Benign Cells (benign + cell)

Distribution by Scientific Domains


Selected Abstracts


Litigation cells: Their incidence and classification in gynecologic smears

DIAGNOSTIC CYTOPATHOLOGY, Issue 6 2002
Wei Sun M.D.
Abstract "Litigation cells" are defined as benign cells which may mimic dysplasia or cancer and might be used by plaintiffs' witnesses to imply that the cytotechnologist or pathologist "missed" cells of dysplasia or cancer. We reviewed 180 cervical smears from 166 patients who had hysterectomy for benign leiomyomas. All smears were performed within 12 months prior to hysterectomy. None of the uteri contained dysplasia or cancer on histologic examination. 90.6% of smears reviewed had at least one cell or cell group with atypia mimicking dysplasia or cancer. These "litigation cells" were classified as follows: parabasal cells, metaplastic squamous cells, degenerated endocervical cells, reactive endocervical cells, endometrial cells, neutrophils, histiocytes, and air-dried cells. Diseases mimicked by these cells included squamous cell carcinoma, high-grade squamous intraepithelial lesion, low-grade squamous intraepithelial lesion, adenocarcinoma, and glandular dysplasia. These "litigation cells" can be correctly classified by experienced cytotechnologists and cytopathologists and recognized as benign. We recommend that in all cases of alleged malpractice against cytotechnologists and/or pathologists the smears should be reviewed by a panel of individuals trained and experienced in cytopathology. The smears should be reviewed without knowledge of the clinical outcome and in an environment that simulates the normal screening practice. Diagn. Cytopathol. 2002;26:345,348. © 2002 Wiley-Liss, Inc. [source]


Differential control of apoptosis by DJ-1 in prostate benign and cancer cells

JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 6 2004
Yaacov Hod
Abstract DJ-1 is a conserved protein reported to be involved in diverse cellular processes ranging from cellular transformation, control of protein,RNA interaction, oxidative stress response to control of male infertility, among several others. Mutations in the human gene have been shown to be associated with an autosomal recessive, early onset Parkinson's disease (PARK7). The present study examines the control of DJ-1 expression in prostatic benign hyperplasia (BPH-1) and cancer (PC-3) cell lines in which DJ-1 abundance differs significantly. We show that while BPH-1 cells exhibit low basal level of DJ-1 expression, stress-inducing agents such as H2O2 and mitomycin C markedly increase the intracellular level of the polypeptide. In contrast, DJ-1 expression is relatively high in PC-3 cells, and incubation with the same cytotoxic drugs does not modulate further the level of the polypeptide. In correlation with the expression of DJ-1, both cytotoxic agents activate the apoptotic pathway in the prostatic benign cells but not in PC-3 cells, which are resistant to their action. We further demonstrate that incubation of BPH-1 cells with TNF-related-apoptosis-inducing-ligand/Apo-2L (TRAIL) also enhances DJ-1 expression and that TRAIL and H2O2 act additively to stimulate DJ-1 accumulation but synergistically in the activation of the apoptotic pathway. Time-course analysis of DJ-1 stimulation shows that while DJ-1 level increases without significant lag in TRAIL-treated cells, there is a delay in H2O2 -treated cells, and that the increase in DJ-1 abundance precedes the activation of apoptosis. Unexpectedly, over-expression of DJ-1 de-sensitizes BPH-1 cells to the action of apoptotic-inducing agents. However, RNA-interference-mediated silencing of DJ-1 expression results in sensitization of PC-3 cells to TRAIL action. These results are consistent with a model in which DJ-1 is involved in the control of cell death in prostate cell lines. DJ-1 appears to play a differential role between cells expressing a low but inducible level of DJ-1 (e.g., BPH-1 cells) and those expressing a high but constitutive level of the polypeptide (e.g., PC-3 cells). © 2004 Wiley-Liss, Inc. [source]


Expression of L-type amino acid transporter 1 (LAT1) in esophageal carcinoma

JOURNAL OF SURGICAL ONCOLOGY, Issue 4 2005
Hideaki Kobayashi MD
Abstract Background and Objectives It has been reported that amino acid transport systems play an important role in cell proliferation. Their activity is increased in malignant cells compared to benign cells. In this study, we investigated whether L-type amino acid transporter 1 (LAT1) is expressed in human non-cancerous esophageal mucosa and esophageal squamous cell carcinoma. We also examined whether LAT1 expression is correlated with histopathological features. Methods From January 1999 to December 2001, sections of formalin-fixed, paraffin-embedded tissue from 11 cases of early esophageal carcinoma (T1) and 19 cases of advanced esophageal carcinoma (T2, T3) were entered in the study. Histopathologically, all 30 cases were squamous cell carcinoma. Immunohistochemical staining was performed using rabbit anti-LAT1 IgG, with the standard avidin-streptavidin immuno-peroxidase method. Measurement was performed by means of computer-assisted image analysis. The ratio of cells with LAT1 expression in esophageal squamous cell carcinoma and non-cancerous esophageal mucosa was used for analysis in this study. Results Non-cancerous esophageal mucosa expressed LAT1 only in the basal layer of the esophageal wall. Esophageal squamous cell carcinoma expressed LAT1 throughout the tumor. LAT1 expression in esophageal squamous cell carcinoma was significantly higher than that in non-cancerous esophageal mucosa. LAT1 expression in esophageal squamous cell carcinoma increased as the depth of invasion progressed (T1,<,T2 (P,=,0.0477), T2,<,T3 (P,=,0.0415), T1,<,T3 (P,=,0.0044)), and as the tumor size increased. Also, high LAT1 expression was significantly associated with well-differentiated carcinoma. Conclusion These results suggest that LAT1 plays a significant role in cell proliferation, differentiation, and invasion in esophageal squamous cell carcinoma. J. Surg. Oncol. 2005;90:233,238. © 2005 Wiley-Liss, Inc. [source]


Selective over-expression of fibroblast growth factor receptors 1 and 4 in clinical prostate cancer,

THE JOURNAL OF PATHOLOGY, Issue 1 2007
K Sahadevan
Abstract Fibroblast growth factor receptors (FGFRs) mediate the tumourigenic effects of FGFs in prostate cancer. These receptors are therefore potential therapeutic targets in the development of inhibitors to this pathway. To identify the most relevant targets, we simultaneously investigated FGFR1,4 expression using a prostate cancer tissue microarray (TMA) and in laser capture microdissected (LCM) prostate epithelial cells. In malignant prostates (n = 138) we observed significant FGFR1 and FGFR4 protein over-expression in comparison with benign prostates (n = 58; p < 0.0001). FGFR1 was expressed at high levels in the majority of tumours (69% of grade 3 or less, 74% of grade 4 and 70% of grade 5), while FGFR4 was strongly expressed in 83% of grade 5 cancers but in only 25% of grade 1,3 cancers (p < 0.0001). At the transcript level we observed a similar pattern, with FGFR1 and FGFR4 mRNA over-expressed in malignant epithelial cells compared to benign cells (p < 0.0005 and p < 0.05, respectively). While total FGFR2 was increased in some cancers, there was no association between expression and tumour grade or stage. Transcript analysis, however, revealed a switch in the predominant isoform expressed from FGFR2IIIb to FGFR2IIIc among malignant epithelial cells. In contrast, protein and transcript expression of FGFR3 was very similar between benign and cancer biopsies. The functional effect of targeting FGFR4 in prostate cancer cells has not previously been investigated. In in vitro experiments, suppression of FGFR4 by RNA interference effectively blocked prostate cancer cell proliferation (p < 0.0001) and invasion (p < 0.001) in response to exogenous stimulation. This effect was evident regardless of whether the cells expressed the FGFR4 Arg388 or Gly388 allele. In parallel experiments, FGFR3 suppression had no discernible effect on cancer cell behaviour. These results suggest evidence of selective over-expression of FGFR1 and FGFR4 in clinical prostate cancer and support the notion of targeted inhibition of these receptors to disrupt FGF signalling. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source]


Endoscopic ultrasound of pancreatic cystic lesions

ANZ JOURNAL OF SURGERY, Issue 9 2010
Shyam Prasad
Abstract Background:, The impact of endoscopic ultrasonography (EUS) on the management of pancreatic cystic lesions remains unclear, and there are no published studies of the Australian experience in this area. The aim of this study was to review the experience of EUS for such lesions within our institution. Methods:, A retrospective review was undertaken of data collected prospectively over a two-year period within the EUS database of St. Vincent's Hospital. Patients who underwent EUS for suspected pancreatic cystic lesions were identified. Data were collected on demographic variables, EUS findings, the results of EUS-guided fine-needle aspiration (FNA) and the findings on clinical and radiological follow-up. Results:, Fifty-nine patients were identified. Two thirds were female. Most lesions were located at the pancreatic head. Median diameter was 25 mm. FNA was performed in 36 cases (61%). On cytology, six (17%) showed features of mucinous tumours and five (14%) showed adenocarcinoma. The remainder contained either non-specific benign cells or insufficient epithelial tissue. Follow-up data on 48 cases (83%), after a median duration of 15 months, revealed that 15 lesions (31%) had been resected, including six serous and six mucinous tumours. The level of carcinoembryonic antigen in FNA specimens appeared to be higher in mucinous than in serous neoplasms. Twenty-four lesions had undergone repeat radiological imaging: only three had grown in size. Conclusions:, EUS and FNA are useful procedures for assessing pancreatic cystic lesions. Malignant features are demonstrated in only a small minority. The majority of the remainder show no signs of progression during follow-up. [source]


Endometrial cells as a predictor of uterine cancer

AUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 1 2007
Adrian R. HEARD
Abstract Background:, With the recent cervix screening national guidelines recommending against reporting of benign endometrial cells, we examined South Australian data to see what impact this would have on detecting uterine cancers. Aims:, To test whether benign endometrial cells detected in cervical cytology testing confer an increased risk of uterine cancer, and to ascertain what percentage of uterine cancers will be missed in cervical screening programs if these cells are not reported. Methods:, The study was a retrospective cohort design of 1585 women with shed endometrial cells, each matched with three women without shed cells. All were linked with cancer registry data to check for uterine cancer diagnosis. Cox proportional hazards regression was used to check for any increase in cancer risk with shed endometrial cells. Using the calculated relative risks for uterine cancer diagnosis, we estimated the number of uterine cancers in South Australia associated with benign endometrial cells. Results:, The presence of benign endometrial cells in a cervical cytology test increases the risk of uterine cancer sixfold. However, screening women with benign cells would involve a major increase in pathology work for only an 18% increase in uterine cancers detected. Conclusions:, Until cytology systems have a higher sensitivity in detecting which benign endometrial cells are associated with uterine cancer, pathology laboratories are unlikely to be required to report these cells on tests. Inability to adjust for symptomatic status may have reduced the relevance of the results in this study. [source]