Complete list of abbreviations of tumor antigens 707-AP 707 alanine proline-AFP alpha (α)-fetoprotein-ART-4 adenocarcinoma antigen recognized by T cells 4 BAGE B antigen-β-catenin/m β-catenin/mutated-Bcr-abl breakpoint cluster region-Abelson - CAMEL CTL-recognized antigen on melanoma CAP-1 carcinoembryonic antigen peptide-1-CASP-8 caspase-8 CDC27m cell-division-cycle 27 mutated-CDK4/m cycline-dependent kinase 4 mutated-CEA carcino-embryonic antigen-CT cancer/testis (antigen)-Cyp-B cyclophilin B DAM differentiation antigen melanoma (the epitopes of DAM-6 and DAM-10 are equivalent, but the gene sequences are different; DAM-6 is also called MAGE-B2. and DAM-10 is also called MAGE-B1) ELF2M elongation factor 2 mutated ETV6-AML1 Ets variant gene 6/acute myeloid leukemia 1 gene ETS G250 glycoprotein 250 - GAGE G antigen GnT-V N-acetylglucosaminyltransferase V -Gp100 glycoprotein 100 kDa-HAGE helicose antigen-HER-2/neu human epidermal receptor-2/ neurological - HLA-A * 0201-R1701 arginine (R) to isoleucine (I) exchange at residue 170 of the α-helix of the α2-domain in the HLA-A2 gene HPV-E7 human papilloma virus E7 HSP70-2M heat shock protein 70-2 mutated HST-2 human signet ring tumor-2 hTERT or hTRT human telomerase reverse transcriptase-iCE intestinal carboxyl esterase KIAA0205 name of the gene as it appears in databases-LAGE L antigen LDLR/FUT low-density lipid receptor/GDP-L-fucose: β-D-galactosidase 2-α-L-fucosyltransferase MAGE melanoma antigen MART-1/Melan-A melanoma antigen recognized by T cells-1/melanoma antigen A MC1R melanocortin 1 receptor Myosin/m myosin mutated-MUC1 mucin 1-MUM-1, -2, -3 melanoma ubiquitous mutated 1, 2, 3 NA88-A NA cDNA clone of patient M88-NY-ESO-1 New York-esophagus 1 - P15 protein 15 p190 minor bcr-abl protein of 190 kDa ber-abl Pml/RARα promyelocytic leukaemia/retinoic acid receptor α-PRAME preferentially expressed antigen of melanoma PSA prostate-specific antigen-PSM prostate-specific membrane antigen-RAGE renal antigen RU1 or RU2 renal ubiquitous 1 or 2 SAGE sarcoma antigen SART-1 or SART-3 squamous antigen rejecting tumor 1 or 3-TEL/ AML1 translocation Ets-family leukemia/acute myeloid leukemia 1 TPI/m triosephosphate isomerase mutated TRP-1 tyrosinase related protein 1, or gp75 TRP-2 tyrosinase related protein 2 TRP-2/ INT2 TRP-2/intron 2 WT1 Wilms' tumor gene Abbreviations used ALL acute lymphoblastic leukemia AML acute myeloid leukemia-APL acute promyelocytic leukemia-CML chronic myelogenous leuke mia-CTL cytotoxic T lymphocytes-Ets E-26 transforming specific (family of transcription factors) H/N head and neck-MHC major histocompatibility complex-NSCLC non-small cell lung carcinoma-ORF open reading frame RCC renal cell carcinoma-SCC squamous cell carcinoma-TSTA tumor-specific transplantation antigens.

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A listing of human tumor antigens recognized by T cells.

Thyroid cancer is one of the few malignancies that are increasing in incidence. Recent advances have improved our understanding of its pathogenesis; these include the identification of genetic alterations that activate a common effector pathway involving the RET-Ras-BRAF signalling cascade, and other unique chromosomal rearrangements. Some of these have been associated with radiation exposure as a pathogenetic mechanism. Defects in transcriptional and post-transcriptional regulation of adhesion molecules and cell-cycle control elements seem to affect tumour progression. This information can provide powerful ancillary diagnostic tools and can also be used to identify new therapeutic targets.

Pathogenetic mechanisms in thyroid follicular-cell neoplasia

The technological advances occurred in the last few years have led to a great increase in the number of tumor associated antigens (TAA) that are currently available for clinical applications. In this review we provide a comprehensive list of human tumor antigens as reported in the literature updated at Feburary 2004. The list includes all T cell-defined epitopes, while excluding analogs or artificially modified epitopes, as well as virus-encoded and antibodies-recognized antigens. TAAs are listed in alphabetical order along with the epitope sequence and the HLA allele which restricts recognition by T cells. Data on the tissue distribution of each antigen are also provided together with an extensive bibliography that allows a rapid search for any additional information may be needed on each single antigen or epitope. Overall, the updated list is a database tool for clinicians, scientists and students who have an interest in the field of tumor immunology and immunotherapy.

A listing of human tumor antigens recognized by T cells: March 2004 update

Purpose An estimated 4% to 7% of the population will develop a clinically significant thyroid nodule during their lifetime. In many cases, preoperative diagnoses by needle biopsy are inconclusive. Thus, there is a clear need for improved diagnostic tests to distinguish malignant from benign thyroid tumors. The recent development of high-throughput molecular analytic techniques should allow the rapid evaluation of new diagnostic markers. However, researchers are faced with an overwhelming number of potential markers from numerous thyroid cancer expression profiling studies. Materials and Methods To address this challenge, we have carried out a comprehensive meta-review of thyroid cancer biomarkers from 21 published studies. A gene ranking system that considers the number of comparisons in agreement, total number of samples, average fold-change and direction of change was devised. Results We have observed that genes are consistently reported by multiple studies at a highly significant rate (P < .05). Compar...

Meta-analysis and meta-review of thyroid cancer gene expression profiling studies identifies important diagnostic biomarkers.

According to the literature thyroid nodules are quite rare in the first two decades of life. However, there are some exceptions, relating to areas with an iodine deficiency or affected by radioactive fallout, where the risk of nodules and carcinomas is increased. Therefore, it is a great challenge for the physician to distinguish between benign and malignant lesions preoperatively, and not only in these areas of greater risk. A careful work-up, comprising the patient’s history, clinical examination, laboratory tests, thyroid ultrasound, scintigraphy, fine-needle aspiration biopsy (FNAB) and molecular studies, is mandatory to improve the preoperative diagnosis. The differential diagnosis should also include benign thyroid conditions such as: (i) congenital hypothyroidism due to dyshormonogenesis or ectopy, (ii) thyroid hemiagenesis, (iii) thyroglossal duct cyst, (iv) simple goiter, (v) cystic lesion, (vi) nodular hyperplasia, (vii) follicular adenoma, (viii) Graves’ disease and (ix) Hashimoto thyroiditis, all of which can predispose to the development of thyroid nodules. The majority of thyroid carcinomas derive from the follicular cell (papillary, follicular, insular and undifferentiated (or anaplastic) thyroid carcinoma), whereas medullary thyroid carcinoma derives from calcitonin-producing cells. Inherited forms of thyroid cancer may occur, especially in relation to medullary thyroid carcinoma. FNAB is a critical factor in establishing the preoperative diagnosis. However, we should keep in mind the fact that a conventional cytological evaluation can miss the neoplastic nature of a lesion and the employment of immunocytochemical and molecular studies of aspirates from FNAB can give us a more precise diagnosis of neoplasia in thyroid nodules once they are detected.

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Pathogenesis, diagnosis and management of thyroid nodules in children.

Although several authors have reported single cases illustrative of some ultrasonographic characteristic of parathyroid carcinoma, the value of ultrasonography for diagnosing this entity remains to be determined. The purpose of our study was to investigate the ultrasonographic features of parathyroid carcinoma in a large number of cases. We assessed the shape, contour, echogenicity, and depth-width (DW) ratio of 16 parathyroid carcinomas and 61 parathyroid adenomas. Ultrasonography showed that parathyroid carcinomas tend to be large, inhomogeneous, hypoechoic masses with lobulated contours. In contrast, parathyroid adenomas were small, homogeneous, hypoechoic masses with smooth borders. The mean (range) DW ratios for parathyroid carcinomas were 1.21 (0.91-2.5) and 0.64 (0.33-1.47) for adenomas; the difference was statistically significant (p or =1 in 15 (94%) of the 16 cases of carcinoma, whereas only 3 (5%) of the 61 adenomas had a similar ratio. Ultrasonographic examination is useful not only for preoperative localization but also for differentiating parathyroid carcinoma from adenoma. Parathyroid tumors with irregular margins, inhomogeneous echogenicity, and a DW ratio > or =1 are likely to be malignant.

Ultrasonographic Features of Parathyroid Carcinoma

This report examines the charcteristics of 10 patients surgically treated for unequivocal parathyroid carcinoma. Seven cases were from our series of 165 patients with primary hyperparathyroidism. Routine determination of serum calcium level by an automated analyzer occasionally led to early tumor detection. A spectrum of clinical and pathological variation was evident in our series. One of 3 patients with simple tumor resection and 1 of 4 patients with wide local excision in the initial operation showed local recurrence. Regional lymph node metastases without local recurrence occurred in another patient 3 years after the initial wide local resection and he was treated by neck and mediastinal dissections.

Surgical treatment of ten cases of parathyroid carcinoma: importance of an initial en bloc tumor resection.

Purpose: Cancer diagnostics and therapeutics are often based on clinically relevant markers that are expressed specifically in a malignant tissue at levels higher than in normal tissue. We examined potential markers for papillary thyroid carcinoma (PTC) by monitoring PTC-specific gene expression using cDNA microarray. Experimental Design: Gene expression profiles for PTC tissue, normal thyroid tissue, and healthy peripheral blood cells were compared by use of a human 4000-gene cDNA microarray. Protein expressions of the up-regulated genes in PTC were examined in thyroid tissues by immunohistochemistry. Results: Sixty-four genes were overexpressed in PTC tissue relative to normal thyroid tissue and healthy peripheral blood cells. The genes that were up-regulated in PTC were involved in cell cycle regulation, DNA damage response, angiogenesis, and oncogenesis. Among these genes, basic fibroblast growth factor and platelet-derived growth factor were identified by immunochemical methods as proteins that are specifically expressed at high levels in thyroid neoplasms. Basic fibroblast growth factor, which has been identified as a biomarker for PTC, was overexpressed in 54% of PTC cases, 67% of follicular thyroid carcinomas, and 36% of benign thyroid neoplasms. Platelet-derived growth factor was overexpressed in 81% of PTC cases and 100% of follicular carcinomas, but was immunonegative in normal thyroid tissues and benign thyroid neoplasms. Conclusions: Platelet-derived growth factor may be a potential biomarker for PTC and follicular carcinoma. Expression profile analysis using a microarray followed by immunohistochemical study can be used to facilitate the development of molecular biomarkers for cancer.

https://clincancerres.aacrjournals.org/content/clincanres/10/6/2035.full.pdf

Gene Expression Profiling Identifies Platelet-Derived Growth Factor as a Diagnostic Molecular Marker for Papillary Thyroid Carcinoma

Background: a-Fetoprotein (AFP) and prostate-specific antigen (PSA) in serum are widely used as tumor markers in the evaluation of prognosis and management of patients with hepatocellular carcinoma and prostate cancer, respectively. To establish the molecular diagnosis of cancer, reverse transcriptase polymerase chain reaction (RT-PCR) for AFPand PSA was used to identify circulating cancer cells in the blood of cancer patients. Here, we examined the tissue-specificity of AFPand PSA and tested whether AFPand PSA are suitable targets in the detection of certain cancer cells by RT-PCR using peripheral blood samples. Methods: Tissue specificity of AFP and PSA was analyzed by Northern blotting and RT-PCR. Probes for AFPand PSA were hybridized with poly A+ RNAs from 50 human tissues. RT-PCR for AFP and PSA mRNA was performed using several cancerous tissues and normal tissues and peripheral blood cells from seven healthy volunteers. Results: Broad expression of AFP was observed in several tissues and a large amount of AFP mRNA was found in fetal liver. PSA was expressed in prostate, salivary gland, pancreas and uterus. By RT-PCR, AFP and PSA mRNA were detected in several tumors, including salivary pleomorphic adenoma, hilar bile duct carcinoma, pancreatic carcinoma, transitional cell carcinoma of urinary bladder and thyroid papillary carcinoma. Furthermore, AFPand PSA mRNAs were frequently detected by RT-PCR, even in peripheral blood cells from healthy volunteers. Conclusions: Neither AFPnor PSA showed tissue-specific expression. AFPand PSA mRNA were detected in several diseased and non-diseased tissues and normal circulating blood by RT-PCR.

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Expression of alpha-fetoprotein and prostate-specific antigen genes in several tissues and detection of mRNAs in normal circulating blood by reverse transcriptase-polymerase chain reaction.

Yuji Aiyoshi

Papers

Ultrasonographic Features of Parathyroid Carcinoma

Surgical treatment of ten cases of parathyroid carcinoma: importance of an initial en bloc tumor resection.

Gene Expression Profiling Identifies Platelet-Derived Growth Factor as a Diagnostic Molecular Marker for Papillary Thyroid Carcinoma

Expression of alpha-fetoprotein and prostate-specific antigen genes in several tissues and detection of mRNAs in normal circulating blood by reverse transcriptase-polymerase chain reaction.

Effects of α2-adrenergic action on cyclic AMP levels in canine thyroid slices