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S Mark

Publications and source records attributed to S Mark.

At least 19 recordsLinked to original sources
PubMed2001

Fluorescence spectroscopy for detection of malignancy: H-ras overexpressing fibroblasts as a model.

Autofluorescence from intracellular chromophores upon illumination of cells by monochromatic light has been studied towards the development of novel noninvasive and sensitive technology for the early detection of cancer. To investigate the relationship between biochemical and morphological changes underlying malignant disease and resulting fluorescence spectra, an in vitro model system of a paired normal and malignant murine fibroblasts cell lines, differing in cancer-associated H-ras expression was employed. A comparison of fluorescence excitation and emission spectra of proliferative cells revealed that fluorescence intensity of malignant cells was significantly less than that of normal cells upon excitation at 290 nm. Fluorescence of both cell lines decreased with decreasing cell concentration, but at each concentration, normal cells had higher fluorescence intensity than malignant cells. Similar differences between the cell lines were observed when brought to quiescence or at stationary phase. Results suggested that the chromophore contributing most significantly to these spectra is tryptophan and its moieties in proteins. This model system demonstrates the specific contribution of H-ras to subcellular chromophores, resulting in a significant difference in their autofluorescence intensity, and implies the potential use of the technique for cancer detection. This model system is potent for analysis of the contribution of other oncogenes and their combinations towards spectral detection of cancer.

3T3 Cells↗
PubMed2001

Helicobacter pylori seropositivity and subsite-specific gastric cancer risks in Linxian, China.

BACKGROUND: Helicobacter pylori carriage (i.e., persistent exposure to the organism without gastric epithelial cell invasion) is an established risk factor for noncardia gastric cancer. However, its association with the risk of cancer of the gastric cardia is controversial. Consequently, we designed this prospective, nested case-control study to further explore the subsite-specific gastric cancer risks associated with H. pylori seropositivity (a surrogate marker for persistent exposure). METHODS: A total of 99 patients with gastric cardia cancer, 82 patients with noncardia gastric cancer, and 192 cancer-free subjects were selected from among the participants (n = 29 584) of a nutrition intervention trial previously conducted in Linxian, China. H. pylori seropositivity was determined by assaying for the presence of H. pylori whole cell and CagA antibodies in baseline serum samples from all subjects. Seropositivity was defined as one or both serum assays being positive. Odds ratios (ORs) for subsite-specific gastric cancer were estimated by multivariate logistic regression analyses. All statistical comparisons were two-sided (alpha =.05). RESULTS: H. pylori seropositivity rates for subjects with gastric cardia cancer, noncardia gastric cancer, and gastric cardia and noncardia cancers combined were 70% (P =.02), 72% (P: =.01), and 71% (P =.003) compared with 56% for cancer-free control subjects. OR estimates for H. pylori seropositivity were 1.87 (95% confidence interval [CI] = 1.10 to 3.17) for gastric cardia cancer, 2.29 (95% CI = 1.26 to 4.14) for noncardia gastric cancer, and 2.04 (95% CI = 1.31 to 3.18) for gastric cardia and noncardia cancers combined. CONCLUSIONS: H. pylori seropositivity was associated with increased risks for both gastric cardia cancer and noncardia gastric cancer in this well-characterized cohort. Thus, H. pylori carriage may increase the risk of cancer throughout the stomach.

Adenocarcinoma↗
PubMed2001

Computed tomography versus intravenous urography in diagnosis of acute flank pain from urolithiasis: a randomized study comparing imaging costs and radiation dose.

The equivalent sensitivity of non-contrast computed tomography (NCCT) and intravenous urography (IVU) in the diagnosis of suspected ureteric colic has been established. Approximately 50% of patients with suspected ureteric colic do not have a nephro-urological cause for pain. Because many such patients require further imaging studies, NCCT may obviate the need for these studies and, in so doing, be more cost effective and involve less overall radiation exposure. The present study compares the total imaging cost and radiation dose of NCCT versus IVU in the diagnosis of acute flank pain. Two hundred and twenty-four patients (157 men; mean age 45 years; age range 19-79 years) with suspected renal colic were randomized either to NCCT or IVU. The number of additional diagnostic imaging studies, cost (IVU A$136; CTU A$173), radiation exposure and imaging times were compared. Of 119 (53%) patients with renal obstruction, 105 had no nephro-urological causes of pain. For 21 (20%) of these patients an alternative diagnosis was made at the initial imaging, 10 of which were significant. Of 118 IVU patients, 28 (24%) required 32 additional imaging tests to reach a diagnosis, whereas seven of 106 (6%) NCCT patients required seven additional imaging studies. The average total diagnostic imaging cost for the NCCT group was A$181.94 and A$175.46 for the IVU group (P < 0.43). Mean radiation dose to diagnosis was 5.00 mSv (NCCT) versus 3.50 mSv (IVU) (P < 0.001). Mean imaging time was 30 min (NCCT) versus 75 min (IVU) (P < 0.001). Diagnostic imaging costs were remarkably similar. Although NCCT involves a higher radiation dose than IVU, its advantages of faster diagnosis, the avoidance of additional diagnostic imaging tests and its ability to diagnose other causes makes it the study of choice for acute flank pain at Christchurch Hospital.

Adult↗
PubMed2001

Innovative mentoring programs to promote gender equity in academic medicine.

The authors describe the history, characteristics, and goals of four innovative programs, each in a medical school, that were established in 1998 to help faculty members of both sexes obtain mentors and thereby facilitate their career advancement. The programs were established as the result of an initiative by the Office on Women's Health (OWH) within the U.S. Department of Health and Human Services. Specifically, the OWH convened the National Task Force on Mentoring for Health Professionals, which determined that two principles are paramount to the success of any mentoring relationship or program: institutional commitment and institutional rewards and recognition to mentors. In accordance with the task force findings, the OWH created the National Centers of Leadership in Academic Medicine, one at each of four medical schools: MCP Hahnemann School of Medicine; the University of California, San Diego, School of Medicine; East Carolina University School of Medicine; and Meharry Medical College School of Medicine. The authors give highlights of each program's goals and progress, and note that, ideally, these programs will eventually serve as models for similar programs at other schools. Programs such as these foster the advancement of a diverse faculty, a more supportive academic environment, and the education of providers who are sensitive to the needs of all their patients, staff, and colleagues.

Faculty, Medical↗
PubMed2000

Partial IGF affinity of circulating N- and C-terminal fragments of human insulin-like growth factor binding protein-4 (IGFBP-4) and the disulfide bonding pattern of the C-terminal IGFBP-4 domain.

Within the IGF axis, the insulin-like growth factor-binding proteins (IGFBPs) are known to play a pivotal role in cell proliferation and differentiation. Defined proteolysis of the IGFBPs is proposed to be an essential mechanism for regulating IGF bioavailability. The generated IGFBP fragments in part exhibit different IGF-dependent and -independent biological activities. Characterizing naturally occurring forms of IGFBPs in human plasma, we identified both a N- and a C-terminal fragment of IGFBP-4 by means of immunoreactivity screening. As a source for peptide isolation, we used large amounts of human hemofiltrate obtained from patients with chronic renal failure. Purification of the IGFBP-4 peptides from hemofiltrate was performed by consecutive cation-exchange and reverse-phase chromatographic steps. Mass spectrometric and sequence analysis revealed an M(r) of 13 233 for the purified N-terminal fragment spanning residues Asp(1)-Phe(122) of IGFBP-4 and an M(r) of 11 344 for the C-terminal fragment extending from Lys(136) to Glu(237). Proteolytic digestion and subsequent biochemical analysis showed that the six cysteines of the C-terminal IGFBP-4 fragment are linked between residues 153-183, 194-205, and 207-228 (disulfide bonding pattern, 1-2, 3-4, and 5-6). Plasmon resonance spectroscopy, ligand blot analysis, and saturation and displacement studies demonstrated a very low affinity of the C-terminal IGFBP-4 fragment for the IGFs (IGF-II, K(d) = 690 nM; IGF-I, K(d) > 60 nM), whereas the N-terminal fragment retained significant IGF binding properties (IGF-II, K(d) = 17 nM; IGF-I, K(d) = 5 nM). This study provides the first molecular characterization of circulating human IGFBP-4 fragments formed in vivo exhibiting an at least 5-fold decrease in the affinity of the N-terminal IGFBP-4 fragment for the IGFs and a very low IGF binding capacity of the C-terminal fragment.

Amino Acid Sequence↗
PubMed2000

Hypotetraploidy in a patient with small cell carcinoma.

While numerical and structural chromosomal abnormalities characterize many hematopoietic and nonhematopoietic malignancies, the occurrence of polyploidy is by and large rare. We report here an interesting patient with small cell carcinoma (SCC) and hypotetraploidy initially referred to us because of a question of acute nonlymphocytic leukemia, M3 subtype, with a question of a 15;17 translocation characteristic of acute promyelocytic leukemia. However, the patient did not have a 15;17 translocation and the final hematopathologic analysis of the bone marrow aspirates and immunohistochemistry studies subsequently revealed the patient to have SCC. Small cell carcinoma is a highly malignant and a very aggressive neoplasm. A review of the literature, using Medline, Cancerlit, and the Science Citation Index, revealed that in most, if not all, reports, the presence of polyploidy is noted as a rare entity. In leukemia, reports of polyploidy point to a distinct category of patients with a poor risk for which more intensive treatment is needed. Limited information is currently available to assess the risk of polyploidy in small cell carcinoma. Our case is important not only because of the relative rarity of polyploidy, but also because insights gained from the study of this and other similar patients may help shed additional light on the mechanism of carcinogenesis, which is not fully known to date. As polyploidization is a manifestation of genetic instability and as genetic instability has been implicated in the genesis and progression of many cancers, it is perhaps not too surprising that polyploidy in our case was associated with a poor disease outcome. The patient has since expired.

Bone Marrow Neoplasms↗
PubMed2000

Fluorescent in situ hybridization study of c-myc oncogene copy number in prostate cancer.

We previously conducted a study of 88 cases of prostate cancer in an attempt to identify potential prognostic biomarkers that can distinguish aggressive cases that must be treated immediately. Prostate cancer is a serious disease affecting men worldwide and compromises the quality of life of its patients. Biomarkers studied included chromosome 7 trisomy, chromosome 8 trisomy, and HER-2/neu oncogene amplification. These biomarkers were initially studied because trisomy 8 and oncogene amplification of the HER-2/neu gene have been reported in many other cancers, including those studied in this laboratory. In view of the fact that HER-2/neu amplification was not found to play a prominent role in the group of prostate cancer specimens that we studied, an exploration of other biomarkers was felt to be warranted. Thus, we began a pilot study of c-myc oncogene copy number in prostate cancer using the same protocol for fluorescent in situ hybridization and a direct-labeled SpectrumOrange LSI c-myc probe (Vysis, Inc., Downers Grove, IL) on formalin-fixed, paraffin-embedded tissue. From a total of 36 cases of prostate cancers successfully analyzed, we found 11 (31%) tumors exhibiting 3 or more positive signals for c-myc in 15% or more of the cells. Of these, only 7 tumors (19% of the total cases studied) had >/=3 signals in 20% or more of the cells. No case had >/=3 signals in 25% or more of the cells. Compared to other molecular probes tested, the c-myc signals were more faint and the quality of the preparation was less optimal than other tumor specimens that we previously studied. Based on the information available thus far, we conclude that an increased copy number in c-myc oncogene copy number was not a prominent finding in our cohort of prostate cancer patients.

Adenocarcinoma↗
PubMed2000

Distribution of fibrillin I in extracellular matrix and epithelia during early development of avian embryos.

Fibrillin microfibrils are widely distributed components of extracellular matrices that function in the formation of elastin, serve structural roles and provide substrates for cell adhesion. To determine when and how fibrillin-1 (fib-1) may function in early development we have examined the temporal and spatial distribution of fib-1 in chicken embryos. Using homologous PCR we amplified and cloned a 407 nt fragment of chicken cDNA that appears to code for an orthologue of FBN-1. Bacterially expressed protein was used to prepare two monoclonal antibodies, both of which recognize a 350 kD band in immunoblots or immunoprecipitates in supernatants of chicken embryonic aorta cells or human MG-63 cells. Both antibodies recognize fibrillar material associated with the surfaces of cultured cells. The antibodies appear to be specific for fib- as there was only weak cross reactivity to a bacterially expressed fragment from the corresponding region of fib-2 and the pattern of immunofluorescence in embryonic tissue is distinctly different from that of JB-3, a fib-2 specific antibody (Rongish et al. 1998). In embryos, fib-1 is first detected at stage 6 in the epiblast during gastrulation. In subsequent stages fib-1 fibers appear in all tissues and are present throughout the first 6 days of development. Immunoreactive fibers are present in basal laminae and mesenchyme filled spaces, but they also form random arrays with an apical-basal polarity within epithelia. Using primers specific for FBN-1 and FBN-2 in RT-PCR reactions we confirm the presence of fib- 1 and fib-2 mRNA in early embryonic stages. This temporal and spatial distribution indicates fib-1 has functions in early development that are distinct from fib-2.

Amino Acid Sequence↗
PubMed2000

The role of government in postgraduate training programs in women's health.

This paper examines the role of the federal government in postgraduate training programs in women's health. Health care professional education has long been an interest of many agencies within the Department of Health and Human Services. Although federal agencies have not been directly involved in the creation of curriculum or funding of training programs in women's health, they have helped to catalyze wide public and private support of these programs. The Office on Women's Health within the Department of Health and Human Services, the National Institutes of Health Office of Research on Women's Health, and the Health Resources and Services Administration have each provided recommendations for the inclusion of women's health in the medical school curriculum. Additionally, the Council on Graduate Medical Education, an advisory body to the Secretary of Health and Human Services and Congress, has recommended that physicians develop a broad understanding of health conditions specific to women. Although federal funding is not available for the development of training programs in women's health, continued public and private interest will foster the development of post-graduate training programs that will improve the delivery of health care for women in the United States.

Curriculum↗
PubMed1999

Strategy for identifying circulating fragments of insulin-like growth factor binding proteins in a hemofiltrate peptide bank.

A differentiated strategy was established to isolate circulating forms of the six human insulin-like growth factor binding proteins (IGFBPs). As starting material we used our peptide bank, a comprehensive blood plasma peptidoma generated from human blood filtrate. The peptides were initially identified in the fractions of the hemofiltrate peptide bank by their immunoreactivity, their capacity to bind the insulin-like growth factors (IGFs), and their molecular masses determined by polyacrylamide gel electrophoresis and matrix-assisted laser desorption ionization-mass spectrometry (MALDI-MS). Fractions revealing both immunoreactivity and IGF-binding capacity were analyzed by direct sequencing of immunoreactive bands from a Coomassie-stained gel. Further purification of the IGFBP peptides was performed by consecutive chromatographic steps guided by sensitive MALDI-MS. Using this strategy, different fragments of IGFBP-3, -4, and -5 were identified and a fragment of IGFBP-4 was purified to homogeneity.

Amino Acid Sequence↗
PubMed1999

Application of a peptide bank from porcine brain in isolation of regulatory peptides.

Over the past years, the introduction of biological assay systems, random peptide sequencing and orphan receptor screening has led to the isolation and identification of new regulatory peptides with potential clinical impact. We have developed a method for separating peptides into about 300 fractions from large amounts of porcine brain tissue. The preparation of this peptide bank consists of three steps including ultrafiltration followed by cation-exchange separation and reversed-phase chromatography. These fractions represent the peptide bank with desalted and lyophilized peptides from brain tissue. Molecular masses of the peptides in the fractions are determined by matrix-assisted laser desorption ionization MS and a mass data bank is subsequently generated. For systematic analysis of the peptides, a subsequent two-step purification procedure is followed by Edman sequencing resulting in the identification of different peptides. A survival assay with a neuronal cell line revealing the stimulatory and inhibitory activities is applied as a model to test the 300 fractions. This primary screen indicates that the biological activities of the extracted peptides are easily characterized and, moreover, can be related to the biochemical entities. We conclude that the established peptide bank is an efficient and useful tool for the isolation of regulatory brain peptides applying different purification strategies.

Animals↗
PubMed1999

OHIO-1 beta-lactamase mutants: the Arg244Ser mutant and resistance to beta-lactams and beta-lactamase inhibitors.

Mutations at residue 244 (Ambler numbering system) in the class A TEM beta-lactamase confer resistance to inactivation by beta-lactamase inhibitors and result in diminished turnover of beta-lactam substrates. The Arg244Ser mutant of the OHIO-1 beta-lactamase, an SHV family enzyme, demonstrates variable susceptibilities to beta-lactamase inhibitors and has significantly reduced catalytic efficiency. The minimum inhibitory concentrations (MICs) for Escherichia coli DH5alpha expressing the Arg244Ser beta-lactamase were reduced when compared to the strain bearing the OHIO-1 beta-lactamase: ampicillin, 512 vs. 8192 micrograms ml-1; cephaloridine, 4 vs. 32 micrograms ml-1, respectively. The MICs for the beta-lactam beta-lactamase inhibitor combinations demonstrated resistance only to ampicillin-clavulanate, 16/8 vs. 8/4 micrograms ml-1 respectively. In contrast, there was increased susceptibility to ampicillin-sulbactam, ampicillin-tazobactam, and piperacillin-tazobactam. When compared to the OHIO-1 beta-lactamase homogenous preparations of the Arg244Ser beta-lactamase enzyme demonstrated increased Km and decreased kcat values for benzylpenicillin (Km=17 vs. 50 microM, kcat=345 vs. 234 s-1) and cephaloridine (Km=97 vs. 202 microM, kcat=1023 vs. 202 s-1). Although the Ki and IC50 values were increased for each inhibitor when compared to OHIO-1 beta-lactamase, the turnover numbers (tn) required for inactivation were increased only for clavulanate. For the Arg244Ser mutant enzyme of OHIO-1, the increased Ki, decreased tn for the sulfones, and different partition ratio (kcat/kinact) support the notion that not all class A enzymes are inactivated in the same manner, and that certain class A beta-lactamase enzymes may react differently with identical substitutions in structurally conserved amino acids. The resistance phenotype of a specific mutations can vary depending on the enzyme.

Drug Resistance↗
PubMed1999

Trisomy 8 in stage I and stage III ovarian cancer detected by fluorescence in situ hybridization.

Ovarian cancer is the leading cause of death from gynecologic maligancy among women in the United States. In 1997, there were nearly 27,000 ovarian cancer cases with over 14,000 deaths. Recent attempts at early detection of ovarian cancer have been aimed at the identification of biomarkers that would indicate an underlining malignant process or reflect the biological behavior of the tumor. Our previous studies revealed that chromosome 8 copy number abnormality, especially trisomy, is common in several cancers. Archival tissues from 24 cases of papillary serous ovarian carcinoma (10 stage I and 14 stage III) were analyzed by fluorescence in situ hybridization (FISH) with a chromosome 8-specific alpha-satellite probe (Oncor, Gaithersburg, MD). The analysis was done according to standard protocols of the Lifespan Academic Medical Center Cytogenetics Laboratory at Rhode Island Hospital. Twenty-one of 24 cases (87.5%) were found to be trisomic for chromosome 8, if a cutoff point of >/=15% cells with three signals is adopted. Overall, 80% of stage I and 93% of stage III tumors had trisomy 8. This study confirms the presence of a high frequency of trisomy 8 in both early and late stages of the disease and suggests that trisomy 8 may be an early event in the multistep process leading to ovarian cancer. It is of interest to note that a higher frequency of trisomy 8 was found in a higher stage of disease, consistent with our previous results on breast cancer. Thus, additional FISH studies of ovarian tumors for chromosome 8 copy number assessment may be warranted.

Adult↗
PubMed1999

Fluorescence in situ hybridization study of HER-2/neu oncogene amplification in prostate cancer.

Prostate cancer is a serious disease affecting men worldwide and treatment compromises the quality of life of prostate cancer patients. We conducted a study of 88 cases of prostate cancer in an attempt to identify prognostic biomarkers that can distinguish aggressive cases that must be treated immediately. HER-2/neu oncogene amplification was initially studied because amplification of this gene has been reported in many other cancers, including those studied in this laboratory. Fluorescence in situ hybridization (FISH) using a HER-2/neu gene probe with a chromosome 17 centromere control probe was performed on formalin-fixed, paraffin-embedded tissues. Of a total of 86 cases successfully analyzed, only 8 (9.3%) were found to be amplified. This frequency was lower than the frequency of amplification found in other cancers studied. Furthermore, no case was found where the level of amplification can be considered high. Only one case was found to have moderate amplification. The rest of the positive cases can all be classified as low amplification. Thus, while we have demonstrated that FISH is a sensitive technique for detecting oncogene amplification, the frequency and level of HER-2/neu amplification detected in prostate cancer seem to be lower than those in most cancers that we studied. In view of the fact that HER-2/neu amplification does not seem to play as significant a role, exploration of other biomarkers in prostate cancer is warranted.

Aged↗
PubMed1999

A variant Klinefelter syndrome patient with an XXY/XX/XY karyotype studied by GTG-banding and fluorescence in situ hybridization.

Klinefelter syndrome is the first human sex chromosomal abnormality to be reported. The majority of Klinefelter syndrome patients have the XXY karyotype. Approximately 15% of Klinefelter patients, however, are mosaics with variable phenotypes. Among the variant Klinefelter genotypes are such karyotypes as XY/XXY and XX/XXY. The variation in phenotypes most likely depends on the number of abnormal cells and their location in body tissues. In this paper we report the case of a 42-year-old patient with Klinefelter syndrome and a rare variant mosaic XXY/XX karyotype initially identified by GTG-banding. This was confirmed by fluorescence in situ hybridization (FISH) using a dual-color X/Y probe. The patient presented with erectile dysfunction and few other physical findings. Thus, this case illustrates a rare variant of Klinefelter syndrome with a relatively mild phenotype. It also illustrates the utility of FISH as an adjunct to conventional cytogenetics in assessing the chromosome copy number in each cell line of a mosaic. In our case, FISH also detected the presence of a small population of cells with the XY karyotype not previously detected in the initial 30-cell GTG-banding analysis. Thus, through a combination of GTG-banding and FISH, the patient was determined to be an XXY/XX/XY mosaic. Given that most individuals with Klinefelter syndrome are infertile, and that these individuals may wish to reproduce with the aid of modern reproductive technology, such as testicular fine needle aspiration and intracytoplasmic sperm injection, it is important that accurate estimation of the frequency of abnormal cells be obtained for accurate risk estimation and genetic counseling, as recent studies in patients with mosaic Klinefelter syndrome revealed that germ cells with sex chromosomal abnormalities were nevertheless capable of completing meiosis.

Adult↗
PubMed1999

Assessment of chromosome 8 copy number in cervical cancer by fluorescent in situ hybridization.

Cervical carcinoma is a malignancy which typically occurs at the transformation zone between squamous and glandular epithelium. The vast majority falls into two histologic types, squamous cell and adenocarcinoma. In an effort to identify a subset of cervical cancer characterized by chromosome 8 trisomy, a biomarker extensively explored by this laboratory, we conducted a study of formalin-fixed, paraffin-embedded materials of cervical cancer. A total of 24 cases of cervical cancer were identified from the archives of the Rhode Island Hospital. Fluorescent in situ hybridization (FISH) using a chromosome 8 centromere enumeration probe was conducted to assess the chromosome 8 copy number in these specimens. Hybridization signals were scored among tumor cells in a blinded fashion. Tumors with >/=15% of cells with three signals were scored as trisomic. Of 24 cases studied, 23 were informative. Of the 23 informative cases, 12 (52.2%) were found to be trisomic. Eleven cases (47.8%) were disomic. The frequency of trisomy in a control chromosome 17 probe was 13.0% (3/23). Selected clinicopathologic characteristics of the tumors were also reviewed. The frequency of trisomy 8 among cases of invasive squamous cell carcinoma was 44.4% (8 of 18 tumors) and that of invasive adenocarcinoma was 80% (4 of 5 tumors). The sole tumor which was both trisomic 8 and amplified for the HER-2/neu oncogene was found to be an invasive adenocarcinoma. While the sample size in this pilot study is not large, the data obtained thus far clearly demonstrate that FISH is an appropriate technique for detecting chromosomal trisomies and that a subset of cervical cancer exists that is characterized by chromosome 8 trisomy. Further exploration of this biomarker is warranted.

Adenocarcinoma↗
PubMed1999

Assessment of chromosomal trisomies in prostate cancer using fluorescent in situ hybridization.

In a previous study, we observed a low frequency of HER-2/neu oncogene amplification in prostate cancer using fluorescent in situ hybridization (FISH). In our continued effort to identify prognostic biomarkers in prostate cancer, we analyzed 74 cases of prostate cancer to assess the presence of chromosomal trisomies in this cohort of patients. Previous results from this laboratory have implicated a role of chromosomal trisomies in various cancers. FISH using a chromosome 7 and a chromosome 8 centromere probe was utilized to study abnormal chromosome copy numbers together with data from a chromosome 17 control. The frequency of trisomy 7 was found to be 58.1% (43 of 74 informative cases), while the frequency of trisomy 8 was found to be 9.5% (7 of 74 informative cases). The frequency of cells showing chromosome 17 trisomy was 18.5% (15 of 81 cases successfully studied). While chromosome 8 trisomy did not seem to play as significant a role here as in other cancers that we studied, the results of chromosome 7 trisomy are consistent with those reported in the literature. Further exploration of selected trisomies as biomarkers in prostate cancer using a larger study sample size is warranted to establish their clinical utilities.

Aged↗