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Biomedical subjects

P C Verhagen

Publications and source records attributed to P C Verhagen.

5 recordsLinked to original sources

Eosinophilic cystitis.

We describe four cases of eosinophilic cystitis in whom no specific cause could be found, and review the literature. Complaints at presentation included urgency, frequency, abdominal pain, and haematuria. In three patients the symptoms and ultrasound pictures suggested a bladder tumour. One patient was treated with anticholinergics and corticosteroids without relief of symptoms; a localised eosinophilic tumour was excised in one patient who remained symptom free; and two patients were managed conservatively with spontaneous resolution of bladder pathology and symptoms. One case was identified by random bladder biopsy in 150 consecutive patients with unexplained irritable micturition complaints. Eosinophilic cystitis is rare in children. After biopsy, we consider a wait and see policy is justified as symptoms tend to disappear spontaneously. Routine bladder biopsies in children with unexplained bladder symptoms is not justifiable.

Adolescent↗

Blood and serum substances for markers of prostate cancer.

Serummarkers for prostate carcinoma are widely applied for the purpose of early detection of cancer and the differentiation between benign and malignant disease, for the pre-treatment staging of detected prostatic cancers, and for the monitoring of prostate cancer after curative or palliative therapies. This review illustrates the limitations of current markers for prostatic disease in blood en serum. It gives an overview of what is known about PSA and its isoforms, hK2, PSMA, and PSCA, and discusses, based on this information, in what direction current research is developing in order to improve these markers.

Antigens, Neoplasm↗

Microdissection, DOP-PCR, and comparative genomic hybridization of paraffin-embedded familial prostate cancers.

There is a clear genetic component to prostate cancer susceptibility. Regions reported to be linked to prostate cancer include 1q24-25 (HPC-1), 1q42.2-43, and Xq27-28. There is limited genetic information on familial prostate tumors. We used the Utah Population Database to identify familial prostate cancer cases and selected 35 cases from high-risk families. Tissue blocks containing discernable tumor were available from 19 cases; 13 of these yielded adequate specimens for analysis. Six cases came from families with linkage to HPC-1, 3 were known to have linkage to Xq27-28, and 4 had no linkage to a known locus; 7 cases were analyzed from patients who showed no known linkage (sporadic tumors) as controls. These paraffin-embedded tumors were laser microdissected, degenerate oligonucleotide (DOP)-amplified, and labeled for fluorescence detection by comparative genomic hybridization (CGH). Loss of 7q, 10q, and 16q and gain of 8q were common abnormalities present in both familial and sporadic tumors. Distinctive abnormalities included loss of 3p12-3p22 in 3 of 6 HPC-7-linked cases and in 2 of 3 X-linked cases and gain of 6q11-6q21 in 2 each of HPC-1 and X-linked tumors. In conclusion, laser microdissection, DOP-PCR, and CGH is a feasible method for analysis of paraffin-embedded prostate tumors. This study provides preliminary data suggesting that familial prostate cancer harbors some unique genetic changes when compared with sporadic prostate tumors.

Chromosomes, Human, Pair 1↗