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PubMed1977

Lymphangiography in the determination of the extent of metastatic carcinoma: the potential value of percutaneous lymph node biopsy.

In determining the extent of disease in patients with carcinoma, lymphangiography when read as positive has an accuracy of 90 to 95%. When considered negative 15 to 20% prove to have metastatic disease. the recent use of percutaneous transperitoneal aspiration biopsy of previously opacified lymph nodes has enhanced the value of lymphangiography. Eighty percent of the aspiration biopsies yield sufficient tissue for cytologic diagnosis.

Adult↗
PubMed1985

Radiation oncology. Programs for the present and future.

Radiation oncology in 1984 continues to make major advances in the multidisciplinary clinical programs. This has been possible by virtue of the radiation oncologist, who is an active participant in these clinical programs. The changing role for the radiation oncologist has dictated a greater participation in the primary management of the patient's disease process and also participation in multidisciplinary research programs.

Breast Neoplasms↗
PubMed1987

The prevalence of pain in four cancers.

Although pain is widely recognized as a major problem in cancer patients, most studies have concentrated on pain among those with advanced or terminal cancer in specialized treatment settings. The study reported here gives a more complete picture of the problem of pain among cancer patients by providing data generalizable to those in early as well as late stages of the disease, and receiving care in the community as well as specialized treatment centers. Having included measures of several distinct features of pain, this study also provides a more complete understanding of the cancer patient's day-to-day pain problem than earlier investigations. The findings presented here indicate that serious pain may occur in all cancer stages, and often represents an ongoing medical problem. The data suggest that many patients may benefit from earlier and more aggressive use of available antipain treatment methods.

Analgesics↗
PubMed1994

The Department of Veterans Affairs' unique clinical cancer research effort.

Without organized clinical trials, we are doomed to repeat our mistakes endlessly. There are many genuine conflicts of interest intrinsic to clinical research. Some of these arise from the necessity of admitting that we as physicians do not know the best way to treat every disease or each patient and that all treatments currently available for this patient's disease are suboptimal. With humility and honesty, these conflicts of interest can be overcome. Surmounting other more palpable ones, however, is equally challenging. Supporting the participation of our patients in clinical trials requires a practical reconfiguration of practice patterns, different and more record keeping, and the surrender of autonomy. Each of these facts has economic implications. Practitioners who are paid according to the specific services they provide risk both significant income loss and cost increase by participating in clinical trials. The Department of Veterans Affairs is a charter member of the cancer clinical trials establishment and the originator of a long string of important firsts in cancer research. The nature of the VA system eliminates or diminishes the impact of many of the conflicts of interest that hinder clinical trial participation. This globally budgeted comprehensive system, which theoretically is responsible for the care of more citizens than is the entire Canadian national health service, is an unique clinical research resource. Some of the high points of the VA contributions to cancer treatment development are listed in this paper. Hopefully, this overview makes the point that the VA clinical research enterprise is a treasure that can ask critical questions that, because of irresolvable economic conflicts of interest, can be asked neither in the fee-for-service nor the prepaid health maintenance settings. This clinical cancer research resource must be nurtured and supported, and it must continue to address critical questions that it alone can answer.

Clinical Trials as Topic↗
PubMed2000

Loss of tissue transglutaminase as a biomarker for prostate adenocarcinoma.

BACKGROUND: Additional molecular tissue biomarkers for prostate carcinoma are needed to stratify patients with clinically suspicious findings, such as an elevated prostate specific antigen (PSA) with a negative biopsy, according to risk. METHODS: Prostate tissues from 43 cancer cases and 47 controls with no evidence of cancer were labeled for transglutaminase by immunohistochemistry. Immunoreactivity was quantified using the Autocyte Pathology Workstation. In addition, quantitative fluorescence image analysis was used to compare transglutaminase concentrations in cells obtained by fine-needle aspiration from excised prostates. Loss of gene expression was evaluated by reverse transcriptase-polymerase chain reaction and growth with 5-azacytidine. RESULTS: Visually, benign glands from controls generally expressed tissue transglutaminase, whereas regions with adenocarcinoma generally were negative. With quantitative immunohistochemistry, 41 of 43 adenocarcinoma of the prostate (CaP) cases expressed lower mean percentage areas positive for transglutaminase than did 30 of 30 benign prostatic hyperplasia (BPH) and 17 of 17 prostatitis cases (P < 0.0001; odds ratio [OR], 1577; 95% confidence interval (CI), 74-33, 820; relative risk [RR], 25; 95% CI, 6-95). Quantitative immunofluorescence of 3277 cells collected by FNA from 19 CaP cases and 645 cells from 5 cases of BPH showed that the mean content of transglutaminase was 93 femtograms (fg) for the CaP-derived cells and 138 fg for the BPH cells (P < 0.0001). Receiver operating curve analysis of the immunohistochemistry data showed an optimized threshold produced 95% sensitivity with 100% specificity. Growth of LNCaP cells with 5-azacytidine failed to stimulate transglutaminase expression, suggesting that loss of expression was likely not attributable to promoter methylation. CONCLUSIONS: Measurements of transglutaminase on tissue sections provides additional diagnostic information that is potentially useful for risk assessment of patients with suspicious clinical findings, such as nodules or positive PSA and negative biopsies, without overdetecting disease.

Adenocarcinoma↗
PubMed2001

The problem of cutoff levels in a screened population: appropriateness of informing screenees about their risk of having prostate carcinoma.

BACKGROUND: Transrectal prostate biopsy decisions often have been based on absolute cutoff values for total and free prostate-specific antigen (PSA). The authors decided that it would be more appropriate to develop risk profiles for the individual patient to allow him to decide whether to undergo a prostate biopsy. METHODS: To develop risk profiles, the authors first used multivariate logistic regression analysis to analyze 2054 males who were part of the Tyrol (Austria) PSA Screening Project. Second, artificial neural network (ANN) analyses were performed using data from 3474 males who also were part of the Tyrol PSA Screening Project and who had undergone prostate biopsy. These analyses were compared with standard cutoff levels of specificity for the detection of prostate carcinoma. RESULTS: To the authors' knowledge, this was the first time that multivariate logistic regression analysis was used to decide whether to perform prostate biopsies based on risk profiles rather than on single cutoff levels. For the detection of prostate carcinoma, at sensitivity levels of 90--95%, the ANN was 150--200% more specific than the standard cutoff points. For screened volunteers with total PSA levels below 4 ng/mL, ANN showed a lower cancer predictive ability in comparison with volunteers with total PSA levels above 4 ng/mL. However, the ANN was approximately 150--200% more specific than the standard cutoff levels in both groups. CONCLUSIONS: At high sensitivity levels, ANN increased the specificity for prostate carcinoma detection in a PSA-based screened population. The improvement in specificity between standard cutoff levels and ANN ranged between 150--200% and was not affected by the presence of benign prostatic hyperplasia or prostatitis.

Aged↗
PubMed2000

Selective activation of the fatty acid synthesis pathway in human prostate cancer.

A substantial subset of breast, colorectal, ovarian, endometrial and prostatic cancers displays markedly elevated expression of immunohistochemically detectable fatty acid synthase, a feature that has been associated with poor prognosis and that may be exploited in anti-neoplastic therapy. Here, using an RNA array hybridisation technique complemented by in situ hybridisation, we report that in prostate cancer fatty acid synthase expression is up-regulated at the mRNA level together with other enzymes of the same metabolic pathway. Contrary to the observations that in many cell systems (including androgen-stimulated LNCaP prostate cancer cells) fatty acid and cholesterol metabolism are co-ordinately regulated so as to supply balanced amounts of lipids for membrane biosynthesis, storage or secretion, no changes in the expression of genes involved in cholesterol synthesis were found. These findings point to selective activation of the fatty acid synthesis pathway and suggest a shift in the balance of lipogenic gene expression in a subgroup of prostate cancers.

Acetyl-CoA Carboxylase↗
PubMed2005

Pitfalls and infrequent findings in fine-needle aspiration of the prostate gland.

Based on the experience accumulated over two decades and in more than 7,000 transrectal fine-needle aspirations (FNAs) of the prostate gland, several benign and malignant unusual cytologic findings are described. Infrequent benign cytologic findings and possible pitfalls are atrophic prostatic epithelium, squamous metaplasia, transitional cells, granulomatous prostatitis, seminal vesicle epithelium, ganglion cells, lubricant artifacts, and treatment effects. Infrequent variants of carcinoma are foamy-cell carcinoma, prostatic duct adenocarcinoma, mucinous adenocarcinoma, transitional-cell carcinoma, small-cell carcinoma, squamous-cell carcinoma of the prostate, metastatic solid tumor within the prostate, and mesenchymal tumors. Cytopathologists must be able to diagnose these variants of prostate adenocarcinoma because on most occasions the variants imply a worse clinical prognosis. Appropriate training is essential to achieve success in this field of cytopathology. FNA of the prostate provides in a matter of minutes useful information concerning clinical management, prognosis, and treatment of patients.

Biopsy, Fine-Needle↗
PubMed2005

Very low intensity alternating current decreases cell proliferation.

Electric fields impact cellular functions by activation of ion channels or by interfering with cell membrane integrity. Ion channels can regulate cell cycle and play a role in tumorigenesis. While the cell cycle may be directly altered by ion fluxes, exposure to direct electric current of sufficient intensity may decrease tumor burden by generating chemical products, including cytotoxic molecules or heat. We report that in the absence of thermal influences, low-frequency, low-intensity, alternating current (AC) directly affects cell proliferation without a significant deleterious contribution to cell survival. These effects were observed in normal human cells and in brain and prostate neoplasms, but not in lung cancer. The effects of AC stimulation required a permissive role for GIRK2 (or K(IR)3.2) potassium channels and were mimicked by raising extracellular potassium concentrations. Cell death could be achieved at higher AC frequencies (>75 Hz) or intensities (>8.5 microA); at lower frequencies/intensities, AC stimulation did not cause apoptotic cellular changes. Our findings implicate a role for transmembrane potassium fluxes via inward rectifier channels in the regulation of cell cycle. Brain stimulators currently used for the treatment of neurological disorders may thus also be used for the treatment of brain (or other) tumors.

Adenylate Kinase↗
PubMedDate not supplied

Histologic variant of the epithelial-myoepithelial carcinoma of the salivary gland: a case report.

BACKGROUND: Epithelial-myoepithelial carcinoma (EMC) of the salivary gland is a low-grade carcinoma. It has been widely accepted as a clinicopathologic entity only in the past decade. Histologically, the classical bimodal differentiation of inner eosinophilic ductal cells and outer layer of clear myoepithelial cells has been well documented by many authors. However, the proportion of each component may vary in different tumors or within the same tumor, and different histologic patterns have been described. The clinicopathologic findings of an epithelial-myoepithelial carcinoma of the parotid gland in a 73-year-old man are presented. METHODS: Light microscopy including immunohistochemistry and ultrastructural studies were done. RESULTS: The various histologic patterns and bimodal differentiation of the tumor were noted. CONCLUSIONS: The present case demonstrates the myriad of histologic patterns that can occur in epithelial-myoepithelial carcinoma. Differentiation from malignant mixed tumor is essential and possible. The importance of the awareness of its histologic variants is emphasized.

Adenocarcinoma↗
PubMed2003

Twenty-three novel BRCA1 and BRCA2 sequence alterations in breast and/or ovarian cancer families in Southern Germany.

BRCA1 and BRCA2 germline mutations cause a substantially increased life time risk of both breast and ovarian cancer. Mutational screening of these genes by means of Denaturing High Performance Liquid Chromatography (DHPLC) in breast and/or ovarian cancer-prone families from Southern Germany revealed 15 novel BRCA1 and 8 novel BRCA2 sequence variants. Predictions on the BRCA1/BRCA2 protein functions lead to the identification of 11 novel deleterious cancer predisposing mutations. Mutation types and their functional relevances are discussed. Our data contribute to phenotype-genotype correlation studies and to the characterisation of the mutation spectrum of BRCA1/BRCA2.

BRCA1 Protein↗
PubMed2001

Preexisting histologic evidence of prostatitis is unrelated to postimplant urinary morbidity.

The presence and extent of prostatitis on the patients' preimplant biopsy slides was correlated with their postimplant course to determine if any relationship exists between histological prostatitis and postimplant morbidity. Biopsy slides from 56 patients treated with I-125 (144 Gy, TG-43), Pd-103 (125 Gy, NIST-1999), or Pd-103 plus supplemental external beam radiation (20-44 Gy) were studied. As part of ongoing prospective protocols, treatment-related morbidity is monitored by mailed questionnaires at 1, 3, 6, 12, and 24 months postimplant, using standard American Urologic Association (I-PSS) and Radiation Therapy Oncology Group criteria. Patient's preimplant biopsies, stained with standard hematoxylin and eosin, were retrieved for review by one uropathologist (LT). Separate evaluations of the degree and extent of inflammation in biopsy cores free of cancer and in cancerous biopsy cores were undertaken. Infiltrates were classified as periglandular if they were within 50 microns of a glandular structure. They were otherwise classified as stromal. Distribution of the inflammation was reported as focal, multifocal, or diffuse. The intensity of inflammation was separately graded as mild if there were fewer than 10 inflammatory cells per high-power field, moderate if there were 10-200 cells per high-power microscopic field, or severe if there were more than 200 cells per field. In all cases the great majority of inflammatory cells were mononuclear, predominantly lymphocytes. Periglandular inflammation was most common, with 18% of patients having focal periglandular and 20% having multifocal periglandular inflammation on their preimplant biopsies. Cancer-related infiltrates were the second most common, with 23% of patients having focal, 13% multifocal, and 13% diffuse cancer-related inflammation on their preimplant biopsies. Eight of the 55 patients developed postimplant urinary retention, requiring catheterization for 2 to 8 days. The overall incidence of postimplant urinary retention was low and there was no obvious relationship between the presence of inflammation on preimplant biopsy and the likelihood of postimplant urinary retention. AUA score changes at 1 and 6 months postimplant were highly variable and unrelated to the presence or severity of periglandular or cancer-related inflammation. Considering the apparent lack of relationship between histological findings and clinical outcomes in the patients reported here, the authors conclude that histologic evidence of prostatitis is not a contraindication to brachytherapy.

Biopsy↗
PubMed2006

A prostate secretory protein94-derived synthetic peptide PCK3145 inhibits VEGF signalling in endothelial cells: implication in tumor angiogenesis.

We have previously observed that the synthetic peptide corresponding to amino acids 31-45 (PCK3145) of PSP94 can reduce prostate tumor growth in vivo. Moreover, a recently concluded phase IIa clinical trial with patients with hormone refractory prostate cancer indicated that PCK3145 down-regulates the levels of plasma matrix metalloproteinase (MMP)-9, a MMP involved in metastasis and tumor angiogenesis. The purpose of our study was to investigate the molecular mechanisms of action of PCK3145 and whether this peptide could antagonize tumor neovascularization. We show that, in a syngeneic in vivo model of rat prostate cancer, the expression of endothelial cell (EC) specific CD31, a marker of tumor vessel density, was decreased by 43% in PCK3145-treated animals. In vitro, PCK3145 specifically antagonized in a dose-dependent manner the VEGF-induced ERK phosphorylation as well as the phosphorylation of the VEGFR-2 in cultured EC (HUVEC). These anti-VEGF effects were partly reproduced by pharmacological inhibitors such as PD98059 and PTK787, suggesting that PCK3145 inhibits the tyrosine kinase activity associated to VEGFR-2, which in turn prevents intracellular signalling through the MAPK cascade. Moreover, PCK3145 was also found to inhibit the PDGF-induced phosphorylation of PDGFR in smooth muscle cells. Finally, PCK3145 inhibited in vitro EC tubulogenesis and VEGF-induced MMP-2 secretion suggesting its potential implication as an antiangiogenic agent. Our study demonstrates that PCK3145 interferes with the tyrosine kinase activity associated with VEGF signalling axis in EC. The antiangiogenic properties of this peptide could be highly beneficial and exploited in novel antiangiogenic therapies, for patients with various cancers.

Animals↗
PubMed2006

Hepatocyte growth factor activation inhibitors (HAI-1 and HAI-2) regulate HGF-induced invasion of human breast cancer cells.

Hepatocyte growth factor (HGF) plays a plethora of roles in cancer metastasis and tumour growth. The interaction between tumour cells and their surrounding stromal environment is a crucial factor regulating tumour invasion and metastasis. Stromal fibroblasts are the main source of HGF in the body, and release HGF as an inactive precursor (pro-HGF). HGF activator (HGFA), matriptase, urokinase-type plasminogen activator and hepsin are the main factors responsible for converting pro-HGF into active HGF. HAI-1 and HAI-2 are 2 novel Kunitz-type serine protease inhibitors that regulate HGF activity through inhibition of HGFA, matriptase and hepsin action. Recent studies demonstrate that HAI-1 and HAI-2 may also potently inhibit a number of other pro-metastatic serine proteases and therefore have direct bearing on the spread of tumours. Our study examined the potential of these HAI's to suppress the influence of HGF and regulate cancer metastasis. We generated a retroviral expression system that induced HAI expression in a human fibroblast cell line. Forced expression of either HAI-1 or HAI-2 in these fibroblasts resulted in a dramatic decrease in the production of bioactive hepatocyte growth factor (HGF). This reduction in HGF activity subsequently suppressed HGF's metastatic influence on breast cancer cells. To further assess the anti-cancer properties of HAI-1 and HAI-2 we generated recombinant HAI proteins. These recombinant HAI proteins possessed the ability to potently quench HGF activity. We also demonstrate that these recombinant HAI's suppressed fibroblast-mediated breast cancer invasion. An additional ribozyme transgenes study revealed that elimination of HAI-1 and HAI-2 expression, in an MDA-MB-231 breast cancer cell line, significantly enhanced the migratory, proliferative and invasive nature of these breast cancer cells. Overall, our data demonstrates the important roles of HAI-1 and HAI-2 in cancer metastasis, and reveals that these serine protease inhibitors display strong therapeutic potential.

Animals↗