Severe periprosthetic osteolytic lesions after the Ankle Evolutive System total ankle replacement.

Between 2002 and 2008, 130 consecutive ankles were replaced with an hydroxyapatite (HA) and titanium-HA-coated Ankle Evolutive System total ankle prosthesis. Plain radiographs were analysed by two independent observers. Osteolytic lesions were classified by their size and location, with cavities > 10 mm in diameter considered to be 'marked'. CT scanning was undertaken in all patients with marked osteolysis seen on the plain radiographs. Osteolytic lesions were seen on the plain films in 48 (37%) and marked lesions in 27 (21%) ankles. The risk for osteolysis was found to be 3.1 (95% confidence interval 1.6 to 5.9) times higher with implants with Ti-HA porous coating. Care should be taken with ankle arthroplasty until more is known about the reasons for these severe osteolyses.

Alpha-smooth muscle actin within epithelial islands is predictive of ameloblastic carcinoma.

Ameloblastoma is the most common clinically significant odontogenic tumor. It is considered benign but locally invasive and associated with variable clinico-pathological behavior. Ameloblastic carcinoma is a malignant tumor having features of ameloblastoma in addition to cytologic atypia with or without metastasis. It is aggressive and associated with poor prognosis. The aim of this study was to examine which epithelial and stromal markers are predictive of histologically diagnosed ameloblastic carcinoma and can sufficiently differentiate it from solid/multicystic ameloblastoma (SA). We examined immunohistochemically Ki-67, epithelial membrane antigen (EMA), alpha-smooth muscle actin (alpha-SMA), calponin, p63 and DNA content using image (ICM) and flow cytometry (FCM) in three ameloblastic carcinomas and up to 18 SAs. The important findings were that Ki-67 labeling index was significantly higher in ameloblastic carcinoma than SA while EMA, calponin, p63, ICM and FCM did not sufficiently differentiate the two groups of lesions. Expression of alpha-SMA was consistently obtained within the epithelial island cells of ameloblastic carcinoma and not in SA, although the marker was well expressed in the stroma of both lesions. We therefore conclude that the presence of alpha-SMA within the epithelial islands is highly predictive of ameloblastic carcinoma.

Mannose receptor is a novel ligand for L-selectin and mediates lymphocyte binding to lymphatic endothelium.

Continuous lymphocyte recirculation between blood and lymphoid tissues forms a basis for the function of the immune system. Lymphocyte entrance from the blood into the tissues has been thoroughly characterized, but mechanisms controlling lymphocyte exit from the lymphoid tissues via efferent lymphatics have remained virtually unknown. In this work we have identified mannose receptor (MR) on human lymphatic endothelium and demonstrate its involvement in binding of lymphocytes to lymphatic vessels. We also show that the binding requires L-selectin, and L-selectin and MR form a receptor-ligand pair. On the other hand, L-selectin binds to peripheral lymph node addressins (PNAds) on high endothelial venules (HEVs) that are sites where lymphocytes enter the lymphatic organs. Interestingly, MR is absent from HEVs and PNAds from lymphatic endothelium. Thus, lymphocyte L-selectin uses distinct ligand molecules to mediate binding at sites of lymphocyte entrance and exit within lymph nodes. Taken together, interaction between L-selectin and MR is the first molecularly defined mechanism mediating lymphocyte binding to lymphatic endothelium.

Cyclin A and Ki-67 with DNA content in benign and malignant prostatic epithelial lesions.

OBJECTIVE: To evaluate the usefulness of immunohistochemical staining of cyclin A and Ki-67 together with DNA content in the classification of benign prostatic hyperplasia, prostatic intraepithelial neoplasm (PIN) and prostatic carcinoma foci and to compare these parameters with each other and with parameters obtained from conventional histopathology. STUDY DESIGN: We selected 37 carcinoma, 18 PIN and 8 hyperplastic foci from prostatectomies done during 1996 and 1997 at Turku University Central Hospital. Cyclin A and Ki-67 staining was assessed by immunohistochemistry and DNA content by image cytometry. RESULTS: The hyperplastic, PIN and carcinoma foci differed clearly in their 2.5c exceeding rates, image cytometric proliferation indices and staining indices for cyclin A and Ki-67. No significant differences were found between these histologic entities in their modal DNA ploidy values. In carcinomas, cyclin A and Ki-67 indices differed between low, intermediate and high Gleason and World Health Organization grading groups. Diploid and tetraploid carcinomas had similar cyclin A and Ki-67 indices, which differed from those of aneuploid carcinomas. CONCLUSION: The 2.5c exceeding rate and image cytometric proliferation index as well as the cyclin A and Ki-67 indices differed significantly between different types of prostatic lesions. Cyclin A and Ki-67 had good correlations with the histologic grade of carcinoma.

Vascular adhesion protein 1 mediates binding of immunotherapeutic effector cells to tumor endothelium.

Tumor-infiltrating lymphocytes (TIL) can be used as an immunotherapeutic tool to treat cancer. Success of this therapy depends on the homing and killing capacity of in vitro-activated and -expanded TIL. Vascular adhesion protein 1 (VAP-1) is an endothelial molecule that mediates binding of lymphocytes to vessels of inflamed tissue. Here, we studied whether VAP-1 is involved in binding of TIL, lymphokine-activated killer (LAK) cells, and NK cells to vasculature of the cancer tissue. We demonstrated that VAP-1 is expressed on the endothelium of cancer vasculature. The intensity and number of positive vessels varied greatly between the individual specimens, but it did not correlate with the histological grade of the cancer. Using an in vitro adhesion assay we showed that VAP-1 mediates adhesion of TIL, LAK, and NK cells to cancer vasculature. Treatment of the tumor sections with anti-VAP-1 Abs diminished the number of adhesive cells by 60%. When binding of different effector cell types was compared, it was evident that different cancer tissues supported the adhesion of TIL to a variable extent and LAK cells were more adhesive than TIL and NK cells to tumor vasculature. These data suggest that VAP-1 is an important interplayer in the antitumor response. Thus, by up-regulating the expression of VAP-1 in tumor vasculature, it can be possible to improve the effectiveness of TIL therapy.

Microscopic acanthosis nigricans in type 2 diabetes.

BACKGROUND: Acanthosis nigricans (AN) has been associated with insulin resistance. Individuals with type 2 diabetes are insulin-resistant and, therefore, could be expected to manifest AN. However, the prevalence and predictors of AN are unknown in this population. OBJECTIVE: An outpatient population with Type 2 diabetes (DM) was compared with matched controls (C) for microscopic and clinical AN along with measurement of body habitus, insulin, glucose, and androgen levels. METHODS: Twenty-four individuals with DM (12M, 12F) from a tertiary care center were compared with 24 C (12M, 12F). Fasting glucose, insulin, sex hormone binding globulin, androstenedione, dihydroepiandrosterone sulfate, and testosterone were measured. Height, weight, waist/hip measures, and a clinical survey for acanthosis were recorded. A 2-mm skin biopsy from midaxilla of the nondominant arm was taken for pathological review. RESULTS: C and DM were matched for age and body mass index (BMI). Prevalence of microscopic AN in C was 12% (3/24) and in DM was 21% (5/24; NS). In C, AN was predicted by waist, waist/hip ratio, and fasting insulin measures, while none of the variables examined was predicative of AN in DM. CONCLUSIONS: Microscopic acanthosis nigricans was found in similar numbers of people with DM when compared with C. Fasting insulin levels most strongly predicted the presence of AN in C, while no significant predictors of AN were found in the population with DM.

Interpretation guidelines of DNA histograms from tissue sections of breast cancer.

BACKGROUND: Evaluation of nuclear DNA staining intensity from histological breast cancer sections has not always been accepted, because of the difficulties in interpreting the histograms. One reason for this is the lack of evidence based interpretation guidelines. MATERIALS AND METHODS: The DNA staining intensity of 140 breast cancer samples was measured with flow cytometry (FCM) and image cytometry (ICM). The methods were compared by using grading efficiency (GE). RESULT: First, the ICM histograms were evaluated with a computer assisted image cytometry system using different cut off points for aneuploidy. The GE results varied from 67.9-76.4%. Subjective interpretation and evaluation according two previously published interpretation methods did not improve the GE. Secondly, we excluded histograms which showed clearly different cell clones in FCM and ICM. The GE of remaining histograms was 77.9%. Comparison of these histograms allowed formulation of interpretation guidelines which improved the GE to 85.3%. CONCLUSIONS: This study suggests that efficient interpretation guidelines of section-based DNA histograms can be created.

Augmented expression of endothelin-1, endothelin-3 and the endothelin-B receptor in breast carcinoma.

AIMS: Endothelins (ETs) are peptides expressed in many tumours which may stimulate angiogenesis and desmoplasia. Because ETs have not been extensively studied mammary neoplasia, we assessed ET protein and mRNA expression and receptor mRNA expression in normal and neoplastic breast tissues. METHODS AND RESULTS: Tissues from five normal breasts, six fibroadenomas, seven ductal carcinomas in situ (DCIS) and 25 invasive carcinomas were stained with anti-ET-1 and anti-ET-3 antibodies and analysed using a grading system. ET-1, ET-3, ETA and ETB mRNA expression was assessed by quantitative RT-PCR from eight carcinomas and five normals. Weak staining for ET-1 and ET-3 was detected in all normals. Moderate to strong staining was seen in 72% and 64% of carcinomas for ET-1 and ET-3, respectively. Most fibroadenomas showed weak positivity for ET-1 (83%) and ET-3 (67%). ET-1 and ET-3 mRNA levels were upregulated in carcinomas compared with normal breast. No ETA mRNA was not detected in any tissue. ETB mRNA was detected in normal breast and was increased in carcinomas. CONCLUSION: These results suggest that the ET system is altered in breast carcinomas and this may be of importance in the progression from in-situ to invasive carcinoma.

Hybrid Capture Human Papillomavirus Testing as an Adjunct to the Follow-Up of Patients with ASCUS and LGSIL Pap Smears: A Study of a Screening Population.

OBJECTIVES: We set out to evaluate Hybrid Capture (Digene Corporation, Silver Spring, MD) testing for human papillomavirus (HPV) in the management of a screening population with atypical squamous cells of undetermined significance (ASCUS) or low-grade squamous intraepithelial lesion (LGSIL). METHODS: A total of 619 patients with ASCUS or LGSIL Papanicolaou smears were tested for high-risk HPV types. They then were followed at 6-month intervals with Papanicolaou smears and repeat HPV testing. Patients with persistent or progressive disease were referred for colposcopy. HPV results were compared to the most significant follow-up cytological or colposcopic diagnosis to determine whether Hybrid Capture HPV testing was predictive of outcome. A cost analysis was performed. RESULTS: Follow-up of 12 to 30 months was available for 471 patients (76.1%). Outcome diagnoses for 190 patients who initially tested HPV-positive were as follows: 49% benign, 14% ASCUS, 19% LGSIL, 18% HGSIL, and 0.5% cancer. For 281 patients who initially tested HPV-negative, outcomes were 77% benign, 14% ASCUS, 6% LGSIL, 2% HGSIL, and 0.3% cancer. Twenty-six of the patients with HGSIL had two or more HPV tests, and all these patients had at least one positive result. CONCLUSIONS: Hybrid Capture testing for high-risk HPV types was predictive of which patients presenting with ASCUS/LGSIL would persist or progress to HGSIL (p < .001). The cost of adding Hybrid Capture testing was intermediate between the cost of cytological follow-up and referral of all patients with ASCUS/LGSIL to colposcopy.

Immunohistochemical labelling for prostate-specific antigen in breast carcinomas.

Immunohistochemical detection of prostate-specific antigen (PSA) is an aid in determining the prostatic origin of metastatic cells. However, small amounts of PSA have also been found in non-prostatic tissues and tumors, for example in some breast carcinomas, by highly sensitive immunofluorometric methods, but also by immunohistochemistry. Our aim was to evaluate the prevalence and prognostic value of histologically confirmed PSA immunoreactivity in breast carcinoma. Sections of formalin-fixed, paraffin-embedded samples from 171 breast carcinomas were immunostained for PSA. The staining results were compared with the mitotic activity, tumor size, histological grade, steroid receptors and follow-up data. For analysis the material was divided into subgroups according to the patients' age (pre- and postmenopausal). PSA was found by immunohistochemistry in 54 (32%) breast carcinomas. In survival analysis of the whole patient material PSA positivity did not show prognostic value. Among premenopausal patients concomitant estrogen receptor and PSA-negativity proved to be associated with high risk of breast cancer death (RR 6.2), also after adjustment for tumor size, histological grade, and axillary lymph node status. Among postmenopausal patients PSA positivity was associated with progesterone receptor positivity and high differentiation but not with age, nodal status, or mitotic activity. PSA can be detected by immunohistochemistry in a considerable number of breast carcinomas. PSA immunoreactivity alone does not seem to have any value as general prognosticator of breast carcinoma patients. However, concomitant absence of PSA and estrogen receptors was an indicator of unfavourable prognosis among premenopausal patients.

Phospholipase A2 in serum and colonic mucosa in ulcerative colitis.

Group II phospholipase A2 is involved in the pathogenesis of various inflammatory diseases and in the host defence against bacteria. The enzyme is expressed in the epithelial cells of colonic mucosa in ulcerative colitis. In this study, we measured the concentration of group II phospholipase A2 in serum and colonic mucosa of patients with ulcerative colitis of different severity and of control patients without any inflammatory disease. The activity of ulcerative colitis was assessed by endoscopy. The concentration of group II phospholipase A2 was measured with an immunoassay. The concentrations of group II phospholipase A2 in serum and colonic mucosa were significantly higher in patients with active and inactive ulcerative colitis than in controls. However, the group II phospholipase A2 levels did not separate patients with different disease activity. The concentration of group II phospholipase A2 in colonic mucosa corresponded with the mucosal inflammatory activity (higher in active colonic areas) intra-individually, but not between different patients with ulcerative colitis. Serum group II phospholipase A2 values were above the normal reference range more often than the values of 11 standard laboratory blood tests widely used for the follow-up of inflammatory activity in ulcerative colitis. These results indicate that the concentration of group II phospholipase A2 is increased in serum and colonic mucosa of patients with ulcerative colitis. The clinical value of the measurement of group II phospholipase A2 in the follow-up of ulcerative colitis remains to be clarified.

Gene expression of group II phospholipase A2 in intestine in Crohn's disease.

OBJECTIVE: Phospholipase A2 (PLA2) has been suggested to play an important role in the pathogenesis of inflammatory bowel diseases. Our aim was to identify cells that express group II phospholipase A2 (PLA2-II) at the mRNA and enzyme protein levels in the intestine in Crohn's disease. METHODS: Tissue samples were obtained from the intestine of 20 patients with Crohn's disease (seven operated and 13 colonoscopied) and from eight control patients without inflammatory diseases. The samples were studied by immunohistochemistry for PLA2-II enzyme protein and in situ hybridization for PLA2-II mRNA. RESULTS: PLA2-II protein and mRNA were detected in the Paneth cells of the small intestinal mucosa in all patients and controls. PLA2-II protein and mRNA were found in the columnar epithelial cells of the small intestinal mucosa in six of eight and eight of eight patients with Crohn's ileitis, respectively. In the eight control patients PLA2-II protein and mRNA were not found in these cells (p = 0.007 and p < 0.001, respectively). Metaplastic Paneth cells, which consistently contained PLA2-II mRNA, were found in the colonic mucosa in five of six patients with Crohn's colitis and of one of eight control patients (p = 0.026). The columnar epithelial cells of the colonic mucosa contained PLA2-II protein in three of six and PLA2-II mRNA in six of six patients with Crohn's colitis, whereas the protein was found in these cells in none of eight of the controls (p = 0.055) and the mRNA in only one of eight (p = 0.005) controls. CONCLUSIONS: In Crohn's disease, Paneth cells and columnar epithelial cells of the small and large intestinal mucosa synthesize PLA2-II at the site of active inflammation.

Elevated group II phospholipase A2 mass concentration in serum and colonic mucosa in Crohn's disease.

Group II phospholipase A2 has been proposed to play an important role in the pathophysiology of inflammatory bowel diseases. This enzyme has also been linked to host defence mechanisms against bacteria. The current study aimed at measuring the mass concentrations of group II phospholipase A2 in serum and colonic mucosa of patients with Crohn's disease of different severity and of appropriate control patients without any inflammatory disease. The activity of the disease was determined by clinical factors (the simple index score) and endoscopic and histological scoring. The mass concentration of group II phospholipase A2 was measured by a time-resolved fluoroimmunoassay. The mass concentrations of group II phospholipase A2 in serum and colonic mucosa were significantly higher both in patients with active and inactive Crohn's disease when compared with controls. There was statistically significant difference in the mass concentration of group II phospholipase A2 in colonic mucosa but not in serum between inactive and active Crohn's disease. The current results indicate that the mass concentration of group II phospholipase A2 is increased in serum and colonic mucosa of patients with Crohn's disease and that the latter is associated with the degree of the inflammatory activity in the intestinal wall. These results support the idea that group II phospholipase A2 is involved in the local and generalised pathological processes of Crohn's disease.

Group II phospholipase A2 in human male reproductive organs and genital tumors.

BACKGROUND: Group II phospholipase A2 (PLA2) is a lipolytic enzyme suggested to play a role in inflammation and antibacterial defence. In seminal fluid, the concentration of PLA2 is exceedingly high under normal circumstances (about 1,000 times the concentration in blood plasma of healthy humans). To elucidate the origin of the enzyme present in seminal plasma, we investigated the expression of group II PLA2 in male reproductive organs both at protein and mRNA levels. In addition, the presence of the enzyme was studied in common male genital tumors. METHODS: The methods used were immunocytochemistry, in situ hybridization, and Northern blotting. RESULTS: Northern blotting gave positive results for group II PLA2 mRNA in normal prostate, whereas other normal genital tissues gave negative results. Immunohistochemistry and in situ hybridization of group II PLA2 gave identical results. The enzyme was produced exclusively by the secretory epithelial cells of the prostatic gland. Surprisingly, expression was restricted to the posterior lobe and paraurethral glands of the prostate. Cells of prostatic adenocarcinoma expressed group II PLA2, whereas cells of other male genital tumors contained neither the enzyme protein nor the mRNA of group II PLA2. In some cases prostatic cancer cell seemed to express group II PLA2 at a higher rate than normal prostatic gland cells. CONCLUSIONS: The high content of group II PLA2 in seminal plasma is due to the local production and secretion of the enzyme by the epithelial cells of the prostatic glands. Group II PLA2 is expressed focally, suggesting that specialized prostatic glands secrete this enzyme. All prostatic adenocarcinomas tested expressed group II PLA2 in variable amounts.

Image cytometry of breast carcinomas that are DNA diploid by flow cytometry: time to revise the concept of DNA diploidy?

OBJECTIVE: To investigate whether breast carcinomas found to be DNA diploid by flow cytometry (FCM) are still diploid if reassessed by image cytometry (ICM). STUDY DESIGN: In a series of 286 breast cancers analyzed by FCM there were 100 (35%) cancers that were classified as DNA diploid. Fourteen of the 100 diploid cases were selected for further analysis with ICM because the patient had died of breast cancer within 11-84 months after the diagnosis (a group with unfavorable outcomes), and 19 cases were selected at random from the cases who had no recurrence of cancer during follow-up of six or more years (a favorable group). RESULTS: Eleven (33%) of the 33 cases turned out to be DNA nondiploid, with a DNA index > or = 1.2 when analyzed by ICM. Nine of the 11 DNA aneuploid samples by ICM were found among the 14 patients with unfavorable prognoses and only 2 among the 19 patients with favorable outcomes (P = .002). The five-year survival rate of the women with DNA diploid cancer by both methods was 86%, whereas that of patients with DNA aneuploid cancer by ICM was 36% (P = .002). CONCLUSION: The results show that some breast carcinomas classified as DNA diploid based on FCM are not DNA diploid by ICM and that such carcinomas are associated with poorer outcomes than the ones that are DNA diploid also by ICM. The prognostic significance of DNA ploidy in breast cancer may need to be reexamined in studies where both FCM and ICM are used.

Assessment of cytologic follow-up as the recommended management for patients with atypical squamous cells of undetermined significance or low grade squamous intraepithelial lesions.

BACKGROUND: The optimal management of low grade Papanicolaou (Pap) smear abnormalities remains controversial. This center's experience with recommending cytologic follow-up for women with atypical cells of undetermined significance (ASCUS) or low grade squamous intraepithelial lesions (LSIL) was reviewed to determine outcome and patient/physician compliance. METHODS: The records were reviewed on women with Pap smears reported as either ASCUS (320) or LSIL (112) who did not have a history of dysplasia. The cytologic and colposcopic follow-up for a 2-year period was obtained from the laboratory data base that includes the colposcopy and cancer referrals for this region. Repeat Pap smear in 6 months was recommended. If patients subsequently demonstrated high grade SIL (HSIL) or persistent ASCUS or LSIL over three time intervals, colposcopic evaluation was recommended. RESULTS: The outcome was determined by the most significant diagnosis among the follow-up Pap smears or colposcopic biopsies. 29% of patients were lost to follow-up. Of the remaining patients, 70.5% reverted to normal or benign cellular changes, 25.3% persisted as ASCUS or LSIL, and 5.2% progressed to HSIL. The majority of patients (68%) were referred for colposcopy for persistent mildly abnormal Pap smears. The timing of referral ranged from 3-30 months. CONCLUSIONS: These results suggest that cytologic follow-up of women with low grade Pap smear abnormalities will identify a large number whose smears will regress to normal. A small but significant proportion of women showed subsequent HSIL. Most HSIL was detected within 1 year of the initial abnormal Pap smear and the majority of intervening Pap smears also were abnormal. Approximately one third of patients did not have follow-up within the study system and their outcome was uncertain. Although the recommendations are standard, patterns of follow-up and referral to colposcopy varied widely, suggesting that the guidelines need to be reinforced to both patients and physicians. [See editorial on pages 1-4, this issue.]

Gene expression of group II phospholipase A2 in intestine in ulcerative colitis.

BACKGROUND: It has been suggested that phospholipase A2 (PLA2) has an essential role in the pathogenesis of inflammatory bowel diseases. AIMS: This study aimed at identifying cells in intestinal and mesenteric tissue samples that might express group II phospholipase A2 (PLA2-II) at the mRNA and enzyme protein levels in patients with ulcerative colitis. PATIENTS AND TISSUE SAMPLES: Tissue samples were obtained from the intestine, mesentery, skeletal muscle, and subcutaneous fat of six patients who underwent panproctocolectomy for severe ulcerative colitis. Mucosal biopsy specimens were obtained from the colon of another group of six patients with ulcerative colitis during routine diagnostic colonoscopies. Tissues from six patients without intestinal inflammatory diseases served as controls. METHODS: Tissue samples were studied by light microscopy, immunohistochemistry for PLA2-II enzyme protein, and in situ hybridisation and northern hybridisation for PLA2-II mRNA. RESULTS: PLA2-II mRNA and PLA2-II protein were detected in metaplastic Paneth cells in six patients and in the columnar epithelial cells of colonic mucosa in four out of six patients with active ulcerative colitis. Positive findings were less numerous in patients with mild ulcerative colitis. Only two out of six control patients had a weak positive signal for PLA2-II mRNA and one of these two patients had a weak positive immunoreaction for PLA2-II in columnar epithelial cells in the colonic mucosa. None of the control patients had metaplastic Paneth cells. CONCLUSIONS: Metaplastic Paneth cells and colonic epithelial cells synthesise PLA2-II in ulcerative colitis. The activity of the PLA2-II synthesis seems to be related to the degree of inflammation in the diseased bowel.

Immunohistochemical labelling for prostate specific antigen in non-prostatic tissues.

Immunohistochemical detection of prostate specific antigen (PSA) in metastases of adenocarcinomas is widely used as an aid to identify the prostatic origin of metastatic cells. However, on the one hand, PSA may not be expressed in some poorly differentiated prostatic carcinomas, while on the other, PSA immunoreactivity has been found in small amounts in non-prostatic tissues. The aim of the current study was to evaluate the prevalence of PSA immunoreactivity in normal non-prostatic tissues and in breast carcinoma. PSA was localized by immunohistochemistry with four commercial antibodies in 34 different normal human tissues, and in 15 ductal and seven apocrine breast carcinomas. Concentrations of PSA in tissue homogenates of prostate and nine non-prostatic tissues from autopsied subjects were measured by a two-site immunoradiometric assay. Weak PSA immunoreactivity was found by immunohistochemistry in kidney, parotid gland and pancreatic tissues. Variable PSA immunoreactivity was seen in three cases of ductal (20%) and two cases of apocrine breast carcinoma (28%). No consistent PSA immunoreactivity was found in homogenates of non-prostatic tissues by the immunoradiometric assay. We conclude that PSA is a quite specific marker of prostatic tissue. However, there are some non-prostatic neoplastic and normal tissues that express PSA. Therefore, a definite diagnosis of metastasis of prostatic origin cannot be made on the basis of immunolabelling for PSA alone.

Metabolic imaging of ovarian tumors with carbon-11-methionine: a PET study.

UNLABELLED: This study examines the potential of 11C-methionine as a PET tracer in metabolic imaging of benign and malignant ovarian tumors. METHODS: Four patients with one or two benign ovarian tumors (endometriomas or cystadenomas), two patients with a tumor of borderline malignancy and seven patients with ovarian cancer were studied with 11C-methionine and PET before laparotomy. CT or MRI were performed as a reference. Tracer uptake was quantitated by calculating tracer standardized uptake values (SUVs) and the kinetic influx constants (Ki values). RESULTS: Benign or borderline malignant tumors did not accumulate 11C-methionine, whereas all carcinomas had significant uptake. The mean SUV of the primary carcinomas was 7.0 (s.d., 2.2) and the mean Ki was 0.14 min-1 (s.d., 0.1 min-1), but the distribution of tracer uptake was highly heterogenous in four of six tumors. CONCLUSION: Ovarian cancer can be imaged with 11C-methionine and PET. This method also may be of value in the differential diagnosis between benign and malignant ovarian neoplasms. Due to physiological accumulations and methodological limitations, the value of 11C-methionine PET in the staging of ovarian cancer appears to be limited.