nature genetics • volume 23 • december 1999 387 The term ‘synteny’ (or syntenic) refers to gene loci on the same chromosome regardless of whether or not they are genetically linked by classic linkage analysis1. This term was introduced in 1971 by John H. Renwick, of the London School of Hygiene and Tropical Medicine, at the 4th Internal Congress of Human Genetics in Paris with one of us (E.P.) in attendance. The need for such a term was suggested to J.H. Renwick by E.A. Murphy, of Johns Hopkins University2. It arose as a consequence of the new methods in gene mapping using somatic cell hybrid cells. Human genes located on the same chromosome with a genetic distance that could not be determined by the frequency of recombination lacked a term of reference. ‘Synteny’ means ‘same thread’ (or ribbon), a state of being together in location, as synchrony would be together in time. Although several textbooks3–10 and other reference works11–15 give a correct definition, the term synteny nowadays is often used to refer to gene loci in different organisms located on a chromosomal region of common evolutionary ancestry. This new usage of the term synteny does not correspond to its original definition and correct language derivation. A survey of 11 articles in Nature Genetics since 1992 using the term syntenic or synteny in either the title or the abstract revealed usage incorrect in 8 and ambiguous in 3. We believe molecular biologists ought to respect the original definition of synteny and its etymological derivation, especially as this term is still needed to refer to genes located on the same chromosome. We recognize the need to refer to gene loci of common ancestry. Correct terms exist: ‘paralogous’ for genes that arose from a common ancestor gene within one species and ‘orthologous’ for the same gene in different species. Eberhard Passarge1, Bernhard Horsthemke1 & Rosann A. Farber2 1Institut für Humangenetik, Universitätsklinikum Essen, Essen, Germany. 2Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA. Correspondence should be addressed to E.P. (e-mail: eberhard.passarge@uni-essen.de).

Analysis of human transcriptomes

A public database, SAGEmap, was created as a component of the Cancer Genome Anatomy Project to provide a central location for depositing, retrieving, and analyzing human gene expression data. This database uses serial analysis of gene expression to quantify transcript levels in both malignant and normal human tissues. By accessing SAGEmap (http://www.ncbi.nlm.nih.gov/SAGE) the user can compare transcript populations between any of the posted libraries. As an initial demonstration of the database’s utility, gene expression in human glioblastomas was compared with that of normal brain white matter. Of the 47,174 unique transcripts expressed in these two tissues, 471 (1.0%) were differentially expressed by more than 5-fold (P < 0.001). Classification of these genes revealed functions consistent with the biological properties of glioblastomas, in particular: angiogenesis, transcription, and cell cycle related genes.

https://cancerres.aacrjournals.org/content/canres/59/21/5403.full.pdf

A public database for gene expression in human cancers.

Lung cancer is the most common cause of cancer death in developed countries. The prognosis is poor, with less than 15% of patients surviving 5 years after diagnosis. The poor prognosis is attributable to lack of efficient diagnostic methods for early detection and lack of successful treatment for metastatic disease. Most patients (>75%) present with stage III or IV disease and are rarely curable with current therapies. Within the last decade, rapid advances in molecular biology, pathology, bronchology, and radiology have provided a rational basis for improving outcome. These advancements have led to a better documentation of morphological changes in the bronchial epithelium before development of clinical evident invasive carcinomas. This has changed our concept of lung carcinogenesis and emphasized the multistep carcinogenesis approach on several levels. Combined with the technical developments in bronchoscopic techniques, e.g., laser-induced fluorescence endoscope (LIFE) bronchoscopy, we now have improved methods to localize preinvasive and early-invasive bronchial lesions. With the LIFE bronchoscope, a new morphological entity (angiogenic squamous dysplasia) has been recognized, which might be an important biomarker and target for antiangiogenic chemopreventive agents. To reduce the mortality of lung cancer, these new technologies have been taken into the clinic in different scientific settings. The use of low-dose spiral computed tomography in the screening of a high-risk population has demonstrated the possibility of diagnosing small peripheral tumors that are not seen on conventional X-ray. A shift in the therapeutic paradigm from targeting advanced clinically manifest lung cancer toward asymptomatic preinvasive and early-invasive cancer is occurring. The present article reviews the recent advances in the diagnosis of preinvasive and early-invasive cancer to identify biomarkers for early detection of lung cancer and for chemoprevention studies.

https://clincancerres.aacrjournals.org/content/clincanres/7/1/5.full.pdf

Early Detection of Lung Cancer: Clinical Perspectives of Recent Advances in Biology and Radiology

Discovery of Inhibitors that Elucidate the Role of UCH-L1 Activity in the H1299 Lung Cancer Cell Line

Comprehensive gene expression profile of LPS-stimulated human monocytes by SAGE

We used the serial analysis of gene expression (SAGE) method to systematically analyze transcripts present in non-small cell lung cancer. Over 226,000 SAGE tags were sequence analyzed from two independent primary lung cancers and two normal human bronchial/tracheal epithelial cell cultures. A total of 226,000 SAGE tags were sequence identified, representing 43,254 unique transcripts. Comparison of the tags present in the tumor with those identified in the normal tissue revealed 175 transcript tags that were overrepresented in the normal tissue and 142 tags that were overexpressed in the tumor by 10-fold or more. Northern hybridization was performed on 15 of the most abundantly expressed tags identified in the tumors. These tags were derived from either a known gene or a matched expressed sequence tag clone. The transcripts for 3 of the 15 genes, PGP 9.5, B-myb, and human mutT, were abundantly expressed in primary lung cancers (10 of 18, 15 of 18, and 6 of 12 tumors, respectively). In contrast, the presence of PGP9.5 and B-myb was much less frequent in primary tumors derived from other tissue origins. These results suggest that at least a portion of the transcripts identified by SAGE are frequently associated with lung cancer, and that their overexpression may contribute to lung tumorigenesis. The identification and further characterization of genes generated by SAGE should provide potential new targets for the diagnosis, prognosis, and therapy of lung cancer.

/pdf/serial-analysis-of-gene-expression-in-non-small-cell-lung-3m3g2eyulk.pdf

Serial Analysis of Gene Expression in Non-Small Cell Lung Cancer

Vectors and vector systems are embodied that include a gene encoding a tumor suppressor protein. In one embodiment, the vector includes a gene encoding a tumor suppressor protein and an inducible promoter controlling the gene encoding a tumor suppressor protein. The tumor suppressor protein may be p53 protein. In another embodiment, there is provided a vector system which comprises a first vector including a gene encoding a tumor suppressor protein, and a second vector containing a nucleic acid sequence encoding an antisense sequence complementary to all or a portion of the gene encoding a tumor suppressor protein. In yet another embodiment, there is provided a vector system which comprises a first vector including a gene encoding a tumor suppressor protein, and a second vector containing a gene which encodes a protein which binds to, and thereby inhibits, the tumor suppressor protein. Such vectors and vector systems enable cells transformed thereby to continue to proliferate such that adequate amounts of infectious viral particles, generated from viral vectors including a gene encoding a tumor suppressor protein, can be harvested for administration to patients.

Vectors and vector systems including genes encoding tumor suppressor proteins and producer cells transformed thereby

Secreted alpha amidating enzymes are generated by specific posttranslational processing of precursors containing transmembrane domains.

This invention provides compositions and methods for the identification of lung cancer cells. In particular, polynucleotide sequences whose presence is indicative of lung cancer are disclosed. In addition, lung cancer can be identified by detecting the presence of the peptides encoded by these sequences. Antibodies to these peptides are also provided. Also included are gene delivery vehicles and host cells comprising these polynucleotides. Kits containing agents and instructions necessary to perform the screening and detecting methods are also provided.

Compositions and methods for the identification of lung tumor cells

Transcriptionally regulated growth-response genes play a pivotal role in the determination o a cell's fate. p53 is known to transcriptionally regulate genes important in regulating cell growth potential. Using differential RT-PCR analysis of rat embryo fibroblast cells containing a temperature-sensitive p53 allele, we were able to isolate several transcripts upregulated specifically in cells harboring the wild-type p53 protein. Two of these genes, SM20 and microsomal epoxide hydrolase (mEH), are previously described genes. Two previously uncharacterized cDNA's, cell growth regulatory (CGR) genes CGR11 and CGR19, were isolated. The predicted amino acid sequences of these novel proteins contain known motifs; EF-hand domains (CGR11) and a ring-finger domain (CGR19), are suggestive of function. CGR11 and CGR19 appear to be primary response genes expressed at 0.05 % and 0.01 % of the total mRNA in wild-type p53 cells. Both CGR11 and CGR19 as well as SM20 and mEH, are able to inhibit growth of several cell lines.

Cell growth regulatory genes

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