of p27(KIP1), p21(WAF1/Cip1) and p53 mRNA in tumors. More than 50% reduction in p27(KIP1) mRNA expression was observed in 42 and 47% of tumors at weeks 18 and 24, respectively; similar reduction in p21(WAF1/Cip1) mRNA expression was observed in 58 and 73% of tumors at weeks 18 and 24, and in p53 mRNA expression in 50 and 73% of tumors at weeks 18 and 24, respectively. None of the 25 tumors we examined by PCR-single-strand conformational polymorphism analysis had p53 mutations. These data imply that abnormal down-regulation of p27(KIP1), p21(WAF1/Cip1) and/or p53 in tumor cells may contribute to the malignant progression of tumors during rat two-stage bladder carcinogenesis.

Animals↗
PubMed2000

B-lymphocyte quiescence, tolerance and activation as viewed by global gene expression profiling on microarrays.

Self-tolerance is achieved by deleting or regulating self-reactive lymphocytes at a series of cellular checkpoints placed at many points along the developmental pathways to plasma cells and effector T cells. At each checkpoint, what are the molecular pathways that determine whether a lymphocyte remains quiescent, begins dividing, differentiates or dies? In splenic B cells, the decision between quiescence, tolerance by anergy, and activation provides a tractable setting to explore these issues by global gene expression profiling on DNA microarrays. Here we discuss the application of microarrays to illuminate a set of cell fate decisions that appear to be determined by summation of numerous small changes in expression of stimulatory and inhibitory genes. Many genes with known or predicted inhibitory functions are highly expressed in naive, quiescent B cells, notably the signal inhibitor SLAP and DNA-binding proteins of the Kruppel family (LKLF, BKLF, GKLF), Tsc-22, GILZ, Id-3, and GADD45. Activation of naive B cells, triggered by acute binding of antigen to the B-cell receptor, involves a rapid decrease in expression of these inhibitory genes. Promitotic genes are induced in parallel, including c myc, LSIRF/IRF4, cyclin D2, Egr-1 and Egr-2, as are the anti-apoptotic gene A1 and genes for the T-cell-attracting chemokines MIP-1alpha and beta. B-cell tolerance through the process of anergy, induced by chronic binding of self antigen, maintains expression of the inhibitory genes found in quiescent B cells and induces an additional set of inhibitory genes. The latter include inhibitors of signaling - CD72, neurogranin, pcp4 - and additional inhibitors of gene expression such as SATB1, MEF2C, TGIF and Nab-2. The effects of tolerance, the immunosuppressive drug FK506 and other modulators of calcium or MAPK signaling allow individual gene responses to be linked to different signal transduction pathways. The global molecular profiles obtained illustrate how quiescence and anergy are actively maintained in circulating B cells, how these states are switched to clonal expansion and how they could be better emulated by pro-tolerogenic drugs.

Animals↗
PubMed1995

The expression profile of alternatively spliced neuronal c-src RNA distinguishes between human tumours of the sympatho-adrenal lineage.

Human neuronal and neuroendocrine tumour specimens and cell lines were analysed regarding proteins and transcripts coded by the proto-oncogene c-src. At the protein level, most of the neuroblastomas and phaeochromocytomas expressed the neuronal c-src form, pp60c-srcN. None of the other neuroendocrine tumours, i.e. paragangliomas, neuroendocrine pancreatic tumours, or carcinoid tumours and small-cell lung carcinomas of different types, appeared to express the neuronal form. In the brain, c-src is transcribed into 3 differently spliced mRNA variants, c-src, c-srcNI, and c-srcNI+NII. The expression of these transcripts was analysed by PCR amplification of fragments covering the mini-exons I and NII of the corresponding cDNAs. The PCR products were analysed by Southern hybridization and characterized by determination of their sequences. Neuroblastomas, paragangliomas, retinoblastomas and the phaeochromocytomas expressed neuronal c-src splice variants. However, whereas neuroblastomas and retinoblastomas contained all 3 transcripts, the phaeochromocytomas and paragangliomas expressed, with 2 exceptions, only the c-src and the c-srcNI+NII mRNA species. To assess whether neuroblastomas display adrenal chromaffin characteristics, they were analysed regarding expression of the chromaffin marker enzyme, phenylethanolamine-N-methyl transferase. Whereas phaeochromocytomas were positive, all neuroblastomas were immuno-chemically negative for this enzyme. These results and the c-src expression profile suggest that neuroblastomas, including those with an adrenal location, do not originate from the adrenal chromaffin differentiation lineage. The data further suggest neuronal c-srcNI mRNA as a marker for sympathetic neuronal cells of the sympatho-adrenal lineage.

Adrenal Gland Neoplasms↗
PubMed1997

Expression profile and subcellular location of the plasmid-encoded virulence (Spv) proteins in wild-type Salmonella dublin.

The plasmid-encoded virulence genes (spvABCD) in nontyphoid Salmonella strains mediate lethal infections in a variety of animals. Previous studies have shown that these genes are transcriptionally regulated by stationary-phase growth. We studied the expression profile and the subcellular locations of the SpvABCD proteins in wild-type S. dublin by using polyclonal antibodies against SpvA, SpvB, SpvC, and SpvD. The cellular levels of the individual proteins were determined during growth by quantitative immunoblotting. As expected, SpvA, SpvB, SpvC, and SpvD were not detectable before the late logarithmic growth phase and appeared in the sequence SpvA, SpvB, SpvC, and SpvD. In contrast to the transcriptional regulation, however, SpvA and SpvB reached their maximal expression shortly after induction and declined during further growth whereas SpvC and SpvD expression remained high throughout the stationary phase, indicating that the Spv proteins are individually regulated at a posttranscriptional level. To localize SpvABCD within the bacteria, the cells were fractionated into the periplasmic, cytoplasmic, inner membrane, and outer membrane components. The cell fractions and the culture supernatant were analyzed by immunoblotting. SpvA was present in the outer membrane, SpvB was present in the cytoplasm and the inner membrane, and SpvC was present in the cytoplasm. SpvD was secreted into the supernatant; however, a substantial portion of this protein was also detected in the cytoplasm and membranes. The molecular weights of SpvD in the supernatant and in the cytoplasm appeared to be equal, suggesting that SpvD is not cleaved upon secretion.

Bacterial Proteins↗
PubMed2001

Targets of transcriptional regulation by transforming growth factor-beta: expression profile analysis using oligonucleotide arrays.

Transforming growth factor-betas (TGF-betas) are potent inhibitors of cell proliferation, and disruption of components of the TGF-beta signaling pathway leads to tumorigenesis. Mutations of transmembrane receptors and Smads mediating intracellular signaling have been reported in various cancers. To identify transcriptional targets of TGF-beta, we conducted an expression profile analysis. HaCaT cells derived from human keratinocytes and highly sensitive to TGF-beta were treated with TGF-beta in the absence or presence of cycloheximide (CHX). mRNAs extracted from the HaCaT cells were used for hybridization of oligonucleotide arrays representing approximately 5600 human genes. TGF-beta increased the expression of PAI-1, junB, p21 cdk inhibitor, Smad7, betaIG-H3, and involucrin that have been reported to be up-regulated by TGF-beta, validating the usefulness of this approach. The induction of betaIG-H3 by TGF-beta was completely abolished by CHX, suggesting that the transcription of betaIG-H3 is not directly regulated by TGF-beta. Unexpectedly, we identified more genes down-regulated by TGF-beta than up-regulated ones. TGF-beta repressed the expression of epithelial specific Ets that may be involved in breast and lung tumorigenesis, which could contribute to tumor suppression by TGF-beta. Among a panel of cell cycle regulators, TGF-beta induced the expression of p21 cdk inhibitor; however, the induction of other cdk inhibitors was not significant in the present study. Taken together, the results suggest that TGF-beta may suppress tumorigenesis through positive and negative regulation of transcription.

Cell Cycle↗
PubMed2001

Expression profiles of BRCA1 splice variants in asynchronous and in G1/S synchronized tumor cell lines.

Disrupting the function of the BRCA1 gene by mechanisms other than germline mutations is suspected to occur in cases of sporadic breast/ovarian cancers. Using ribonuclease protection assay and multiplex RT-PCR, we examined the change of the total BRCA1 mRNA pool and the expression profile of four predominant BRCA1 splice variants in asynchronous and in G1/S synchronized tumor cell populations compared to normal breast cells. Experiments were carried out on MCF-7 and MDA-MB-231 breast cancer, OVCAR-5 ovarian cancer, and K562 leukemia cell lines. The ratio of the full length, the delta(11q), the delta(9,10), and the delta(9,10,11q) BRCA1 isoforms showed different expression patterns in the examined breast and ovarian tumor cell lines as compared to the leukemia cell line. This observation raises the possibility that the dysregulation of alternative splicing of the BRCA1 gene could be involved in tumor formation in the breast and the ovary, even in the absence of germline mutations.

Alternative Splicing↗
PubMed1998

Expression profile of receptor-type protein tyrosine kinase genes in the human thyroid.

Protein tyrosine kinases (PTKs) play a role in regulating the growth and differentiated functions of thyroid cells and are probably involved in tumorigenesis of papillary-type thyroid carcinoma. To better understand the roles of PTKs in the physiology and pathophysiology of the thyroid, we analyzed the expression profile of receptor-type PTKs in normal human thyroid tissues. Highly conserved regions in the catalytic domains of receptor-type PTKs were amplified by RT-PCR using degenerate oligonucleotide primers. Nucleotide sequencing of about 100 clones identified 21 PTKs, including 16 receptor type and 5 nonreceptor type; no novel PTK was identified. Insulin-like growth factor I receptor, platelet-derived growth factor receptor (PDGFR), TrkE, Axl, epidermal growth factor receptor, etc., appear to be the most abundant receptor-type PTKs in the thyroid; many of which (PDGFR, TrkE, Axl, etc.) have never previously been demonstrated to be expressed in the thyroid. The expression of messenger RNAs (mRNAs) for PDGFR, axl, and trkE in normal thyroid cells was confirmed by Northern blot analysis, and interestingly, the expression levels of PDGFR and trkE mRNAs were decreased in all three thyroid carcinoma cell lines examined (FRO, WRO, and NPA), whereas axl mRNA and protein were overexpressed in 2 of 3 thyroid carcinoma cell lines (FRO and WRO) compared with that in normal tissue. The axl gene was, however, neither amplified nor rearranged. The biological activity of the ligand for Axl, the product of growth arrest-specific gene 6 (Gas6), was then evaluated, demonstrating modest mitogenic activity in thyroid carcinoma cells overexpressing Axl. Furthermore, gas6 mRNA was expressed in FRO cells. Thus, we here identify a variety of PTKs expressed in the thyroid gland, many of which may participate in the regulation of thyroid cell function. Variable expression levels of some PTKs in normal and cancerous cells suggest that there may be an imbalance and disarray of phosphorylation events in thyroid carcinoma cells. Furthermore, Gas6 is identified as a novel growth factor for thyroid carcinoma cells overexpressing Axl receptor tyrosine kinase.

Amino Acid Sequence↗
PubMed1997

Protein expression profiles in human breast ductal carcinoma and histologically normal tissue.

Reference two-dimensional (2-D) gels are presented for human breast ductal carcinoma and histologically normal tissue. Whole biopsy fragments were analyzed, including epithelial and nonepithelial components. Thirty-five spots have been assigned by gel matching to the human liver SWISS-2DPAGE reference map and/or to the human primary keratinocyte IPG map from the Danish Center for Human Genome. N-terminal microsequencing was applied to confirm randomly chosen matching assignments and to identify six new spots. Protein expression profiles in ductal carcinoma and in normal breast tissue appeared to be similar, except for a pattern consisting of 32 spots, which were highly expressed in all carcinoma specimens, and less intense and occasionally undetectable in normal tissue. This difference was statistically significant. Assignment has been obtained for several spots, namely GRP94, GRP78, GRP75, mitochondrial HSP60, calreticulin, protein disulfide isomerase, peptidyl-prolyl cis-trans isomerase, collagen-binding protein 2, fructose bisphosphate aldolase, glyceraldehyde-3-phosphate dehydrogenase, thioredoxin, cytochrome c oxidase VA subunit, tubulin beta isoform and macrophage migration inhibitory factor (MIF). The cancer- and tissue-specificity of the described pattern was assessed by matching to the Swiss-2DPAGE human liver, hepatoma, lymphoma, erythroleukemia reference maps. The pattern of 32 spots was found to be indicative of epithelial neoplasia.

Aged↗