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PubMed1997

A testicular antigen aberrantly expressed in human cancers detected by autologous antibody screening.

Serological analysis of recombinant cDNA expression libraries (SEREX) using tumor mRNA and autologous patient serum provides a powerful approach to identify immunogenic tumor antigens. We have applied this methodology to a case of esophageal squamous cell carcinoma and identified several candidate tumor targets. One of these, NY-ESO-1, showed restricted mRNA expression in normal tissues, with high-level mRNA expression found only in testis and ovary tissues. Reverse transcription-PCR analysis showed NY-ESO-1 mRNA expression in a variable proportion of a wide array of human cancers, including melanoma, breast cancer, bladder cancer, prostate cancer, and hepatocellular carcinoma. NY-ESO-1 encodes a putative protein of Mr 17,995 having no homology with any known protein. The pattern of NY-ESO-1 expression indicates that it belongs to an expanding family of immunogenic testicular antigens that are aberrantly expressed in human cancers in a lineage-nonspecific fashion. These antigens, initially detected by either cytotoxic T cells (MAGE, BAGE, GAGE-1) or antibodies [HOM-MEL-40(SSX2), NY-ESO-1], represent a pool of antigenic targets for cancer vaccination.

Amino Acid Sequence↗
PubMed1993

Increased immunodetection of acidic fibroblast growth factor in bladder cancer, detectable in urine.

Acidic fibroblast growth factor is a regulatory peptide involved in cell proliferation, differentiation and motility. We used a polyclonal antiserum raised against purified native bovine acidic fibroblast growth factor, with no cross-reactivity for basic fibroblast growth factor to detect acidic fibroblast growth factor in tissue extracts and urine samples by means of a competitive enzyme immunoassay. Histochemical analysis was also performed on 10 specimens of normal urothelium and 50 of bladder cancer. Acidic fibroblast growth factor immunoreactive material was found in normal urothelium (1.77 +/- 2 ng./gm. tissue) and was increased more than 10-fold in patients with transitional cell carcinoma of the bladder (20.36 +/- 12 ng./gm. tissue). Immunohistochemical analysis localized immunoreactivity in the epithelial compartment of bladder tumors. Acidic fibroblast growth factor was assayed in urine from 579 individuals comprising a control group (114) and patients with benign prostatic hypertrophy (133), carcinoma of the prostate (96) or transitional cell carcinoma of the bladder (236). There was a significant difference in the frequency of urinary acidic fibroblast growth factor detection among the patients with invasive transitional cell carcinoma, the control group (p < 0.001) and the patients with prostatic disease (p < 0.01). The sensitivity was 72% and the specificity was 91%. Furthermore, the frequency of acidic fibroblast growth factor detection by enzyme immunoassay in the urine and the intensity of immunostaining was correlated with the stage of the disease. These data strongly suggest that acidic fibroblast growth factor is a potential marker for bladder tumors that may be of use in the noninvasive followup of patients with bladder cancer. We present a simple and reliable enzyme immunoassay for the detection of acidic fibroblast growth factor in voided urine that might be useful to quantitate this marker.

Biomarkers, Tumor↗
PubMed2003

The probability of malignancy in small pulmonary nodules coexisting with potentially operable lung cancer detected by CT.

The aim of this study was to assess the probability of malignancy in one or two small nodules 1 cm or less coexisting with potentially operable lung cancer (coexisting small nodules). The preoperative helical CT scans of 223 patients with lung cancer were retrospectively reviewed. The probability of malignancy of coexisting small nodules was evaluated based on nodule size, location, and clinical stage of the primary lung cancers. Seventy-one coexisting small nodules were found on conventional CT in 58 (26%) of 223 patients, and 14 (6%) patients had malignant nodules. Eighteen (25%) of such nodules were malignant. The probability of malignancy was not significantly different between two groups of nodules larger and smaller than 0.5 cm ( p=0.1). The probability of malignancy of such nodules within primary tumor lobe was significantly higher than that in the other lobes ( p<0.01). Metastatic nodules were significantly fewer in clinical stage-IA patients than in the patients with the other stage ( p<0.01); however, four (57%) of seven synchronous lung cancers were located in the non-primary tumor lobes in the clinical stage-I patients. Malignant coexisting small nodules are not infrequent, and such nodules in the non-primary tumor lobes should be carefully diagnosed.

Adult↗
PubMedDate not supplied

Evaluation of a series of new 99mTc-labeled bombesin-like peptides for early cancer detection.

Bombesin (BN) is a peptide exhibiting a high affinity for the gastrin-releasing peptide (GRP) receptor, which is overexpressed by a variety of tumors, including breast or prostate cancer. The aim of the present study was the investigation of the complexes formed between a series of BN-like peptides and the nuclides (185/187)Re and 99mTc. The (185/187)Re complexes were formed via the precursor Regluconate. The radiolabeling of the derivatives with 99mTc was performed using either 99mTc-gluconate or 99mTc-MDP as the intermediate complex. For the in vitro evaluation of the new peptides, the cancer cell line PC3 was used. The in vivo behavior of the 99mTc-labeled BN-like peptides was evaluated in normal mice. All the derivatives showed specific uptake in the pancreas, an organ rich in BN receptors and high affinity for the cancer cell line PC3. The above preliminary results indicated that the new BN derivatives are promising for human cancer studies.

Adenocarcinoma↗
PubMed2005

Significant involvement of chromosome 13q deletions in progression of larynx cancer, detected by comparative genomic hybridization.

Head and neck squamous cell carcinoma (HNSCC) is a heterogeneous group of tumours with various clinical characteristics. These tumours generally exhibit complex karyotypes. Few studies of genomic imbalances have been performed exclusively in subgroups of larynx cancer samples at different stages of the disease. In the present study, chromosomal gains and losses were investigated in 52 larynx tumours, by using comparative genomic hybridization (CGH). The mean number of observed alterations was 37.7 per tumour. The most common sites of losses were 1p, 13q, Xp, and the most common gains were located in 1p, 9q, 16q. The overall number of gains was negatively associated with cancer grading. G1 tumours were also characterized by a higher frequency of deletions in 13q32 and amplifications in 1q23, than tumours in other grades (p < 0.05). The frequency of losses of 13q22 also positively associated with tumour size. There was no association between the frequency of losses in 13q and the presence of lymph node metastases at the time of diagnosis. Another statistically significant association was observed for gains at 1q22-23 and tumour size (p < 0.01). No statistically significant difference in the frequency of most common imbalances was detected between primary tumours with lymph node metastases and those without metastases. In conclusion, we discovered a significant involvement of 13q deletions in the progression of larynx cancer. All the other significant changes observed in the present study were reported previously as being important for HNSCC progression. It seems that multiple genes are disrupted in the process of neoplastic transformation in the larynx, and the networks of events remain to be elucidated.

Carcinoma, Squamous Cell↗
PubMed2001

Differentiation of mammographically suspicious lesions: evaluation of breast ultrasound, MRI mammography and electrical impedance scanning as adjunctive technologies in breast cancer detection.

AIM: Various modalities are used as an adjunct to mammography for differentiation of potentially suspicious breast lesions. Electrical impedance scanning (EIS) is a new technique based upon the principle that cancer cells exhibit altered local dielectric properties and thus show measurably higher conductivity values. The accuracy of differentiation of benign and malignant breast lesions was evaluated to determine whether EIS duplicates or supplements the results obtainable from ultrasound (US) or magnetic resonance imaging (MRI). MATERIALS AND METHODS: One hundred mammographically suspicious lesions were examined using US, MRI and EIS. Definitive histology was acquired through either lesion biopsy or surgical excision. RESULTS: Fifty of 62 malignant lesions were correctly identified using EIS (81% overall sensitivity), 24/38 benign lesions were correctly identified as benign (63% specificity). Negative predictive value and positive predictive value of 67 and 78% were observed, respectively. kappa-factor evaluation revealed a value of 0.82 between MRI and EIS and 0.62 between US and EIS. CONCLUSIONS: EIS may be a valuable adjunct for differentiation of suspicious mammographic lesions. Based upon the calculated kappa-factor, EIS results supplement US examinations. Artifacts (superficial skin lesions, poor contact, air bubbles) currently result in the high false-positive rate of EIS.

Breast Neoplasms↗
PubMed2002

Fruit and vegetable intakes and the risk of colorectal cancer in the Breast Cancer Detection Demonstration Project follow-up cohort.

BACKGROUND: Recent findings have cast doubt on the hypothesis that high intakes of fruit and vegetables are associated with a reduced risk of colorectal cancer. OBJECTIVE: In a large prospective cohort of women, we examined the association between fruit and vegetable intakes and colorectal cancer. DESIGN: Between 1987 and 1989, 45490 women with no history of colorectal cancer satisfactorily completed a 62-item Block-National Cancer Institute food-frequency questionnaire. During 386142 person-years of follow-up, 314 women reported incident colorectal cancer, searches of the National Death Index identified an additional 106 colorectal cancers, and a match with state registries identified another 65 colorectal cancers for a total of 485 cases. We used Cox proportional hazards regression analysis to estimate the relative risks (RRs) and 95% CIs in both energy-adjusted and fully adjusted models. RESULTS: In models using the multivariate nutrient-density model of energy adjustment, RRs for increasing quintile of fruit consumption indicated no significant association with colorectal cancer [RR (95% CI)]: 1.00 (reference), 0.94 (0.70, 1.26), 0.85 (0.63, 1.15), 1.07 (0.81, 1.42), and 1.09 (0.82, 1.44). For vegetable consumption, there was also no significant association in the multivariate nutrient-density model with increasing quintiles of consumption: 1.00 (reference), 0.77 (0.58, 1.02), 0.83 (0.63, 1.10), 0.90 (0.69, 1.19), and 0.92 (0.70, 1.22). Additionally, 3 alternative models of energy adjustment showed no significant association between increases in vegetable intake and the risk of colorectal cancer. CONCLUSION: Although the limitations of our study design and data merit consideration, this investigation provides little evidence of an association between fruit and vegetable intakes and colorectal cancer.

Cohort Studies↗
PubMed2005

Lymph node metastasis in patients with clinical early-stage cervical cancer: detection with integrated FDG PET/CT.

PURPOSE: To prospectively determine the accuracy of combination positron emission tomography-computed tomography (PET/CT) in lymph node staging in patients with early-stage cervical cancer, with histopathologic results as the reference standard. MATERIALS AND METHODS: The study was institutional review board approved, and all patients gave informed consent. Forty-seven consecutive women aged 29-71 years with clinical stage IA or IB cervical carcinoma were included in the study. All 47 patients were scheduled for radical hysterectomy with pelvic lymph node dissection. Before surgery, all patients underwent fluorine 18 fluorodeoxyglucose (FDG) PET/CT. PET/CT findings were interpreted by two readers in consensus and then compared with histopathologic results. At histopathologic examination, the dissected lymph nodes were classified as nonmetastatic or metastatic. RESULTS: Fifteen (32%) patients had metastatic lymph nodes at histopathologic examination, and 32 (68%) had no histopathologically confirmed nodal metastasis. Of the total 1081 lymph nodes histopathologically sampled, 18 were found to be positive for malignant cells. The overall node-based sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), and accuracy of PET/CT were 72% (13 of 18), 99.7% (1060 of 1063), 81% (13 of 16), 99.5% (1060 of 1065), and 99.3% (1073 of 1081), respectively. Corresponding values for PET/CT-based diagnosis of lymph nodes larger than 0.5 cm in diameter were 100% (13 of 13), 99.6% (675 of 678), 81% (13 of 16), 100% (675 of 675), and 99.6% (688 of 691), respectively. The overall patient-based sensitivity, specificity, PPV, NPV, and accuracy of PET/CT were 73% (11 of 15), 97% (31 of 32), 92% (11 of 12), 89% (31 of 35), and 89% (42 of 47), respectively. CONCLUSION: PET/CT proved to be valuable for lymph node staging in patients with early-stage cervical cancer, with short-axis diameter greater than 0.5 cm being the size threshold for accurate depiction of metastatic nodes.

Adult↗
PubMed1996

Genetic alterations in untreated metastases and androgen-independent prostate cancer detected by comparative genomic hybridization and allelotyping.

A newly developed method of comparative genomic hybridization (CGH) employing quantitative statistical comparisons was applied to DNA from two different types of advanced prostate cancer tissue. Multiple CGH analyses were obtained for each chromosome in each tumor, and the results of point-by-point comparison of the mean tumor:normal color ratio to a control normal:normal color ratio in each of 1247 evenly distributed data channels constituting the entire human genome were interpreted as loss, gain, or no change in copy number in the tumor genome. Group I tissue was obtained from prostate cancer metastases from 20 patients, 19 of whom had received no prior prostate cancer treatment. This DNA also was analyzed by Southern and microsatellite allelotyping at 53 different loci on 20 different chromosome arms. CGH results agreed with allelotyping results at 92% of the informative loci studied. These samples, which contained highly enriched tumor DNA, showed the highest rates of alteration yet reported in several chromosomal regions known to be altered frequently in prostate cancer: 8q gain (85%), 8p loss (80%), 13q loss (75%), 16q loss (55%), 17p loss (50%), and 10q loss (50%). Group II tissue was obtained predominately from primary or recurrent tumor from 11 patients who had been treated with long-term androgen-deprivation therapy and developed androgen-independent metastatic disease. Quantitative CGH analysis on DNA from these tissues showed chromosomal alterations that were very similar to those found in group I, suggesting that untreated metastatic tumors contain the bulk of chromosomal alterations necessary for recurrence to occur during androgen deprivation. In the entire data set, a number of previously undetected regions of frequent loss or gain were identified, including losses of chromosomes 2q (42%), 5q (39%), 6q (39%), and 15q (39%) and gains of chromosomes 11p (52%), 1q (52%), 3q (52%), and 2p (45%). Chi-squared analysis showed a significantly higher frequency of gain of the 4q25-q28 region in tumors from African-American patients, indicating a possible oncogene whose activation may play a role in the higher rate of progression seen in this ethnic group. Additional study of these frequently altered regions may provide insight into the mechanism of prostate cancer progression and lead to important tools for tumor-specific prognosis and therapy.

Adult↗
PubMed2003

Single nucleotide polymorphism of the human kallikrein-2 gene highly correlates with serum human kallikrein-2 levels and in combination enhances prostate cancer detection.

PURPOSE: We examined the relationship between a mutant (T) for wild-type (C) allele substitution of the human kallikrein-2 gene (KLK2), circulating human kallikrein-2 (hK2) levels and prostate cancer risk. PATIENTS AND METHODS: We studied 1,287 consecutive men who underwent prostate biopsies because of an abnormal prostate-specific antigen level. Serum and DNA were obtained before biopsy. Cases were patients with cancer, and controls were patients with no cancer. The mutant and wild-type alleles of the KLK2 gene were designated as the T and C alleles, respectively. RESULTS: Of the 1,287 men, 616 had cancer, and 671 had no cancer. The overall distribution of the CC, CT, and TT KLK2 genotypes was 55.1%, 38.2%, and 6.8%, respectively. The median hK2 levels for men with the CC, CT, and TT genotypes were 0.24, 0.18, and 0.062 ng/mL and correlated with the genotypes, respectively (P =.0001). The adjusted odds ratios for prostate cancer for patients with the TT and CT genotypes compared with patients with the CC genotype, were 2.13 (95% confidence interval [CI], 1.3 to 3.5; P =.004) and 1.51 (95% CI, 1.2 to 2.0; P =.002), respectively. The adjusted odds ratio for prostate cancer for patients in the fourth quartile of hK2 compared with the first quartile was 4.33 (95% CI, 2.9 to 6.4; P =.0001). When combined, the adjusted odds ratio for having prostate cancer was 13.92 (95% CI, 6.6 to 29.2; P =.0001) for patients with high hK2 levels and at least one T allele. CONCLUSION: The C/T polymorphism of the KLK2 gene and circulating levels of hK2 are correlated and, in combination, are highly predictive for prostate cancer.

Adenocarcinoma↗
PubMed2004

High-resolution serum proteomic features for ovarian cancer detection.

Serum proteomic pattern diagnostics is an emerging paradigm employing low-resolution mass spectrometry (MS) to generate a set of biomarker classifiers. In the present study, we utilized a well-controlled ovarian cancer serum study set to compare the sensitivity and specificity of serum proteomic diagnostic patterns acquired using a high-resolution versus a low-resolution MS platform. In blinded testing sets, the high-resolution mass spectral data contained multiple diagnostic signatures that were superior to the low-resolution spectra in terms of sensitivity and specificity (P<0.00001) throughout the range of modeling conditions. Four mass spectral feature set patterns acquired from data obtained exclusively with the high-resolution mass spectrometer were 100% specific and sensitive in their diagnosis of serum samples as being acquired from either unaffected patients or those suffering from ovarian cancer. Important to the future of proteomic pattern diagnostics is the ability to recognize inferior spectra statistically, so that those resulting from a specific process error are recognized prior to their potentially incorrect (and damaging) diagnosis. To meet this need, we have developed a series of quality-assurance and in-process control procedures to (a) globally evaluate sources of sample variability, (b) identify outlying mass spectra, and (c) develop quality-control release specifications. From these quality-assurance and control (QA/QC) specifications, we identified 32 mass spectra out of the total 248 that showed statistically significant differences from the norm. Hence, 216 of the initial 248 high-resolution mass spectra were determined to be of high quality and were remodeled by pattern-recognition analysis. Again, we obtained four mass spectral feature set patterns that also exhibited 100% sensitivity and specificity in blinded validation tests (68/68 cancer: including 18/18 stage I, and 43/43 healthy). We conclude that (a) the use of high-resolution MS yields superior classification patterns as compared with those obtained with lower resolution instrumentation; (b) although the process error that we discovered did not have a deleterious impact on the present results obtained from proteomic pattern analysis, the major source of spectral variability emanated from mass spectral acquisition, and not bias at the clinical collection site; (c) this variability can be reduced and monitored through the use of QA/QC statistical procedures; (d) multiple and distinct proteomic patterns, comprising low molecular weight biomarkers, detected by high-resolution MS achieve accuracies surpassing individual biomarkers, warranting validation in a large clinical study.

Biomarkers, Tumor↗
PubMed1987

Breast cancer detection centers and case-control studies of the efficacy of screening.

Case-control studies of screening efficacy have been proposed as a cost- and time-efficient alternative to randomized controlled trials. Possible source populations for such retrospective studies of breast cancer screening are considered, including women from (i) pre-existing randomized trials, (ii) non-experimental population-based studies and (iii) detection centers. On practical grounds women attending detection centers are seen to comprise the most readily accessible source of adequate numbers of cases and controls. Potential biases are addressed, involving incomplete case ascertainment, self-selection, and different screening recommendations. Data from the Guttman Breast Diagnostic Institute are used for illustration.

Age Factors↗
PubMed2006

Signs of positive selection of somatic mutations in human cancers detected by EST sequence analysis.

BACKGROUND: Carcinogenesis typically involves multiple somatic mutations in caretaker (DNA repair) and gatekeeper (tumor suppressors and oncogenes) genes. Analysis of mutation spectra of the tumor suppressor that is most commonly mutated in human cancers, p53, unexpectedly suggested that somatic evolution of the p53 gene during tumorigenesis is dominated by positive selection for gain of function. This conclusion is supported by accumulating experimental evidence of evolution of new functions of p53 in tumors. These findings prompted a genome-wide analysis of possible positive selection during tumor evolution. METHODS: A comprehensive analysis of probable somatic mutations in the sequences of Expressed Sequence Tags (ESTs) from malignant tumors and normal tissues was performed in order to access the prevalence of positive selection in cancer evolution. For each EST, the numbers of synonymous and non-synonymous substitutions were calculated. In order to identify genes with a signature of positive selection in cancers, these numbers were compared to: i) expected numbers and ii) the numbers for the respective genes in the ESTs from normal tissues. RESULTS: We identified 112 genes with a signature of positive selection in cancers, i.e., a significantly elevated ratio of non-synonymous to synonymous substitutions, in tumors as compared to 37 such genes in an approximately equal-sized EST collection from normal tissues. A substantial fraction of the tumor-specific positive-selection candidates have experimentally demonstrated or strongly predicted links to cancer. CONCLUSION: The results of EST analysis should be interpreted with extreme caution given the noise introduced by sequencing errors and undetected polymorphisms. Furthermore, an inherent limitation of EST analysis is that multiple mutations amenable to statistical analysis can be detected only in relatively highly expressed genes. Nevertheless, the present results suggest that positive selection might affect a substantial number of genes during tumorigenic somatic evolution.

Amino Acid Sequence↗
PubMed2002

Bombesin receptor subtypes in human cancers: detection with the universal radioligand (125)I-[D-TYR(6), beta-ALA(11), PHE(13), NLE(14)] bombesin(6-14).

PURPOSE: Bombesin and bombesin receptors have been shown to play a role in cancer. Whereas the gastrin-releasing peptide (GRP) receptor is a bombesin receptor subtype frequently expressed by tumors, the other three subtypes, the neuromedin B (NMB), BB3, and BB4 receptors, have been poorly investigated in human tissues. EXPERIMENTAL DESIGN: We investigated 161 human tumors for their bombesin receptor subtype expression using in vitro receptor autoradiography with the universal bombesin radioligand (125)I-[D-Tyr(6), beta-Ala(11), Phe(13), Nle(14)]bombesin(6-14) in displacement experiments with unlabeled GRP, bombesin, NMB, and [D-Tyr(6), beta-Ala(11), Phe(13), Nle(14)]bombesin(6-14). The distinct rank order of potencies of these analogues for each receptor subtype allows us to identify the predominant subtype expressed by each tumor. RESULTS: Twelve of 12 prostate cancers, 41 of 57 breast cancers, and 5 of 5 gastrinomas expressed predominantly GRP receptors; 11 of 24 intestinal, 1 of 26 bronchial, and 1 of 1 thymic carcinoids had preferentially NMB receptors; 9 of 26 bronchial carcinoids, 1 large cell neuroendocrine lung carcinoma, and 4 of 9 small cell lung carcinomas had preferentially BB3 receptors, whereas 3 of 9 small cell lung carcinomas had GRP receptors. Renal cell carcinomas had GRP receptors in 6 of 16 cases and BB3 receptors in 4 of 16 cases. Finally, 2 of 10 Ewing sarcomas had BB3 receptors. In situ hybridization detected BB3 receptor mRNA in neuroendocrine tumors expressing the BB3 protein. CONCLUSIONS: This is the first study detecting the proteins of BB3, NMB, and GRP receptors in a group of human tumors using differential binding techniques. Particularly relevant is the BB3 expression in lung carcinoids and other neuroendocrine lung tumors, whereas gastrointestinal carcinoids preferably express NMB receptors. These tumors may be targets for diagnostic and radiotherapeutic applications of subtype-selective bombesin analogues.

Autoradiography↗
PubMed1992

p53 gene mutations in esophageal cancer detected by polymerase chain reaction single-strand conformation polymorphism analysis.

Mutations of the p53 gene play an important role in the development of common human malignancies. We investigated mutations of this gene in 26 surgical specimens of esophageal cancer using the polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) analysis. The results were correlated with histological findings, DNA ploidy and the short-term relapse of the disease. PCR-SSCP analysis detected mutations of the p53 gene in 10 tumors (38%), eight in exons 5-6 and two in exons 7-8. A higher incidence of lymph node metastasis, poorly differentiated tumor, DNA aneuploidy and short-term relapse of the disease was observed in cases with p53 gene mutations, although the findings were not statistically significant.

Base Sequence↗
PubMed2002

Insulin-like growth factor-1 and insulin-like growth factor binding protein-3 for prostate cancer detection in patients undergoing prostate biopsy.

PURPOSE: Laboratory and epidemiological studies suggest that high circulating insulin-like growth factor (IGF)-1 and low IGF binding protein-3 are associated with increased prostate cancer risk. However, the usefulness of serum IGF-1 or IGF binding protein-3 for predicting pathology results in men undergoing prostate biopsy is unclear. We examined the relationships of serum IGF-1, IGF binding protein-3 and the results of prostate biopsy. MATERIALS AND METHODS: A total of 652 consecutive patients with elevated serum prostate specific antigen (PSA) or abnormal digital rectal examination who were referred for transrectal ultrasound sextant prostate needle biopsy underwent blood sampling before biopsy. PSA, free PSA, IGF-1 and IGF binding protein-3 were measured. There were 244 men (37.4%) with cancer and 408 controls with benign conditions. RESULTS: Mean IGF-1 plus or minus SD in the cancer and control groups was 176.1 +/- 58.3 and 178.7 +/- 54.7 ng./ml., respectively (p = 0.57). Mean IGF binding protein-3 in the cancer and control groups was 2,724 +/- 647 and 2,673 +/- 589 ng./ml., respectively (p = 0.3). Adjustment for age and PSA showed significantly lower IGF-1 in cancer cases, while IGF binding protein-3 was not significant. ROC values were significantly higher for free-to-total PSA and PSA than for crude and age adjusted IGF-1 and IGF binding protein-3. CONCLUSIONS: Our data indicate that serum IGF-1 or IGF binding protein-3 does not predict the results of prostate biopsy in men with elevated PSA or abnormal digital rectal examination. This finding implies that while there is evidence that the IGF-1 level is a risk factor for prostate cancer, neither IGF-1 nor IGF binding protein-3 can be used as a tumor marker for this disease.

Aged↗
PubMed2005

Distinct chromosomal aberrations of ampulla of Vater and pancreatic head cancers detected by laser capture microdissection and comparative genomic hybridization.

Despite the continuous progress in molecular methodology, the genetic events involved in the carcinogenesis of pancreatic head ductal carcinomas (PHDCs) and ampulla of Vater cancer (AVC) remain largely unknown. Their proximity within the confined region lends them to very similar clinical presentations and operative approaches. However, it is unclear why AVC has a significantly better outcome than PHDCs. The drastic difference may arise from the distinct tumor origins. Therefore, the study of genetic alterations within these two neighboring tumors may elucidate their mechanisms. However, previous genetic analysis of PHDCs may have been influenced by contamination of excessive stromal and inflammatory cells in the background. To date, most comparative genomic hybridization (CGH) studies of pancreatic cancer are based in cell lines or specimens that were not microdissected. Even AVC has a paucity of data. To determine the differences of the genetic alterations of PHDCs and AVC, we used laser capture microdissection combined with degenerated oligonucleotide polymerase chain reaction and CGH to identify the chromosomal aberrations. Frequent gains were found on 5p, 13q, 3q, 8q, 1p, 2p, 2q, 3q, 7p, 8p, 9p, 13q, and 21q, while frequent losses were located on 7p, 18q, 1p, 11q, 16q, 19q, 1q, 2q, 3p, 19p, and 17p in PHDCs. In AVC, chromosomal gains occurred frequently in 7p, 8q, 1q, 2q, 3p, 4p, 7p, 3q, 5p, 20p, 20q, 4q, 5q, 7q, 11p, 12p, 13q, 14q, 18p, 18q, 21q, 9p, 10p, and 15q, and losses frequently in 17q, 1p, 18q, 19p, 5q, 10p, and 10q. This is the first report on the CGH profiles of AVC. These data provide evidence that chromosomal gains/amplifications of AVC differ from those of PHDCs. Among them, chromosomal gains on 1q25, 7p15, 8q23, and 3p21, and losses on 17q24, were statistically higher in AVC than PHDCs (P<0.05). The gains and losses suggest possible putative tumor suppressors and oncogenes that may be involved in the different carcinogenic pathways of AVC.

Adult↗