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Cancer Detection and Prevention Volume 22 / Issue 5 (Sep-Oct 1998)Table of Contents and Editor's NotesThe peer review process occasionally results in approval of controversial publications that do not necessarily reflect the viewpoint of the editors. Readers of the journal are encouraged to critically review and comment on presented data by submitting a "Letter to the Editor" that may be reprinted in a subsequent issue. Genetic Instability and Chromosomal Aberrations in Colorectal Cancer: A Review of the Current ModelsTwo mechanisms that may lead to genomic instability. One involves loss of nuclear chromosomal fragments; the other is characterized by microsatellite instability. Generally carcinogenesis depends upon multiple mutations of growth regulatory genes; multistep carcinogenesis evolves from accumulation of specific genetic lesions. >>> Genetic Abnormalities and Microsatellite Instability in Colorectal CancerIn 63 cases of resected colorectal adenocarcinomas 46% showed microsatellite instability for one or more loci. Molecular markers such as k-ras mutation, c-myc mRNA overexpression and p54 mutation were used either as prognostic indicators or to determine the metastatic potential of colorectal adenocarcinomas. >>> Epidemiology of Sociodemographic characteristics, lifestyle, Medical History and Colon Cancer: A Case-Control Study Among French Canadians in MontrealIncreased risks of colon cancer were associated with a positive family history of colon cancer, never-married status, decreased physical activity, increased weight and constipation. >>> Expression of Lymphomagenic Oncogenes in T-Cell Lymphomas of Hpv 16 Transgenic MiceOne of the two oncogenic pathways to tumors in HPV16 transgenic mice had E6/E7 and c-myc expression. The other pathway involved E2 and lymphomagenic oncogenes. E6 expression may result in oncogenesis by binding and degradation of p53. E7 may bind Rb gene and inactivate Rb suppressor function with activation of c-myc expression, leading to HPV16 tumorigenesis. In 23 T-cell lymphomas, 10 of 17 animal tumors expressed E2 as well as E6/E7; 4 tumors expressed E2 only and 3 tumors expressed E6/E7 only. >>> Cytokeratin Markers in Malignant Pleural MesotheliomaIn 95 patients tissue polypeptide-specific antigens (TPS) and cytokeratin 19 fragments (CYFRA 21-1) were significantly higher in malignant pleural mesothelioma (MPM), pulmonary squamous cell carcinomas (SQC) and adenocarcinoma (AC) than in benign lung and pleural diseases (BLPD). The TPS levels were significantly higher in MPM than in SQC. The main markers were CYFRA 21-1 for SQC and CEA for AC. The combination of CYFRA 21-1 and CEA offered a marker with the highest specificity. >>> Predictive Value of Molecular Alterations for the Prognosis of Urothelial CarcinomaIn 52 patients with progressive urothelial carcinoma, p53 accumulation was associated with recurrent tumors in 73% of the cases. p53 accumulation correlated significantly with tumor grade. In superficial urothelial tumors, c-myc overexpression occurred more frequently than p53 accumulation with the exception of carcinoma in situ. However c-myc overexpression did not discriminate between benign and aggressive urothelial tumor growth. >>> Rapid Increase in Diagnosis of Cutaneous Melanoma in Situ in Sweden 1968-1992In Sweden the average annual percentage increase in incidence rates of malignant melanoma in situ during 1968 to 1992 was 15% in men and 12.8% in women. This exceeded, by far, the trend of invasive malignant melanoma, which increased yearly by 4.9% and 3.7% respectively. Age-specific rates increased from 1978 onwards, especially in men aged 45 years or older, whereas the rates in women increased in all ages. >>> Interstitial Collagenase and the Ed-B Oncofetal Domain of Fibronectin are Markers of Angiogenesis in Human Skin TumorsBlood vessels in normal adult human skin were negative for fibronectin (Fn-f) and for collagenase-1 (C1), the predominant matrix metalloproteinase. In aggressive skin tumors and squamous cell carcinomas, angiogenesis was associated with a marked increase in the number of C1 and Fn-f positive microvessels. >>> Viral and Non-Viral Gene Delivery Vectors for Cancer Gene TherapyInfection of cells with recombinant adenovirus (Adv) carrying the gene for the tumor suppressor p53 (Adv/p53) was carried out by injection of subcutaneous H1299 tumors. A significant inhibition of growth occurred during and immediately after treatment, compared to tumors injected with PBS or with the replication-defective adenovirus d1312. A higher level of tumor growth inhibition and increased gene transduction fo the tumor was obtained by pretreatment of the cells with the DNA-damaging agent cisplatin. >>> The Role of Protein Glycosylation Inhibitors in the Prevention of Metastasis and Therapy of CancerThe indolizidine alkaloid swainsonine, produced by a variety of plants and fungi, was used for treatment of tumor bearing mice. A reduction in solid tumor growth and metastasis was observed in several tumor cell types. Although swainsonine blocked the cytotoxicity of various chemotherapeutic agents, murine tumors remained sensitive to chemotherapy. >>> Phorbol Ester Synergizes the Dimethyl Sulfoxide-Dependent Programmed Cell Death Through Diacyiglycerol IncrementThe dimethyl sulfoxide (DMSO) induced cell death of RPMI 8402 thymic lymphoma cells was increased by phorbol ester acetate (PMA) supplementation. The association between PMA and DMSO treatment provided an early activation of an intracellular signaling mechanism that resulted through sustained diacylglycerol (DAG) elevation in a long-term protein kinase (PKC) activation. DMSO treatment produced an accumulation of cells in the G1 phase with a decrease in the S phase. In DMSO/PMA-cotreated cells, the newly synthesized DAG resulted in an enhanced apoptotic effect. >>> Nucleosome-Releasing Treatment Makes Surviving Tumor Cells Better Targets for Nucleosome-Specific Anticancer AntibodiesDexamethasone or vincristine induced partial death of S49 T lymphoma cells. The subsequent release of intact surface bound nucleosomes (NSs) from dead tumor cells into the extracellular space resulted in a 50-fold increase in the anticancer effect of the monoclonal antibody (MoAb2C5) binding to the surface of surviving S49 cells. >>> Apoptosis and Other Mechanisms in Androgen Ablation Treatment and Androgen Independent Progression of Prostate Cancer: A ReviewAmong apoptosis-associated oncoproteins c-myc, p53 and in particular Bcl-2 may be of importance in the regulation of prostate apoptosis as well as androgen-independent progression of prostate cancer (PC). Overexpression of c-myc may induce proliferation in the presence of growth factor and apoptosis in its absence. Bcl-2 expression confers androgen independence in experimental PC models and may significantly contribute to androgen independent progression in PC patients. >>>
Herbert E. Nieburgs, MD |
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