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Priya N Werahera

Publications and source records attributed to Priya N Werahera.

4 recordsLinked to original sources

Clinical staging of prostate cancer: a computer-simulated study of transperineal prostate biopsy.

OBJECTIVE: To identify the precise location of prostate cancer within the gland and thus possibly permit more aggressive therapy of the lesion, while potentially sparing the noncancerous gland from ablative therapy. MATERIALS AND METHODS: Three-dimensional "solid" computer models were reconstructed for 86 autopsy specimens and 20 stage T1c radical prostatectomy specimens. Transperineal biopsies were simulated for grid sizes of 5-mm (method A) and 10-mm (method B) with an 18 G, 23-mm long biopsy needle. One or two biopsies per grid point were obtained for a total of 12-108 biopsies, depending on the size of the prostate. Clinically threatening cancers were defined as having volumes of > or = 0.5 mL or Gleason sum > or = 7. RESULTS: Method A detected significantly more carcinomas than method B in both the autopsy and prostatectomy specimens (autopsy, 72 vs 51; prostatectomy, 50 vs 32, both P < 0.001). Method A also detected more clinically threatening cancers found at autopsy (38/40 vs 31/40, P = 0.008). Among autopsy patients with negative sextant biopsies whose disease was localized to one side, method A detected 72% and method B detected 29-43% (P < 0.001). CONCLUSIONS: The results of this computer simulation show that 5- and 10-mm grid biopsies detect three-quarters and a third, respectively, at autopsy, of patients with the disease localized to one side of the prostate, which may be useful when planning highly selective ablative treatments in the future.

Adult↗

Biomorphometric analysis of human prostatic carcinoma by using three-dimensional computer models.

Advances in the detection of carcinoma of the prostate during the last 15 years have accounted for a sharp increase and then an abrupt decrease in the incidence of the disease. A more recent decline in its mortality rates has been variously interpreted as either the success of early detection and improved treatment or lead-time bias. The recently reported Prostate Cancer Prevention Trial had an overall detection rate that approached the 30%-40% prevalence rates reported in autopsy series in which men died of other causes. However, the prognostic information that can be obtained from prostate cancer found on biopsy is limited. Three-dimensional computer modeling is one technique that allows multiple studies on "immortal" prostates to test methods of biopsy sampling accuracy and to assist in the determination of the disease's severity. Computer modeling can assess detection rates and assesses tumor multifocality and heterogeneity. It can provide a more accurate representation of tumor volume, aiding in therapeutic decision making, and can assess sampling errors of various biopsy methods. It has been shown to be superior to wire-frame technique by immortalizing the original shape and dimensions of the surgically excised prostate gland. Moreover, our 3-dimensional computer modeling system improves upon other systems: It is more than a simple extension of the planimetric technique, and it is able to demarcate clearly the boundaries of Gleason grades just 1 grade apart.

Adenocarcinoma↗

Laterally directed biopsies detect more clinically threatening prostate cancer: computer simulated results.

BACKGROUND: The purpose of this study was to determine, whether a modified fan-shaped biopsy (MFSB) technique which utilizes six laterally directed biopsies would lead to higher detection rates of clinically threatening prostatic carcinoma than the six random systematic core biopsy (SRSCB) method. METHODS: We reconstructed 3-dimensional solid computer models of 86 autopsy prostates and 40 radical prostatatectomy specimens. Simulations of SRSCB and MFSB were then performed using the same biopsy sites except that the biopsy probe was rotated 45 degrees toward posterolateral peripheral zone for MFSB. When the Gleason sum was less than 7, clinically threatening cancers were defined as having a tumor volume > or =0.25 cc or > or =0.5 cc. RESULTS: When the cut off volume was 0.25 cc, MFSB detected significantly more threatening carcinomas in autopsy prostates than did SRSCB (P < 0.0082). This was also true for the surgical prostates (P < 0.0047) as well as for a sub-group of non-palpable carcinomas (P < 0.0047). When the cut off volume was increased to 0.5 cc, MFSB detected significantly more threatening carcinomas in the radical series (P < 0.0047) and for the non-palpable carcinomas (P < 0.0082), but not in the autopsy series. CONCLUSIONS: The MFSB technique, which utilizes laterally directed biopsies, appears to be an effective approach to improve the detection of clinically threatening prostatic carcinoma.

Adult↗

Aberrant HOXC expression accompanies the malignant phenotype in human prostate.

Dysregulation of HOX gene expression has been implicated as a factor in malignancies for a number of years. However, no consensus has emerged regarding specific causative genes. Using a degenerate reverse transcription-PCR technique, we show up-regulation of genes from the HOXC cluster in malignant prostate cell lines and lymph node metastases. When relative expression levels of the four HOX clusters were examined, lymph node metastases and cell lines derived from lymph node metastases exhibited very similar patterns, patterns distinct from those in benign cells or malignant cell lines derived from other tumor sites. Specific reverse transcription-PCR for HOXC4, HOXC5, HOXC6, and HOXC8 confirmed overexpression of these genes in malignant cell lines and lymph node metastases. Laser capture microdissection and examination of paired tumor/normal prostate epithelial cells also indicated overexpression of these HOXC genes in primary tumor cells. Our data indicate a possible link between expression of HOXC genes and malignancy in prostate cells. Overexpression of HOXC8 in LNCaP prostate cancer cells suppressed transactivation by androgen receptors. We speculate that HOXC overexpression may predispose tumor cells to androgen independence by necessitating adaptation to diminished androgen signaling.

Androgens↗