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Malignant thymoma in the United States: demographic patterns in incidence and associations with subsequent malignancies.

The cause of thymoma is unknown. No population-based study has described demographic patterns of thymoma incidence. Previous reports have linked thymoma with diverse subsequent malignancies, but these associations are uncertain. We used Surveillance, Epidemiology and End Results (SEER) data to study the incidence of malignant thymoma by sex, age and race in the United States (1973-1998). Incidence was modeled with joinpoint regression (for age) and Poisson regression. We also used SEER data to compare malignancies following thymoma diagnosis with those expected from general population rates, calculating the standardized incidence ratio (SIR, observed/expected cases) to measure risk. The overall incidence of malignant thymoma was 0.15 per 100000 person-years (849 cases). Thymoma incidence increased into the 8th decade of age and then decreased. Incidence was higher in males than females (p=0.007) and was highest among Asians/Pacific Islanders (0.49 per 100000 person-years). Following thymoma, there were 66 malignancies (SIR 1.5, 95%CI 1.2-1.9). The most notable excess risk for subsequent malignancy was for non-Hodgkin's lymphoma (B immunophenotype) where the SIR was 4.7 (95%CI 1.9-9.6, 7 cases). There were also excess digestive system cancers (SIR 1.8, 95%CI 1.1-2.9) and soft tissue sarcomas (SIR 11.1, 1.3-40.1). No other cancers were increased after thymoma. In conclusion, malignant thymoma is extremely rare. The peak in late adulthood deserves further study. Variation in incidence by race suggests a role for genetic factors. Our study did not demonstrate broadly increased risk for malignancies following thymoma.

Adult↗

Oncogenesis by interspecific interaction of malignant murine and non-malignant hamster cells in vitro.

A clone of Cloudman S91 murine melanoma was fused in vitro with non-malignant hamster cheek pouch cells by means of lysolecithin, and the putative hybrid progeny cells, HCP-MM, were found to be highly malignant in hamster, but not in appropriate mice. A malignant clone of HCP-MM cells was shown to have hamster species-specific surface antigens (as demonstrated by immunofluorescence and the cytotoxic antibody) and hamster-like lactate dehydrogenase and NAD-dependent malate dehydrogenase isoenzyme profiles. Nevertheless, chromosomes similar to those of both murine and hamster parental cells could be distinguished in cells of this malignant clone and in hamster tumor grafts by the method of trypsin-Giemsa banding. A majority of the murine chromosomes, however, appeared to be lost. This study indicates that a murine melanoma previously found untransplantable in hamsters could produce a highly malignant and lethal tumor for hamsters after being mixed in vitro with non-malignant hamster cells, in the presence of a fusing chemical. It is not as yet certain whether the production of transformed cells in vitro and of highly malignant tumors in the hamster (both with predominantly hamster properties) required heterosynkarion formation between the murine melanoma and hamster cheek pouch cells. Nevertheless, our results suggest that the presence of the murine melanoma, and possibly the interaction of its genome with non-malignant hamster cells, was implicated in this process.

Animals↗

Immunocytochemistry of malignant mesothelioma: OV632 as a marker of malignant mesothelioma.

In pleural or ascitic effusions the cytomorphological distinction of adenocarcinoma cells, reactive mesothelial cells, and malignant mesothelioma cells often causes a diagnostic dilemma. The value of immunocytochemistry was investigated on cytological smears of 24 well-established cases of malignant mesothelioma, a selected series of 31 metastatic adenocarcinomas, and 20 smears of patients without known malignancy. In these smears we scored the immunoreactivity with a panel of four monoclonal antibodies. In addition to antibodies for epithelial membrane antigen (EMA) and carcinoembryonic antigen (CEA), the monoclonal antibody MOC31 and the ovarian carcinoma specific antibody OV632 were incorporated in the panel. With none of these four antibodies was immunostaining of reactive mesothelial cells found. CEA- and MOC31-positive tumour cells were frequent in metastatic adenocarcinomas, but occurred rarely in malignant mesotheliomas. EMA-positive tumour cells were found in all metastatic adenocarcinomas (100 per cent) and in most malignant mesotheliomas (83 per cent). In addition to the expected reactivity of OV632 with ovarian carcinomas, 22 of 24 malignant mesotheliomas contained immunopositive tumour cells, while only a small proportion of non-ovarian adenocarcinomas reacted with this antibody. This selective staining of malignant mesothelioma cells, but not reactive mesothelial cells, with OV632 now permits the positive identification of malignant mesothelioma cells in male patients.

Adenocarcinoma↗

Malignant progression of a weakly malignant rat mammary tumor cell line, ER-1, by tumor microenvironmental factors.

Malignant progression is the process by which tumor cells acquire more malignant properties, such as invasiveness and metastasis, during tumor development. The process is thought to be regulated by the microenvironment surrounding tumor cells, which can modify the malignant properties of tumor cells directly or through various humoral factors. Using a cloned weakly malignant cell line, ER-1, which we established, we demonstrated that growth factors such as epidermal growth factor (EGF) and transforming growth factor-beta (TGF-beta) derived from host cells play an important role in promoting malignant progression of ER-1 cells. It is noteworthy that EGF treatment induced not only reversible but also irreversible progression to ER-1 cells depending on the treatment period. An increase in intracellular reactive oxygen species by EGF stimulation was thought to be one of the key factors involved in EGF-induced malignant progression of ER-1 cells. Morphological investigations revealed that ER-1 cells that had acquired malignant properties showed more abundant microvilli on the surface compared to ER-1 cells. Thus, the ER-1 cell line is a useful tool for biological and morphological analyses of the mechanisms of malignant progression of tumor.

Journal Article↗

In vitro modelling of epithelial and stromal interactions in non-malignant and malignant prostates.

To study the effects of stromal epithelial cell interactions on prostate cancer metastasis, we have used primary human prostatic stromal cells derived from malignant and non-malignant tissues and established epithelial cell lines from normal (PNT1a and PNT2-C2) and tumour (PC-3, DU145 and LNCaP) origins. The effects of stromal cells on epithelial cell growth were studied in direct and indirect (using culture inserts) co-culture and by exposure to stromal cell-conditioned medium (assessed by MTT assay). The influence of stromal cells on epithelial cell invasion was measured using matrigel invasion chambers and on epithelial cell motility using time lapse microscopy. Results indicated that epithelial cell line growth was similarly unaffected or inhibited by stromal cells derived from malignant (n = 8) or non-malignant tissue (n = 8). In contrast, PNT2-C2 and PC-3 cells were found to be the least and the most invasive and motile epithelia respectively. Stromal cultures enhanced the invasion of both epithelial cells, but no differences were observed between the use of malignant and non-malignant tissues. All stromal cultures modestly stimulated PNT2-C2 motility but displayed a greater stimulation of PC-3 cell motility, while stromal cells derived from malignant tissue stimulated PNT2-C2 and PC-3 cell motility more than stromal cultures from non-malignant tissues.

Cell Division↗

Mutagen sensitivity as a risk factor for second malignant tumors following malignancies of the upper aerodigestive tract.

BACKGROUND: Second malignant tumors in patients successfully treated for an initial cancer of the upper aerodigestive tract are an important cause of morbidity and mortality. Biologic markers capable of identifying high-risk subgroups of patients who could be targeted for intensive clinical surveillance, therefore, have immense therapeutic and prognostic relevance. We previously demonstrated in a pilot study of 84 patients with cancers of the upper aerodigestive tract that mutagen sensitivity was a significant predictor of risk of developing second malignant tumors. PURPOSE: We extended the study to include 278 patients diagnosed with previously untreated cancers of the upper aerodigestive tract from 1987 to August 1993. METHODS: For each patient, base-line (pretreatment) mutagen sensitivity was measured in vitro in 50 metaphases established from peripheral lymphocyte cultures. Patients with an average of more than 1 chromosomal break/cell were deemed mutagen hypersensitive. Cox proportional hazards analysis was used to predict the risk of developing second malignant tumors associated with mutagen sensitivity. RESULTS: Overall, 44% of the case group exhibited mutagen hypersensitivity. There were no differences in the distribution of mutagen hypersensitivity by site, sex, stage of disease, or smoking status. There were 17 synchronous and 11 metachronous cancers, of which 15 (54%) were smoking-related malignancies. Sixteen (13.1%) of the mutagen-sensitive patients developed second malignant tumors, compared with 12 (7.7%) of the nonsensitive patients. The mean break/cell value (+/- SD) for patients developing second malignant tumors was 1.17 (+/- 0.54), compared with 0.98 (+/- 0.44) for patients with only one cancer (P = .04). Mutagen hypersensitivity conferred a relative risk of 2.67 (95% confidence interval = 1.22-5.79) of developing second malignant tumors. CONCLUSIONS: Mutagen hypersensitivity increases the risk of developing second malignant tumors. IMPLICATIONS: Future research should focus on the molecular mechanisms underlying mutagen sensitivity.

Adult↗

Case report: malignant pericardial effusion as the initial manifestation of malignancy.

Although malignant pericardial effusion is a common complication of malignancy, it is rarely the initial manifestation. A case of a nonsmoking 36-year-old woman who had pericardial tamponade due to malignant pericardial effusion as the initial manifestation of malignancy is presented. Case reports of patients with malignant pericardial effusion as the initial manifestation of malignancy published since 1974 are reviewed. The clinical presentation, histology, and survival of these patients is compared with those cases published prior to 1974. Survival of patients with primary malignancy in the lung who present with malignant pericardial effusion has not improved.

Adenocarcinoma↗

True histiocytic malignancy associated with a malignant teratoma in a patient with 46XY gonadal dysgenesis.

The relatively frequent association of hematologic neoplasia and primary mediastinal germ cell tumors has been reported. Of these hematologic malignancies, nine were classified as malignant histiocytosis or acute monoblastic leukemia, and all occurred in males. We now report on a patient who was phenotypically female, with 46XY gonadal dysgenesis, and who developed a true histiocytic malignancy that presented as a large hepatic tumor and also involved the spleen, right kidney, and lymph nodes. Twenty-six months before the development of the histiocytic malignancy, an ovarian malignant teratoma with yolk sac elements was removed; the patient subsequently received chemotherapy. The neoplasm was composed of large pleomorphic cells and the histiocytic nature was established by cytologic, cytochemical, immunologic, and ultrastructural studies. In the course of her illness, the patient developed classic acute monoblastic leukemia 8 months after the diagnosis of histiocytic malignancy. Karyotypic analysis of the hepatic tumor, bone marrow, and blood showed 46XY gonadal dysgenesis. We believe that this is the first reported case of a phenotypically female patient who developed these two rare malignancies. It suggests that the association between germ cell tumors and histiocytic malignancy in genotypically male individuals may not be coincidental or secondary to therapy, but may be a phenomenon related to dysgenetic gonads in the presence of a Y chromosome.

Adolescent↗

The behavior of serous tumors of low malignant potential: are they ever malignant?

Although the literature describing the clinicopathologic features of serous borderline or low malignant potential (LMP) tumors of the ovary is extensive, the behavior of these neoplasms is not well understood. While some studies indicate a 30 to 40% mortality for advanced stage tumors, it is not clear whether this poor outcome is related to "benign" complications of the disease, such as bowel obstruction from adhesions, or to development of carcinomatosis from malignant transformation. In an effort to determine more clearly the cause of death of patients with serous LMP tumors and to assess the malignant potential of these tumors, defined by progression to invasive serous carcinoma, we reviewed 22 series, totalling 953 patients. Analysis of these studies reveals that for patients with stage I tumors, survival is 99%. For advanced stage disease, survival is 92%. Advanced-stage tumors associated with so-called invasive implants were excluded from this analysis because they were considered invasive serous carcinomas at the time of diagnosis rather than noninvasive LMP tumors. Various causes of death in patients with advanced-stage tumors include complications of the disease, complications of therapy, and, rarely, malignant transformation. Our review of 953 cases disclosed only seven (0.7%) tumors that appeared to have undergone malignant transformation, resulting in death from intraabdominal carcinomatosis. Because the rate of malignant transformation is exceedingly low and because classifying these tumors as malignant often leads to unnecessary treatment, we believe that the term low malignant potential or borderline tumor is not justified.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗

Incidence and mortality patterns of malignancy and factors affecting the risk of malignancy in dialysis patients.

A questionnaire study was performed among 23,209 dialysis patients in 589 institutions together with a retrospective study at Keio University Hospital to determine the risk of malignancy and factors affecting the risk ratio in dialysis patients. The incidence and mortality were 1.4-fold and 1.9-fold higher in dialysis patients than the expected rates in the general population. Incidence and mortality were 1.9-fold and 2.6-fold higher in males than in females. The risk ratios were remarkably high in university hospitals, followed by public hospitals. However, there was no significant difference between those in private hospitals and in the general population. The incidence was very high during the first 6 months of dialysis treatment and rather low in the 7th-10th year. The risk ratio of malignancy was higher in younger patients. Beyond the age of 60, the influence of age was greater than that of renal failure. Malignancies of the digestive organs were frequent and constituted 56% of all malignancies. Frequencies of malignancy in the liver, colon, rectum, bladder and kidney were higher than expected, whereas in the pancreas the frequency was lower than expected. Metastasis of malignancy was observed in 30% of the cases. Our study demonstrated a slight to moderate overall increase in the risk of malignancy and a widely differing risk ratio of malignancy by organ involved, sex, age, hospital group, epidemiological index and length of dialysis treatment in a large single racial population of maintenance dialysis patients.

Adult↗

Creatine kinase-BB activity in malignant tumors and in sera from patients with malignant diseases.

Creatine kinase (CK EC 2.7.3.2) and CK-BB activity was analyzed in 41 malignant tumors of 6 different sites and different histological structures. The same analyses were done on 150 sera of patients with malignant diseases of various localizations. The rate of CK activity was determined kinetically, whereas tissue and serum CK-BB were separated chromatographically (Mercer). Insofar as malignant tumor tissues are concerned, the highest average rate of CK-BB activity was detected in tumors of the prostate (mean 1450 IU/g), and the lowest in tumors of the parotid gland (mean 5.2 IU/g). CK-BB was detected by the Mercer technique in 56 (37.3%) of 150 analyzed sera of patients with malignant diseases. The rate of CK activity in sera of patients with malignant diseases was 8 to 74 IU/I. In comparison with the site of the malignant process no significant CK serum activity differences were observed. T2-T3 tumors did not significantly influence the activity of either CK or CK-BB in the case of either tissues or sera (T1-T3). Enzyme activity was found to be much higher--both in tumoral tissue and in sera--with T4 tumors. The highest rate of CK-BB activity was found in sera of patients with malignant tumors of the stomach (mean 8.1 IU/I), and the lowest in malignant tumors of the rectum (mean 1.8 IU/l).

Adenocarcinoma↗

Reduced-intensity conditioning for the treatment of malignant and life-threatening non-malignant disorders.

Allogeneic bone marrow or blood stem cell transplantation (BMT) represents an important therapeutic tool for the treatment of an otherwise incurable broad spectrum of malignant and non-malignant diseases. Until recently, BMT was used primarily to replace a malignant, genetically abnormal or deficient immunohematopoietic compartment and therefore, highly toxic myeloablative regimens were considered mandatory for more effective eradication of all undesirable host-derived hematopoietic cells, including stem cells and their progeny. Our preclinical and ongoing clinical studies indicated that much more effective eradication of host immunohematopoietic system cells can be mediated by donor lymphocytes in the process of adoptive allogeneic cell therapy following BMT. Thus, eradication of all malignant cells, especially in patients with CML and, to a lesser extent, in patients with other hematologic malignancies can be accomplished despite complete resistance of puch tumor cells to maximally tolerated doses of chemoradiotherapy. Our cumulative experience suggested that graft-versus-malignancy effects might be used as a tool for eradication of otherwise resistant tumor cells of host origin. We speculated that the therapeutic benefit of BMT may be improved by using safer conditioning for engraftment of donor stem cells induce host-versus-graft unresponsiveness to enable engraftment of donor lymphocytes for subsequent induction of graft-versus-malignancy effects, or even graft-versus-autoimmunity and graft-versus-genetically abnormal cells. In other words, focusing on more selective and smarter rather than stronger modalities. Effective BMT procedures may be accomplished without lethal conditioning of the host, using a new, well-tolerated and user-friendly non-myeloablative regimen, thus eliminating or minimizing immediate and late procedure-related toxicity and mortality. It appears that initial induction of graft tolerance, mediated by engraftment of donor stem cells, leads to durable engraftment of immunocompetent donor lymphocytes, which may be necessary for induction of effective biologic warfare against host-type immunohematopoietic cells. Consequently, stem-cell therapy following induction of transplantation tolerance by selective elimination of alloreactive donor lymphocytes may represent the treatment of choice for a wide range of otherwise incurable diseases, including cancer (hematologic malignancies and certain metastatic solid tumors), genetic disorders (hemoglobinopathies and enzyme deficiency disorders), diseases caused by self-reactive lymphocytes (autoimmune diseases such as multiple sclerosis, rheumatoid arthritis) to mention just a few. Using reduced intensity conditioning, non-myeloablative stem cell transplantation (NST) can be accomplished with no major procedure-related toxicity or mortality. Thus, NST offers the feasibility of safe stem cell transplantation and cell-mediated procedures for a large and constantly growing spectrum of clinical indications for all patients in need without lower or upper age limit. Future strategies currently under investigation include developing new approaches for control of alloreactivity of host-versus-graft and graft-versus host reactivity reactions and developing better approaches for maximizing the capacity of donor lymphocytes to eliminate cancer cells more selectively, while avoiding or minimizing GVHD for safer and more effective treatment of patients in need of BMT.

Animals↗

[Multiple primary malignant tumors in patients with malignant melanoma of the skin].

The incidence of further malignant tumors was analyzed by means of a retrospective study in 2335 melanoma patients. During the follow up 85 patients (3.64%) developed a second malignant tumor: 29 patients multiple primary malignant melanomas (mm), 49 a mm and a further nonmelanocytic malignant tumor, and 7 multiple primary mm and an additional non-melanocytic malignant tumor. Statistical calculations revealed that female melanoma patients have a 20 fold, and male melanoma patients a 30 fold increased risk to develop further malignant melanomas. In contrast, there was no increased incidence of non-melanocytic malignant tumors, breast carcinoma included. A total skin examination has therefore to be performed during follow up investigations of melanoma patients for early detection of further malignant melanomas.

Adult↗

[Unusual and unknown aspect of cutaneous malignant melanoma: minimal deviation malignant melanoma. Retrospective study of 45 cases].

Minimal deviation malignant melanoma (MDMM) is a rare melanocytic tumor of the skin that shares both malignant and benign histologic features: 1) a vertical growth phase similar to that of malignant melanomas with expansile nodules invading throughout the reticular dermis (Clark's level IV), and even the subcutaneous fat (Clark's level V); 2) but a monotonous and uniform proliferation of melanocytic cells that are only moderately atypical. A very slight cellular maturation from the top to bottom of the lesions may be observed, but usually there is no maturation at all. By themselves, the cells do not appear as malignant. A borderline variant of MDMM shows identical cytological and growth pattern features, but remains confined to a Clark's level III of invasion. Over the past 14 years, 45 cases (female to male ratio: 1.5:1.0) of MDMM, 8 of which were of the borderline variant, were observed. The lesions appeared as acquired pigmented tumors, 0.5 to 1.0 cm in size which predominated on the trunk. Young adults (mean age: 34 years) were most frequently involved. Based on the cytological characteristics of the cellular proliferation, they could be subdivided in 4 groups: 1) epithelioid and spindle cell type (15 cases); 2) epithelioid type (14 cases); 3) spindle cell type (7 cases); and 4) pigmented spindle cell type (9 cases). The mean thickness of the 45 cases was 3.06 mm (1.24 mm for the borderline lesions; 3.40 mm for the MDMM). Tumors with a spindle cell component appeared thicker than those without. Mitoses were numerous (mean: 3.2/10 high power fields). Each tumor but one showed a junctional component. This appeared as melanocytic hyperplasia or melanocytic nests at the dermoepidermal interface. Moreover, 10 cases (7 MDMM and 3 borderline tumors) disclosed intraepidermal spread of melanocytes. However, as observed with the dermal component of the lesions, these intraepidermal melanocytes never appeared cytologically malignant, although moderate atypism could be observed. At last, an association with a compound or dermal nevus was seen in 8 cases. MDMM appears as a particular subgroup of cutaneous malignant melanomas with distinct and characteristic histologic features. Its differential diagnosis includes blue nevus, especially the cellular variant, combined nevus, spindle and epithelioid cell nevus (Spitz-Allen's nevus) and cutaneous metastasis of malignant melanoma. The most important features for the differential diagnosis are the growth pattern, the absence of cellular maturation, the absence of real malignant cells and moderate cellular atypism.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

Biological behavior and natural course of acral malignant melanoma. Clinical and histologic features and prognosis of palmoplantar, subungual, and other acral malignant melanomas.

This study, based on 67 Japanese cases of acral malignant melanomas, presents their gross clinical and histologic features and the natural history of the lesions with respect to anatomic locations, thicknesses, and sex of patients afflicted. We found that the anatomic locations of malignant melanomas in Japanese are unique in the sense that more than 40% of cutaneous melanomas occurred in palmoplantar and subungual sites, about 80% showed the clinical and histologic features of the acral lentiginous type, 15% were in the form of nodular malignant melanoma, and 3% in the form of superficial spreading malignant melanoma. We did not find any difference in prognosis of acral malignant melanomas from that of malignant melanomas on other parts of the body. Neither was there significant difference in the overall survival rates or in the survival rates within same range of thickness. There was some difference in the survival rates of patients with palmoplantar and subungual malignant melanoma of men and women, the women being younger and having better survival rates than the men. However, no significant difference was found in survival rates from the factor of thickness of lesion. Our study indicates the usefulness of specifications of thickness and anatomic site in predicting biological behavior and natural course of acral malignant melanomas.

Aged↗

[Late phase II clinical study of irinotecan hydrochloride (CPT-11) in the treatment of malignant lymphoma and acute leukemia. The CPT-11 Research Group for Hematological Malignancies].

A nationwide multi-center cooperative phase II clinical study of irinotecan hydrochloride (CPT-11) was conducted to evaluate its efficacy in intractable malignant lymphoma and acute leukemia. In malignant lymphoma, one course of CPT-11 consisted of intravenous drip infusion at a dose of 40 mg/m2 once daily for 3 consecutive days, performed once a week. In acute leukemia, one course of CPT-11 consisted of intravenous drip infusion at a dose of 15 to 20 mg/m2 a day twice daily for 7 consecutive days (1 cycle), performed every 2 to 4 weeks. Among the 79 patients with malignant lymphoma and 50 patients with acute leukemia enrolled in the study, 66 and 41 patients, respectively, completed treatment. These patients had all undergone chemotherapy prior to treatment. Among the malignant lymphomas, the response rate in non-Hodgkin's lymphoma (NHL), including 9 CRs, was 42% (26/62, 95% CI: 30-54%); of these there was a response rate of 39% (5/13), including 1 CR, in adult T-cell leukemia (ATL) as well. In Hodgkin's disease (HD), on the other hand, there were no cases in which efficacy was demonstrated (0/4). The overall response rate in malignant lymphoma was 39% (26/66), and the response rate even among the recurrent intransigent cases was 42% (16/38). The 50% survival time (MST) in the 74 eligible cases of malignant lymphoma was 153 days. In acute leukemia, on the other hand, partial remission was observed in 2 of 17 cases (12%) of acute lymphocytic leukemia (ALL), but no cases of remission were observed in the 24 patients with acute myelogenous leukemia (AML). The overall remission rate in acute leukemia was 5% (2/41, 95% CI: 1-14%). The principal adverse effects were myelosuppression in malignant lymphoma and gastrointestinal symptoms, including diarrhea, nausea/vomiting, anorexia and abdominal pain, in both malignant lymphoma and acute leukemia, and there was little organ damage to the heart, liver or kidney. Myelosuppression and gastrointestinal adverse effects were severe in some of the patients, so caution is required. Based on the above findings, CPT-11 appears to be efficacious in the treatment of non-Hodgkin's lymphoma.

Adolescent↗

Value of ascitic fibronectin and cholesterol concentration in the differentiation between malignancy-related and non-malignant ascites.

In this prospective study, we tried to evaluate various "humoral tests of malignancy" regarding their efficiency of discriminating between malignancy-related and non-malignant ascites. Fibronectin, total protein, number of cells, LDH, pH, specific gravity and cytology were compared in the ascitic fluid of 51 patients with malignancy-related and 52 patients with non-malignant ascites; patients with tuberculous peritonitis were not included. Ascitic fluid cholesterol was determined in 36 of 51 malignancy-related and in 37 of 52 non-malignant ascites. Cytology and fibronectin were found 100% specific with diagnostic efficiency 87.5% and 94.2% respectively under optimal conditions. Cholesterol was neither sensitive nor specific. It is concluded that fibronectin was a valuable test for malignancy-associated ascites.

Ascitic Fluid↗

[A survey of malignant gliomas accompanied with visceral malignancies].

From January 1984 to December 1997, a total of six patients with malignant gliomas accompanied with visceral malignancies were treated in our department. We reviewed their radiological findings and clinical course. They consisted of four patients with glioblastoma and two patients with anaplastic astrocytoma. Classified according to visceral malignancies, three cases had colon cancer and the rest consisted of thyroid, uterus and prostate cancers. In radiological examinations of the brain (CT scans and MR images), these gliomas were relatively well-circumscribed, as if they were metastatic brain tumors. Of all these six cases, two cases survived more than five years and there were two cases in which there was recurrence within a year. Particularly, in four cases, whose gliomas developed after the treatment for visceral malignancies, two cases survived long-term (more than five years) and there was recurrence in only one case. We speculated that visceral malignancies could affect the nature of glioma progression. Thinking about its mechanisms, we hypothesized as follows; (1) visceral malignancies may activate non-specific, or common antitumor, immunity. (2) visceral malignancies may produce some factors which could affect the biological nature of gliomas. (3) glioma accompanied with visceral malignancy may have genetic uniqueness. Although the cases were limited in number, the present study may be helpful in designing the treatment for such cases and in elucidating the invasive nature of gliomas.

Adult↗