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PubMed2005

Usefulness of ascitic fluid cholesterol as a marker for malignant ascites.

BACKGROUND: The differential diagnosis of ascites is a common clinical problem. However, the capability to distinguish malignant from non-malignant causes of ascites using available biochemical techniques would obviate many expensive and time-consuming diagnostic studies on patients presenting with ascites of unknown etiology. Therefore, this study was planned to evaluate the diagnostic efficacy of ascitic fluid cholesterol in comparison to the efficiency of ascitic/serum total protein, pH, glucose, total leukocyte count, and the serum/ascitic albumin gradient in differentiating "malignant" from non-malignant ascites. MATERIALS/METHODS: A total of 50 patients (25 with malignant ascites and 25 with non-malignant) were evaluated for total ascitic protein, ascites/serum (A/S) total protein ratio, serum ascites albumin gradient (SAAG), ascitic pH, serum & ascitic cholesterol with glucose. RESULTS: The mean ascitic cholesterol level was significantly higher in malignant ascites than in non-malignant ascites, with a cut off level of 70 mg/dl for ascitic fluid cholesterol; 22/25 (88%) patients with malignant ascites could be separated from the 25 patients with non-malignant ascites. The specificity (100%) and diagnostic efficiency (94%) of ascitic fluid cholesterol is better than the 84% specificity and 86% diagnostic efficiency of serum ascitic albumin gradient. CONCLUSIONS: Total Ascitic protein (70%), Ascitic serum protein ratio (74%), ascitic leukocyte count (54%), and malignant cytology (82%) yielded much lower diagnostic efficiency than ascitic fluid cholesterol (94%) or SAAG (86%) in the diagnosis of malignant ascites.

Adolescent↗

PubMed1991

Malignant transformation of human fibroblasts correlates with increased activity of receptor-bound plasminogen activator.

To determine whether a relationship exists among urokinase plasminogen activator (u-PA) activity, tissue plasminogen activator (t-PA) activity, and the malignant transformation of human fibroblasts, we measured receptor-bound and secreted u-PAs and t-PA activity in fibroblast cell strains of a unique cell lineage and compared the results with the values obtained in human fibrosarcoma-derived cell lines and control cell lines. The lineage consists of four nonmalignant, infinite life span cell strains, clonally derived from a finite life span, neonatal foreskin-derived cell line or one of its derivatives and 10 malignant cell strains clonally derived from that same derivative. Seven of the latter were malignantly transformed by K-, H-, or N-ras oncogene transfection, two were obtained following carcinogen treatment, and one arose spontaneously. All 10 malignant strains in this lineage exhibited significantly higher levels of activity of receptor-bound u-PA than was found in the cell strain from which they arose or the nonmalignant cell strains derived from it. The ras oncogene-transformed malignant strains also exhibited significantly higher levels of activity of receptor-bound t-PA than their cell strain of origin. The other three malignant strains showed undetectable levels, consistent with their attaining the malignant state by an alternate process. The five fully malignant fibrosarcoma-derived cell lines tested also showed high levels of receptor-bound u-PA and t-PA. The majority (greater than or equal to 80%) of the nonmalignant control cell lines did not do so. The 10 malignant cell strains in the lineage also exhibited higher levels of activity of secreted high molecular weight u-PA or t-PA than did their cell strain of origin and the nonmalignant cell strains derived from it, as did the malignant fibrosarcoma-derived cell lines. The data suggest that the malignant state of human fibroblasts is always associated with high levels of activity of receptor-bound u-PA, and in addition cells transformed to the malignant state are very likely to exhibit high levels of receptor-bound t-PA and secreted forms of plasminogen activators.

Cell Transformation, Neoplastic↗

PubMed1995

Interval changes in nonpalpable breast lesions as an indication of malignancy.

OBJECTIVE: To determine whether the patterns of interval changes in nonpalpable breast lesions can be used to determine malignancy. PATIENTS AND METHODS: The authors reviewed the records for 128 nonpalpable breast lesions detected by mammography between March 1990 and May 1992 for which previous imaging studies were available. Changes in size, density and contour of the 59 masses and changes in size, number, configuration and pattern for the 69 cases involving microcalcifications were determined from comparison of the current mammograms with the earlier imaging studies, obtained 6 to 42 months previously. These findings were correlated with the pathological diagnosis based on needle localization and excisional biopsy. RESULTS: Twelve (55%) of the 22 new masses and 15 (48%) of the 31 masses that changed were malignant, but none of the 6 masses that did not change were malignant (chi 2 test, p < 0.01). All of the 31 masses that changed increased in size (and of these, 15 [48%] were malignant). In addition, 14 (45%) of the masses that changed exhibited increased density (and of these 9 [64%] were malignant), and 11 (35%) became irregular (and all of these were malignant). Eight (47%) of the 17 cases of new calcifications, 18 (43%) of the 42 cases of calcifications that changed and none of the 10 cases of unchanged calcifications were malignant (chi 2 test, p < 0.01). Twelve (44%) of the 27 calcifications that changed in area and 14 (40%) of the 35 that changed in number were malignant. Fifteen (60%) of the 25 calcifications that changed from scattered to grouped and 8 (53%) of the 15 that changed from punctate to linear were malignant. CONCLUSION: A change in the density or contour of a mass is a fairly definite sign of malignancy. The authors conclude that interval observation is a good method of detecting malignancy in breast masses but is less reliable for detecting malignancy in calcifications.

Biopsy↗

PubMed1996

Long-term results and prognostic factors after repair of abdominal aortic aneurysm with concomitant malignancy.

OBJECTIVE: Long-term results after repair of abdominal aortic aneurysm (AAA) with concomitant malignancy were reviewed, and factors which may affect survival were analyzed. DESIGN: Retrospective series with follow-up of three to 125 months. Setting. Department of Surgery, Matsuyama Red Cross Hospital, Matsuyama, Japan. PATIENTS: Among 112 consecutive repairs of AAA, 16 cases had concomitant malignancy. The malignant lesions included eight gastric cancers and eight other malignant tumours. The malignancies were divided using TNM Classification into an early stage (stage O or I) group (n=9) and an advanced stage (stage II, III, or IV) group (n=7). INTERVENTIONS: All aneurysms were successfully repaired, and simultaneous resection of the concomitant malignancy was performed in five cases. While 13 malignant lesions were resected completely, three could not be resected completely, but were treated by other surgical procedures. MEASURES: Survival rates were predicated using the Kaplan-Meier method. The log-rank test was used to compare survival rates. RESULTS: The one-, two-, and five-year survival rates after repair of AAA were 80%, 72% and 63%, respectively. The survival rates for the early stage group were significantly higher than those for the advanced stage group (p<0.05). Patients with concomitant gastric cancer or who underwent complete resection of the malignant lesion survived longer. CONCLUSION: In patients with concomitant AAA and malignancy, factors influencing survival for those with malignant lesions also affected survival after aneurysmectomy. Detection of early-stage concomitant malignancy and more aggressive treatment for the malignancy may improve the outcome.

Age Factors↗

PubMed1996

An association between renal cell carcinoma and lymphoid malignancies. A case series of eight patients.

BACKGROUND: Second primary malignancies have been described in patients with both solid tumors and hematologic malignancies. However, an association between renal cell carcinoma and lymphoid malignancies has rarely been described. Eight patients with both disorders are described and possible explanations for the association are reviewed. METHODS: A retrospective review of records from patients with renal cell carcinoma, lymphoma, leukemia, or myeloma discharged from the University of California at Los Angeles between July 1, 1993 and June 30, 1995 was performed. Renal cell carcinoma was diagnosed in 186 patients, whereas 405 had a lymphoid malignancy. Eight patients with both disorders were identified. RESULTS: In four of the eight patients, the renal cell carcinoma was diagnosed prior to their hematologic malignancy, whereas in the remaining four patients, the lymphoid malignancy was diagnosed first. Renal cell carcinoma is observed in the general population in 12.5 persons per 100,000 and hematologic malignancies in 31.8 per 100,000. The number of cases of lymphoid malignancies expected in the 186 renal cell carcinoma patients is lower than the 4 cases actually observed (P < 0.01). Likewise, the number of renal tumors expected in the 405 patients with hematologic malignancies is fewer than the 4 cases observed (P < 0.01). CONCLUSIONS: The incidence of renal cell carcinoma and lymphoid malignancy occurring in the same patient is higher than that expected in the general population. This association cannot be explained by treatment-related development of a second malignancy. A common genetic mutation or an immunomodulatory role of the first malignancy predisposing to the second are possibilities but further investigation is warranted.

Aged↗

PubMed1996

Prognostic parameters for survival of patients with malignant mesenchymal tumors of the uterus.

BACKGROUND: Malignant mesenchymal uterine neoplasms are the most aggressive type of primary uterine tumors, with most patients dying within a few years of diagnosis. Thus, it would be very important to define prognostic factors for predicting the malignancy potential of at least some of their subtypes. METHODS: Flow cytometric cell cycle analysis (proliferative activity, DNA ploidy, and DNA index) was performed on archival paraffin embedded blocks from 80 patients with malignant mesenchymal uterine neoplasms (endometrial stromal sarcomas, malignant smooth muscle tumors, and malignant Müllerian mixed tumors). The Cox proportional hazards regression model was used to assess relative effects of the following factors on patient survival: clinical stage, mode of therapy, DNA+proliferative activity, DNA index, histologic type, cellularity, degree of atypia, mitotic activity, and depth of myometrial invasion. RESULTS: There were 9 low grade stromal sarcomas, 17 high grade stromal sarcomas, 8 smooth muscle neoplasms with uncertain malignant potential, 23 leiomyosarcomas, and 16 homologous and 7 heterologous malignant Müllerian mixed tumors. In univariate analysis for stromal sarcomas, statistical significance was found for DNA ploidy+proliferative activity (P < 0.001), histologic type (P = 0.005), and DNA index (P < 0.001). In multivariate analysis, DNA index appeared to be the only significant parameter influencing patient survival (P = 0.005). In univariate analysis for malignant smooth muscle neoplasms, statistical significance was detected for mitotic activity (P = 0.049) and International Federation of Gynecology and Obstetrics classification (P = 0.021), but in multivariate analysis, clinical stage appeared to be the only significant parameter influencing patient survival (P = 0.032). In univariate analysis for malignant Müllerian mixed tumors, statistical significance was found for the depth of myometrial invasion (P = 0.039), DNA index (P = 0.037), and clinical stage (P = 0.013), but in multivariate analysis, only the depth of myometrial invasion (P = 0.036) and clinical stage (P = 0.025) were of statistical significance. CONCLUSIONS: The most powerful prognostic indicator for stromal sarcomas was the DNA index, for malignant smooth muscle neoplasms it was the clinical stage, and for malignant Müllerian mixed tumors it was the depth of myometrial invasion.

Analysis of Variance↗

PubMed1995

Effects of propofol on Ca2+ regulation by malignant hyperthermia-susceptible muscle membranes.

BACKGROUND: The effects of inhalation anesthetics on Ca2+ regulation in malignant hyperthermia-susceptible skeletal muscle are considered to be responsible for triggering malignant hyperthermia. The intravenous anesthetic propofol does not trigger malignant hyperthermia in susceptible patients or experimental animals, suggesting that there are important differences between the effects of propofol and the effects of inhalation anesthetics on Ca2+ regulation in malignant hyperthermia-susceptible muscle. Understanding these differences may help to clarify the mechanisms responsible for triggering malignant hyperthermia. METHODS: To investigate the effects of propofol on Ca2+ regulation by malignant hyperthermia-susceptible skeletal muscle, we determined its effects on the membrane channels and pumps that control myoplasmic Ca2+ concentrations: the sarcoplasmic reticulum ryanodine receptor, the transverse tubule dihydropyridine receptor, and the sarcoplasmic reticulum Ca(2+)-adenosine triphosphatase (Ca(2+)-ATPase). Terminal cisternae-derived sarcoplasmic reticulum vesicles enriched in the junctional proteins of the sarcoplasmic reticulum and the transverse tubule membranes were isolated from the muscle of malignant hyperthermia-susceptible and normal pigs. Ca2+ flux, Ca(2+)-ATPase, and ligand binding measurements on these isolated vesicle preparations were performed in the presence of varying propofol concentrations. RESULTS: Propofol (10-500 microM) had no effect on ryanodine receptor-mediated Ca2+ efflux from muscle membrane vesicles. Propofol (1-100 microM) also had no effect on sarcoplasmic reticulum vesicle [3H]ryanodine binding, whereas higher concentrations (200-300 microM) slightly inhibited [3H]ryanodine binding. Binding of the dihydropyridine receptor Ca2+ channel blocker [3H]PN200-110 to these preparations was inhibited by propofol (10-300 microM). Ca(2+)-ATPase activity was stimulated by 10-100 microM propofol but was inhibited by higher concentrations. In all cases, the effects of propofol on malignant hyperthermia-susceptible and normal membrane preparations were similar. CONCLUSIONS: In contrast to malignant hyperthermia-triggering inhalation anesthetics, propofol does not stimulate malignant hyperthermia-susceptible or normal ryanodine receptor channel activity, even at > 100 times clinical concentrations. Effects on dihydropyridine receptor and Ca(2+)-ATPase function, however, are similar to the effects of inhalation anesthestics and require much lower concentrations of propofol. These findings, demonstrating that propofol does not activate ryanodine receptor Ca2+ channels, suggest a plausible explanation for why propofol does not trigger malignant hyperthermia in susceptible persons.

Animals↗

PubMed1998

Pleural fluid pseudouridine in malignant and benign pleural effusions.

Pseudouridine in urine and plasma has been proved to be a useful tumour marker in many malignant conditions. We studied its usefulness in pleural fluid for distinguishing malignant from non-malignant pleural effusions. Pleural fluid pseudouridine concentrations in different groups of patients with pleural effusion (31 malignant, 29 benign, 16 unknown, 1 double pathology) was measured and compared. Its usefulness in distinguishing malignant from non-malignant pleural effusions was analysed by receiver-operating characteristic (ROC) curve analysis. Pseudouridine concentrations in the malignant group were significantly higher than the non-malignant group (P < 0.017, Bonferroni adjustment) with values overlapping extensively at the lower end. The area-under-the curve (AUC) value in the ROC curve analysis was 0.675 (P < 0.05). We conclude that the pleural fluid pseudouridine is of limited clinical value in distinguishing malignant from non-malignant pleural effusion due to its extensive overlap. However, it is useful when the concentration is higher than 65 mumol/L, which indicates malignancy.

Area Under Curve↗

PubMed2005

Downregulation of metastasis suppressor genes in malignant pheochromocytoma.

There is no reliable method currently available to predict malignant potential of pheochromocytoma based on conventional histology or genetic, molecular or immunohistochemical markers. Metastasis suppressor genes affect the spread of several cancers and, therefore, may provide promise as prognostic markers or therapeutic targets for malignant pheochromocytoma. We hypothesized that the downregulation of metastasis suppressor genes in malignant pheochromocytoma may play a role in malignant behavior. We applied quantitative real-time polymerase chain reaction (QRT-PCR) to 11 metastasis suppressor genes. These genes are known to be involved in the regulation of important cancer-related cellular events, such as cell growth regulation and apoptosis (nm23-H1, TIMP-1, TIMP-2, TIMP-3, TIMP-4, TXNIP and CRSP-3), cell-cell communication (BRMS-1), invasion (CRMP-1) and cell adhesion (E-Cad and KiSS1). The study included 15 benign and 10 malignant pheochromocytomas. Six metastasis suppressor genes (nm23-H1, TIMP-4, BRMS-1, TXNIP, CRSP-3 and E-Cad) were downregulated significantly in malignant compared to benign pheochromocytoma (p < 0.05, Mann-Whitney U-test). We applied a non-linear rule using median malignant value (MMV) as a threshold to use metastasis suppressor genes to distinguish malignant from benign samples. After cross-validation, the non-linear rule produced no errors in 10 malignant samples and 3 errors in the 15 benign samples, with an overall error rate of 12%. These results suggest that downregulation of metastasis suppressor genes reflect malignant pheochromocytoma with a high degree of sensitivity. Thus, we conclude that altered function of these metastasis suppressor gene pathways may play an important role in the malignant behavior of pheochromocytoma.

Adrenal Gland Neoplasms↗

PubMed1977

Identification of a chromosome that controls malignancy in Chinese hamster cells.

A chromosome that controls malignancy in Chinese hamster cells has been identified by analysis of the Giemsa banding pattern of a malignant cell line transformed by simian virus 40 (SV40), non-malignant revertants from this line, segregants from the revertants that were again malignant and a cell line transformed by methylcholanthrene. The malignant cell line transformed by SV40 was near diploid and had gained additional material of chromosome 3. Revertants with a suppression of malignancy and malignant revertants from which they were derived. Malignancy of these cells was associated with the ability to form colonies in agar. Cells of a line transformed by methylcholanthrene were malignant, formed almost no colonies in agar and the only chromosome change from the normal diploid chromosome banding complement was the addition of a long arm of chromosome 3. The results indicate that chromosome 3 carriers gene(s) that control malignancy in Chinese hamster cells in cell lines transformed by a viral or a chemical carcinogen and that malignancy was induced in both cell types by an increase of these genes.

Animals↗

PubMed1999

[Second malignancies after the therapy of Hodgkin's disease: the Freiburg collective 1940 to 1991].

AIM: To quantify the risk of second malignancies in patients with Hodgkin's disease treated at the Department of Radiotherapy, University Clinic Freiburg, with the object of comparing this risk with the international experience and as a contribution to the discussion about future treatment. PATIENTS AND METHODS: Second malignancies were reviewed in 1,588 patients treated for Hodgkin's disease between 1940 and 1991. Treatment consisted of involved or extended field radiotherapy as a single modality or in combination with chemotherapy. Before the early 1970's, chemotherapy used (sequential) monodrug regimens. The mean follow-up was 8.3 years. The cumulative risk was calculated using the Kaplan-Meier method and related to the risk of a normal population taken from epidemiological data of the National Cancer Institute. An estimate of radiation dose at the site of origin of the second malignancy was obtained from representative measurements employing an Alderson phantom. RESULTS: After 5, 10, 15 and 20 years the cumulative risk for all malignancies was 1.5%, 4.2%, 9.4% and 21%, respectively; for solid tumors it came to 1.2%, 3.1%, 7.9% and 19%; for non-Hodgkin lymphoma (NHL) the risk amounted to 0.1%, 0.9%, 1.4% and 1.9%; and for leukemia it was 0.1%, 0.3%, 0.6% and 0.6%. For the same time points the relative risk for all malignancies was calculated to be 1.1, 1.4, 1.8 and 2.5; for solid tumors it came to 1.0, 1.1, 1.6 and 2.5; for NHL it amounted to 3.3, 11.8, 9.3 and 8.0; and for leukemia it was 3.3, 3.1, 3.4 and 2.1. For combinations of radiotherapy and chemotherapy the risk for second malignancies was highest in patients receiving ABVD any time during their treatment. 51% of the second malignancies were located infield, 22% at the field border and 27% outfield. In those cases for which the cause of death was known, Hodgkin's disease accounted for 79% followed by second malignancies accounting for 8%. The results obtained in Freiburg fell within the range reported in international publications. CONCLUSION: The increased incidence of second malignancies in cured Hodgkin's patients is along-term risk making regular follow-up mandatory. Although part of the second malignancies are unrelated to therapy, there is a need to carefully collect the data from patients treated according to new protocols in order to detect any changes in the number or kind of second malignancies in due time. This may well lead to a reassessment of therapeutic concepts.

Adult↗

PubMed1993

Malignant melanoma in xeroderma pigmentosum: search for a precursor lesion.

BACKGROUND: Malignant melanomas occur with increased frequency and at an early age in patients with xeroderma pigmentosum (XP). OBJECTIVE: The purpose of this study was to describe the histologic features of malignant melanomas in patients with XP and to search for a possible precursor lesion. METHODS: Clinical records and hematoxylin-eosin-stained sections of 19 malignant melanomas from seven patients with XP were examined. A search was conducted for malignant melanoma precursor lesions (melanocytic nevi and solar lentigines lateral to and contiguous with the malignant melanomas). Basal cell carcinomas removed from the same patients were used as controls. RESULTS: Malignant melanomas were characteristically found in biopsy specimens of small elevations and/or changed color foci arising in large, flat, darkly pigmented, gradually enlarging macules. Histologically, solar lentigo was lateral to and contiguous with malignant melanoma in 88% of the malignant melanomas. Transitional areas were present. A significantly lower number (22%) of contiguous solar lentigines, without transitional areas, were observed in the basal cell carcinoma controls. Most of the invasive malignant melanomas were spindle cell malignant melanomas. CONCLUSION: We propose that solar lentigo is the most common precursor lesion of malignant melanoma in patients with XP.

Adolescent↗

PubMed2004

The malignant potential of endometrial polyps.

OBJECTIVES: To determine the pre-malignant and malignant potential of endometrial polyps and to assess whether different clinical parameters are associated with malignancy in the polyps. STUDY DESIGN: Four hundred and thirty consecutive cases of hysteroscopic diagnosis of endometrial polyp were retrieved. The medical records, preoperative vaginal sonography results and histopathology findings were reviewed. Statistical analysis was performed. RESULTS: Hysteroscopy truly identified endometrial polyps in 95.7% of the cases. In 11.4% cases, hyperplasia without atypia was found in the endometrial polyp. In 3.3 and 3.0% of women pre-malignant or malignant conditions were found in the polyp. Older age, menopause status and polyps larger than 1.5 cm were associated with significant pre-malignant or malignant changes, although the positive predictive value for malignancy was low. All the malignant polyps were diagnosed only in postmenopausal women. The presence of postmenopausal or irregular vaginal bleeding, was not a predictor of malignancy in the polyp. CONCLUSIONS: Postmenopausal women with endometrial polyps are at increased risk of malignancy in the polyp. Those patients, whether symptomatic or not should be evaluated by hysteroscopic resection of the polyps. Asymptomatic premenopausal patients with polyps smaller than 1.5 cm can be observed.

Adult↗

PubMed2005

Comparison of secondary and primary ovarian malignancies reveals differences in their pre- and perioperative characteristics.

OBJECTIVE: Preoperative differentiation of primary and metastatic ovarian tumors is difficult. Young age of the patient, bilateralism and reduced multilocularity are cited characteristics of secondary ovarian malignancies. We sought to identity pre- and perioperative factors which may aid in differentiating metastatic ovarian tumors from primary ovarian malignancies. PATIENTS AND METHODS: We performed a retrospective analysis of demographic parameters, preoperative serum tumor marker levels and ultrasonographic as well as operative findings in 38 patients with secondary ovarian malignancies and 76 control patients with primary epithelial ovarian cancer. All patients were treated at our institute from 1996 to 2003. RESULTS: The proportion of secondary ovarian tumors, of all ovarian malignancies, was 5.2%. The most common sites of origin were the gastrointestinal tract (42%), breast (29%) and peritoneum (16%). Fifty-eight percent of the patients with a secondary ovarian tumor had a history of previous malignancy; 42% of the primary malignancies were detected only following diagnosis of ovarian metastasis. The two patient groups (primary or secondary ovarian malignancy) could not be distinguished by age, parity, menopausal status or history of hysterectomy. Of the serum markers, the preoperative level of serum CA 125 was not different between the two groups. Both serum tumor-associated trypsin inhibitor (TATI) (7.2 +/- 9.6 vs. 4.7 +/- 9.4 mug/l [mean +/- SD]) and carsinoembryonic antigen (CEA) levels (19.7 +/- 30.8 vs. 6.7 +/- 120.0 mug/l) were higher in the group with secondary malignancies (P < 0.02). The metastatic ovarian tumors, as measured preoperatively by ultrasonography (US), were smaller (64 mm, 62-89 mm [median, 95% Cl]) than the primary tumors (105 mm, 104-134 mm) (P < 0.0005). The same was true for tumor sizes measured at surgery (P < 0.05). Furthermore, the secondary tumors were more often solid (50 vs. 10%) (P < 0.005), and more seldom cystic-solid (17 vs. 55%) (P < 0.001). Presence of ascites was more common among patients with primary ovarian malignancies in both preoperative US (P < 0.01) and at operation (P < 0.0001). Bilateralism, presence of adhesions, and carcinosis did not differ between the two groups. CONCLUSIONS: When evaluating a patient with an ovarian tumor, a history of malignancy strongly suggests a metastatic nature. Size less than 9 cm, solid structure, absence of ascites and elevated serum CEA and TATI levels were typical features associated with secondary ovarian malignancies.

CA-125 Antigen↗

PubMed1975

The accuracy of radiological diagnosis of benign, primarily and secondarily malignant gastric ulcers and their correlation with three simplified radiological types.

Two radiologists individually gave 'blind' diagnoses of benignancy or malignancy to 145 radiographic representations of gastric ulcers, all with gastrectomy histological proof of benignancy or malignancy. A radiological diagnosis of malignancy was shown to be 98-6% reliable. A diagnosis of benignancy was less reliable (85-4% true positives) but this was a surgical series containing thereby an abnormally high proportion (over a third) of malignant ulcers. A correct diagnosis was mde in 99-5% of the proven benign ulcers, but in only 68-6% of the proven malignant ulcers. Analysis of the pathology reports on the malignant ulcers has shown that it was mainly those arising on the basis of pre-existing benign ulcers (i.e. secondarily malignant ulcers) that were wrongly diagnosed radiologically, thus suggesting that they have fundamentally different radiographic appearance from that of primarily malignant ulcers. It was then found that the ulcers could be divided into three simplified radiological types based on their in-profile appearances: type 1 (projecting), type 2 (intraluminal) and type 3 (so shallow as to be neither projecting nor intraluminal). Statistical association with the histological types led to the following conclusions: (a) radiological type 2 or 3 ulcers should be diagnosed as almost certainly malignant (usually primarily malignant) and (b) radiological type 1 ulcers are almost always benign but should be followed up until healed because the rare secondarily malignant ulcers are also usually of this type.

Diagnosis, Differential↗

PubMed2003

Preoperative differentiation of malignant from benign ovarian tumors: the efficacy of morphology indexing and Doppler flow sonography.

OBJECTIVE: The goal of this study was to determine the efficacy of morphology indexing and Doppler flow sonography as methods to predict risk of malignancy in sonographically confirmed ovarian tumors. METHODS: Risk of malignancy was assessed preoperatively in 442 ovarian tumors using a new morphology index (MI) based on tumor volume and wall structure. Each tumor was assigned a score of 0 to 10 based on increasing volume and morphologic complexity. Doppler flow studies were performed on 371 of these tumors. Following morphologic evaluation, all ovarian tumors were removed surgically. RESULTS: Of 315 tumors with a MI < 5 there was only 1 malignancy (a stage IA granulosa cell tumor <2 cm in diameter) whereas there were 52 malignancies in 127 tumors with a MI > or = 5. Stage of disease was as follows: stage I, 33; stage II, 6; stage III, 14. Risk of malignancy was related directly to MI score, varying from 0.3% in tumors with a MI < 5 to 84% in tumors with a MI > or = 8. A MI value of > or = 5 as indicative of malignancy was associated with the following statistical parameters: sensitivity 0.981, specificity 0.808, PPV 0.409, NPV 0.997. A pulsatility index (PI) < 1.0 as indicative of malignancy was associated with: sensitivity 0.528, specificity 0.776, PPV 0.288, NPV 0.906. A resistive index (RI) < 0.4 as indicative of malignancy was associated with: sensitivity 0.222, specificity 0.867, PPV 0.222, and NPV 0.867. The addition of Doppler flow indices to MI did not improve the accuracy of predicting malignancy. Likewise, the absence or presence of ovarian tumor blood flow was not reliable as a means to differentiate benign from malignant ovarian tumors. CONCLUSIONS: Morphology indexing is an accurate and inexpensive method of differentiating benign from malignant ovarian tumors, and can be a valuable adjunct in treatment planning. The addition of Doppler flow studies did not improve diagnostic accuracy of MI.

Adolescent↗

PubMed1999

MCP-1 expression as a potential contributor to the high malignancy phenotype of murine mammary adenocarcinoma cells.

The search for mechanisms that regulate tumor progression has motivated the authors' laboratory to establish a unique murine model system, consisting of two lines of DA3 mammary adenocarcinoma cells that were derived originally from a common ancestor but differed in their malignant potential. Studies indicated that the highly malignant phenotype manifested by one of the cell lines (termed Ly-6hi DA3 cells) was associated with high expression of the Ly-6E.1 antigen. To characterize the mechanisms controlling the high malignancy phenotype expressed by Ly-6hi DA3 cells, the study was focussed on the potential contribution of tumor-derived factors to the high malignancy phenotype expressed by these cells. To this end, the expression of CC chemokines, major chemoattractants of monocytes and T cells, by the highly malignant Ly-6hi DA3 cells as compared to the low malignancy Ly-6lo DA3 cells was evaluated. The results indicate that the highly malignant cells express higher levels of factors that induce monocyte migration than the low malignancy cells. Two CC chemokines were shown to be highly produced by Ly-6hi DA3 cells, MIP-1alpha and MCP-1, of which only the latter was shown to contribute to the high migratory activity expressed by the high malignancy Ly-6hi DA3 cells. Since MCP-1 may attract monocytes to tumor sites, these findings suggest that monocyte-derived mediators, such as growth factors or angiogenic cytokines, have pro-malignancy effects that contribute to the high malignancy phenotype expressed by Ly-6hi DA3 cells.

Adenocarcinoma↗

PubMed2001

Chromosomal aberrations in malignant gastrointestinal stromal tumors: correlation with c-KIT gene mutation.

Gastrointestinal stromal tumors (GISTs) are distinctive, KIT positive mesenchymal neoplasms. The genetic alterations leading to the malignant behavior of these tumors are not well known. In this study, we looked for recurrent numerical chromosomal changes, which may be associated with malignant GISTs, using interphase fluorescence in situ hybridization (FISH). Fourteen malignant primary tumors and two intra-abdominal recurrences were analyzed. Nine benign tumors were studied for comparison. In all cases, the presence of mutations in exons 9, 11 and 13 of the KIT gene were evaluated. Sixteen centromeric enumeration probes (CEP) for chromosomes 1, 2, 3, 4, 6, 7, 8, 9, 10, 11, 12, 15, 16, 17, 18, and X and three locus specific probes (LSI) for 22q11.2 (BCR-locus), 13q14 (RB1-locus) and 14q32 (IgH-locus) were used. The most common changes seen in malignant GISTs were losses of 14q32 and 22q11. However, these changes were commonly detected in benign tumors and represent early changes related to the pathogenesis of GISTs. Losses of chromosomes 1 and 9 were the only recurrent numerical changes seen exclusively in malignant GISTs. Other recurrent numerical changes seen predominantly in malignant tumors were gain of chromosome 8 and losses of chromosomes 7 and 15. The concurrent loss of chromosome 7 and gain of chromosome 8 (in 4 cases) was never seen together with loss of chromosomes 9 or 15 and only once with loss of chromosome 1. Mutations in KIT were found in the majority of malignant GISTs (64%) confirming a previously shown correlation between presence of such mutations and malignancy. KIT mutations were seen in four of five malignant GISTs with loss of chromosome 9, but only in one of four malignant tumors with loss of chromosome 1. These observations may reflect the different pathways leading to malignant transformation of GISTs.

Adult↗