Prostatic Neoplasms: Srigley J

Epstein JI, Srigley J, Grignon D, Humphrey P, Otis C. · The Johns Hopkins Hospital, 401 N Broadway St, Rom 2242, Baltimore, MD 21231, USA. · Virchows Arch. · Pubmed #17674043 No free full text.

This publication has no abstract.

Epstein JI, Srigley J, Grignon D, Humphrey P, Anonymous00049. · Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA. · Hum Pathol. · Pubmed #17707261 No free full text.

Abstract: It has been evident for decades that pathology reports are very variable even within a single institution. Standardization of reporting is the optimal way to insure that information necessary for patient management, prognostic and predictive factor assessment, grading, staging, analysis of outcomes, and tumor registries are included in pathology reports. The ADASP has chosen a pathologist expert in each field to assemble a group from within the pathology community (with clinician input if desired) to write specific cancer protocols. These were then approved by the ADASP council and subsequently by the membership. The American College of Surgery Commission on Cancer (COC) accredits cancer centers in the United States. Recently, the COC decided to require elements, deemed as essential by the CAP, to be described in all pathology reports in their accredited cancer centers as of January 2004. Importantly, they do not require that the specific College of Pathologists (CAP) protocols or synoptic reports be used. ADASP has updated all of its protocols to comply with the COC requirements in the form of uniform checklists. The checklists use the staging criteria cited in the American Joint Committee on Cancer 2002 staging manual (sixth edition) but include a variety of other references listed in each of the checklists. Moreover, the checklists are formatted for ease of use. They may be used as templates for uniform reporting and are designed to be compatible with voice-activated transcription. The different elements in these revised ADASP diagnostic checklists have been divided into Required and Optional. The term Required in this context only signifies compliance with the COC guidelines. ADASP realizes that specimens and practices vary, and it will not be possible to report these elements in every case. However, ADASP hopes that pathologists will find these checklists useful in daily clinical practice while facilitating compliance with the new COC requirements.

Epstein JI, Srigley J, Grignon D, Humphrey P, Anonymous00022. · The Johns Hopkins Medical Institutions, Baltimore, MD, USA. · Am J Clin Pathol. · Pubmed #18089486 links to  free full text

This publication has no abstract.

Joshua AM, Vukovic B, Braude I, Hussein S, Zielenska M, Srigley J, Evans A, Squire JA. · Department of Medical Biophysics, University of Toronto, Toronto, Canada. · Neoplasia. · Pubmed #17325746 links to  free full text

Abstract: The causes of early genomic events underlying the development of prostate cancer (CaP) remain unclear. The onset of chromosomal instability is likely to facilitate the formation of crucial genomic aberrations both in the precursor lesion high-grade prostatic intraepithelial neoplasia (HPIN) and in CaP. Instability generated by telomere attrition is one potential mechanism that could initiate chromosomal rearrangements. In this study, normalized telomere length variation was examined in a cohort of 68 men without CaP who had HPIN only on prostatic biopsies. Multiple significant associations between telomere attrition and eventual diagnosis of CaP in the HPIN and in the surrounding stroma were found. Kaplan-Meier analysis of telomere length demonstrated a significantly increased risk for the development of cancer with short telomeres in the surrounding stroma [P = .035; hazard ratio (HR) = 2.12; 95% confidence interval (95% CI) = 0.231-0.956], and a trend for HPIN itself (P = .126; HR = 1.72; 95% CI = 0.287-1.168). Cox regression analysis also demonstrated significance between the time from the original biopsy to the diagnosis of cancer and telomere length in HPIN and in the surrounding stroma. These analyses showed significance, both alone and in combination with baseline prostate-specific antigen, and lend support to the hypothesis that telomere attrition in prostatic preneoplasia may be fundamental to the generation of chromosomal instability and to the emergence of CaP.