Angiogenesis and lymphangiogenesis are downregulated in primary breast cancer.

BACKGROUND: Angiogenesis and lymphangiogenesis are considered to play key roles in tumour growth, progression and metastasis. However, targeting tumour angiogenesis in clinical trials showed only modest efficacy. We therefore scrutinised the concept of tumour angiogenesis and lymphangiogenesis by analysing the expression of crucial markers involved in these processes in primary breast cancer. METHODS: We analysed the expression of angiogenic, lymphangiogenic or antiangiogenic factors, their respective receptors and specific markers for endothelial and lymphendothelial cells by quantitative real-time RT-PCR in primary breast cancer and compared the expression profiles to non-cancerous, tumour-adjacent tissues and breast tissues from healthy women. RESULTS: We found decreased mRNA amounts of major angiogenic and lymphangiogenic factors in tumour compared to healthy tissues, whereas antiangiogenic factors were upregulated. Concomitantly, angiogenic and lymphangiogenic receptors were downregulated in breast tumours. This antiangiogenic, antilymphangiogenic microenvironment was even more pronounced in aggressive tumours and accompanied by reduced amounts of endothelial and lymphatic endothelial cell markers. CONCLUSION: Primary breast tumours are not a site of highly active angiogenesis and lymphangiogenesis. Selection for tumour cells that survive with minimal vascular supply may account for this observation in clinical apparent tumours.

Squamous cell carcinoma of the oropharynx: Ki-67 and p53 can identify patients at high risk for local recurrence after surgery and postoperative radiotherapy.

PURPOSE: To assess the prognostic value of biologic (p53, Ki-67) and clinical factors in squamous cell carcinoma of the oropharynx after radical surgery and postoperative radiotherapy (RT). METHODS AND MATERIALS: Between 1985 and 1995, a total of 102 patients with 104 tumor sites were entered onto the study. Fifty-five primary tumors (53%) involved the tonsils, 26 (25%) the soft palate, and 23 (22%) the base of the tongue. Median age was 53 years (range 36-80 years). The clinical T- and N-categories (UICC 1997) were: T1 (30), T2 (47), T3 (22), T4 (5), N0 (33), N1 (28), N2 (42), and N3 (1). Histologically-clear margins were achieved in all patients by initial surgery. Postoperative RT to the primary and regional lymphatics was given, to a total of 60 Gy in 6 weeks, and single daily fractions of 2 Gy. The expression of the nuclear p53- and Ki-67-labeling index (LI) was investigated by immunostaining using the monoclonal antibodies DO-7 and MIB 1. The nuclear p53-intensity (p53-I) was graded into 4 categories (0/+/++/) by densitometry. Median follow-up was 43 months (range 14-132 months). RESULTS: Cancer-specific survival, disease-free survival, and locoregional tumor control rates were 74%, 69%, and 75%, respectively, at 5 years. Significant prognostic factors for disease-free survival were: T-category (T1/2: 77% vs. T3/4: 53%, p = 0.02), tumor site (tonsils: 79% vs. soft palate: 70% vs. base of tongue: 45%, p = 0.05), duration of RT (< or = 46 days: 80% vs. > 46 days: 60%, p = 0.04), Ki-67 LI (< or = 20%: 84% vs. > 20%: 49%, p = 0.006) and p53-I (0/+: 56% vs. ++/ : 79%, p = 0.008). A significant prognostic impact on locoregional control was noted for the duration of RT (< or = 46 days: 86% vs. > 46 days: 68%, p = 0.01), tumor site (tonsils: 88% vs. soft palate: 67% vs. base of tongue: 51%, p = 0.02), Ki-67 LI (< or = 20% LI: 87% vs. > 20% LI: 56%, p = 0.018), and the p53-I (0/+: 58% vs. ++/ : 88%, p = 0.0006). On multivariate analysis, the p53 nuclear intensity (p = 0.002) and the Ki-67 index (p = 0.01) remained the only significant factors for locoregional control. CONCLUSION: Ki-67 labeling index above 20% and a weak p53 nuclear intensity (0/+) are both able to identify patients with squamous cell carcinoma of the oropharynx being at high risk for local recurrence after surgery and postoperative RT. Consequently, in this subgroup an intensification of treatment may be contemplated in prospective trials.

Nodal CT density and total tumor volume as prognostic factors after radiation therapy of stage III/IV head and neck cancer.

PURPOSE: To determine whether the immunohistochemical expression of proliferation-associated antigens (proliferating cell nuclear antigen, MIB1) and the nuclear p53 reactivity in addition to total tumor volume, nodal CT density and T and N category are predictive for overall survival and locoregional tumor control in patients with squamous cell carcinoma of the head and neck region. MATERIALS AND METHODS: Between October 1989 and September 1993, 87 patients with biopsy proven head and neck cancer were randomly allocated to receive radiation alone or simultaneous radiation and chemotherapy as part of a multicenter trial with a total of 298 randomized patients. There were only inoperable lesions in UICC (1992) stage III (8%) and IV (92%). Radiotherapy was delivered with 180 cGy twice daily up to a total dose of 7020 cGy in 51 days. Three cycles of 2340 cGy each were separated by a rest period of 11 days. Chemotherapy consisted of cis-DDP, 5-fluorouracil and leucovorin and was repeated on days 22 and 44. Routinely-processed paraffin-embedded sections were stained using monoclonal antibodies for detection of proliferation-associated antigens (MIB1 and PCNA) and p53 oncoprotein to determine the labeling index (LI). In addition, the total tumor volume and the percentage of necrosis were measured using CT data. The median follow-up was 3.9 years (range 1.9-5.0 years). RESULTS: The overall survival and locoregional control for all 87 patients were 34 and 39% at 3 years, respectively. The addition of chemotherapy resulted in a better overall survival (27 versus 47%, P = 0.03) but did not influence locoregional control (31 versus 47%, P = 0.08). In univariate analysis, nodal CT density (P < 0.0001), total tumor volume (P < 0.0001), age (P = 0.001) and the MIB1-LI (P = 0.04) had a significant impact on overall survival. However, in the final Cox model only the nodal CT density (P = 0.0003) and age (P = 0.05) were independent prognostic factors for survival and only the nodal CT density (P = 0.0006) was an independent prognostic factor for locoregional control. The expression of the p53 oncoprotein was not found to have a clear predictive value. CONCLUSION: Nodal CT density, total tumor volume and age will remain the relevant prognostic factors in stage III/IV head and neck cancer.

Pattern of genomic imbalances in oral squamous cell carcinomas with and without an increased copy number of 11q13.

Among 23 squamous cell carcinomas (SCC) of the oral cavity which were screened for DNA copy number alterations (CNAs) using comparative genomic hybridization, 14 showed a gain of, and 5 of these 14 even an amplification of band 11q13. Amplification of 11q13 was also detected in three of the four studied SCC cell lines and was confirmed by interphase FISH. The number of CNAs in addition to 11q13 varied from 14 to 47 in these carcinomas. All these tumors had seven other specific CNAs in common, i.e. gain on 1p36.3-36.6, 5p15, 9q34, 12p12-13, 14q32, 19 and 20q, all but one showed also an increase of copy number in 7p22, 8q24, 10q26, 12q26, 15q24-25, 16p, 16q23-24, 17q and 22q12-qter. These imbalances were distinctly rarer in the tumors without CNA in 11q13. Loss of material apparently played a minor role in these tumors with gain of 11q13, the most frequent losses (3p12-14 and 5q21) being present in 10 of the 14 cases and loss of 9p13-21 in 5/14 tumors. The three tumors with the highest number of CNAs in addition to 11q13, were histologically classified as pT4, three of the five tumors with 11q13 amplification were highly node-positive (pN 2b-2c). Two of the pT4 tumors shared as many as 23 specific chromosomal segments affected by CNA. Thus, gain of 11q13, though being found at different stages of karyotypic evolution, is apparently associated with a rather specific pattern of other CNAs and involved in progressed stages of malignancy in oral squamous cell carcinoma. In addition, the proportion of patients deceased within one year after diagnosis was clearly higher in the group whose tumors showed an increased 11q13 copy number as compared to the group without this increase. This could point to an association of gain in 11q13 and aggressiveness of the respective tumor.

Gp130 and ras mediated signaling in human plasma cell line INA-6: a cytokine-regulated tumor model for plasmacytoma.

INTRODUCTION: Cytokines of the gp130-family, particularly interleukin(IL)-6, play a crucial role in the propagation of malignant plasma cells. MATERIALS AND METHODS: The role of IL-6 and other gp130-cytokines was studied in the human plasma cell line INA-6 in vitro and in INA-6 xenografts. The proliferative response to gp130-cytokines was evaluated and activated components of gp130-signaling pathways were identified by Western blotting and DNA binding studies. Specifically, expression of IL-6 and receptors for IL-6 and leukemia inhibitory factor were analysed by RT-PCR and ELISA. RESULTS: The plasma cell line INA-6 was cultured for several years remaining strictly dependent on exogenous IL-6. Other gp130-cytokines had no significant effect on INA-6 cell proliferation in vitro. Due to an activating mutation in the N-ras gene, mitogen-activated protein kinases (MAPK) were constitutively phosphorylated. In contrast, signal transducer and activator of transcription(STAT)-3 activation was dependent on stimulation with IL-6. Blocking of either one of these pathways resulted in a significant decrease of INA-6 cell proliferation. Remarkably, INA-6 xenografts did not require exogeneous IL-6 for proliferation in vivo. Instead, an autocrine IL-6 loop and, in certain tumor sublines, responsiveness to additional gp130-cytokines was induced during in vivo growth. CONCLUSION: Activation of the gp130 signal transducer is mandatory for INA-6 cell growth in vitro and in vivo. Both the MAPK and the Jak/STAT pathway are operative in malignant plasma cells and either one is essential for plasma cell growth. The INA-6 cell line provides a preclinical model to study growth regulation of human plasmacytoma cells and to evaluate novel therapeutic strategies.

Evidence of novel pathogenic pathways for the formation of antigastric autoantibodies in Helicobacter pylori gastritis.

Autoantibodies against gastric epithelial cells are detectable in up to 50% of patients with chronic, active Helicobacter pylori gastritis. Presence of autoantibodies against canalicular structures within human parietal cells (anticanalicular autoantibodies) correlate with gastric mucosa atrophy. It has been suggested, that molecular mimicry between H pylori and the host on the level of Lewis X and Lewis Y blood group antigens leads to these autoantibodies. This study aimed at analysing whether antigastric antibodies can be absorbed to Lewis X or Y positive H pylori strains. Sera from 14 H pylori infected patients with anticanalicular autoantibodies were effectively absorbed to H pylori. Immunohistochemical studies of the absorbed sera showed no decrease of antigastric autoreactivity. Pathogenic mechanisms other than molecular mimicry lead to the formation of antigastric autoantibodies, and epitopes other than Lewis antigens are the autoimmune targets.

Antigastric autoantibodies in Helicobacter pylori gastritis: prevalence, in-situ binding sites and clues for clinical relevance.

Colonization of human gastric mucosa with Helicobacter pylori leads to chronic active gastritis and induces the occurrence of an acquired mucosa-associated lymphoid tissue (MALT) in the stomach. This remodelling of the gastric mucosa together with chronic antigen persistence may induce autoimmune reactions. The aim of this study was to investigate humoral autoimmune reactions to human gastric mucosa in H. pylori gastritis and their clinical relevance. Sera from patients with dyspeptic symptoms were tested for presence of IgG immunoglobulins against H. pylori. Gastric infection with H. pylori and alterations of gastric mucosa were demonstrated by histological examination of gastric biopsy specimens. All sera were tested for reactivity against human gastric mucosa by immunohistochemistry. Two different in-situ binding sites of antigastric autoantibodies were observed. Binding to canalicular structures within parietal cells was significantly correlated with antibodies to H. pylori, elevated basal gastrin levels and atrophy of gastric corpus glands. Our data indicate that autoimmune reactions to antigens in the human gastric mucosa occur in H. pylori gastritis and that they may play a role in the pathogenesis of the disease.

Apoptosis in chronic gastritis and its correlation with antigastric autoantibodies.

In the course of time, chronic gastritis may result in gastric atrophy, as in type A gastritis, where autoimmune reactions against parietal cells result in a loss of corpus glands. Two antigastric autoantibodies have been detected in Helicobacter pylori gastritis and are described as anti-luminal and anti-canalicular autoantibodies. The aim of this study was to determine whether increased apoptosis may be responsible for the loss of gastric epithelium and whether this apoptosis is correlated with antigastric autoimmunity. Gastric biopsies from normal mucosa and Helicobacter pylori gastritis were analysed for the presence of apoptosis using the TUNEL method. Helicobacter pylori gastritis was divided into cases (1) without autoantibodies, (2) with anti-luminal, and (3) with anti-canalicular autoantibodies. Apoptotic cells of the foveolar and of the glandular epithelium in the antrum and corpus were counted. The number of apoptotic cells in the gastric mucosa was significantly increased in all cases of gastritis. The highest number of apoptotic cells was observed in the gastric glands of the corpus mucosa in Helicobacter pylori gastritis with anti-canalicular autoantibodies. Apoptosis contributes to the development of gastric atrophy and there are various types of Helicobacter pylori gastritis. The positive correlation between apoptotic cell loss in the glandular zone of the corpus mucosa and the presence of anti-canalicular autoantibodies indicates a possible link between anti-gastric autoimmunity and atrophy in this type of Helicobacter pylori gastritis--similar to that in classic type A gastritis.

Oral squamous cell carcinomas are characterized by a rather uniform pattern of genomic imbalances detected by comparative genomic hybridisation.

Total genomic DNA sampled from 20 oral squamous cell carcinomas (SCCs) and from four SCC cell lines, was examined for genomic imbalances using comparative genomic hybridisation (CGH). Gains and losses of DNA copy number aberrations (CNAs) were found in the primary tumours, but also in the cell lines at a varying number. The patterns of CNAs proved to be rather peculiar in oral SCCs, gains of genetic material clearly dominating compared with losses, and a rather high uniformity of these patterns was an impressive finding. Hypersomies of whole chromosomes, e.g. numbers 17 and 19 or of whole chromosome arms, e.g. 20q, were particularly evident. The segments most frequently gained in oral SCCs were 3q26-q27, 5p15 and 9q34 (16 of 20 tumours each), as well as 1p36.3, 8q24, 10q26, 19 and 20q (15/20 each). Among the 15 tumours with more than 10 CNAs, all showed these imbalances. 11q13 was a band often involved in increases (14/20 tumours), but in several tumours was involved in amplification of DNA copy number. Several other chromosomal segments over represented in more than 60% of the tumours, as, for example, 12q24, 15q22-q24, 16p13.2 and 17q (14/20 tumours each), 6q26-qter, 7p22, 12p12.2-p13, 14q31-q32.2 (13/20) and 1q32-q41, 2q37, 16q23-q24 (12/20 each). In contrast, loss of material affected only a few chromosomal segments, as, for example, 3p12 (12 of the 20 tumours), 5q21 (10/20), 6q13 (8/20). The peculiarities of these findings, in some respect, differ from those found in other epithelial tumours, suggesting a high impact of environmental factors in the generation and progression of these tumours.

p53 mutation and detection of p53 protein expression in oral leukoplakia and oral squamous cell carcinoma.

In many studies the detection of p53 protein by immunohistochemistry (IHC) with one antibody is assumed to be consistent with a mutation of the gene. To determine the correlation of protein detection by immunohistochemistry and gene mutation, paraffin embedded specimens of 60 oral leukoplakias (OL) and 73 oral squamous cell carcinomas (OSCC) were analysed by IHC with two different antibodies (Do7; Pab 1801), PCR-SSCP and sequencing. In 98% of OLs and 94% of OSSCs p53 protein expression was detected with at least one antibody. Only 49% of all tissue specimen were positive with both antibodies. Molecular analysis of the same specimen showed mutations of the p53 gene in 13.3% of OLs and 9, 6% of OSCCs. p53 protein expression was not detected by IHC in 3 out of 7 OSCC with p53 mutations. According to these results detection of p53 expression by IHC is not always correlated with p53 gene mutation and failure to detect p53 protein by IHC does not prove the absence of mutation of the gene in the carcinogenesis in the oral mucosa.

Correlation of telomerase activity, clinical prognosis and therapy in oral carcinogenesis.

Telomerase activity is associated with most malignant tumors. To evaluate the role of telomerase reactivation as a diagnostic and prognostic marker in oral carcinogenesis activity was investigated in mortal and immortal cell lines in eight oral leukoplakias (OL) and 46 oral squamous cell carcinomas (OSCC). Activity was also investigated in 13 histopathologically unaffected mucosas from distant sites or tumor-free margins of the same patients using a modified, highly sensitive, non-radioactive telomeric repeat amplification protocol (TRAP). This was correlated with histopathological stages and the clinical course of the disease. 50% of OL and 46% of OSCC showed activity. One patient with positive, high dysplastic OL developed an OSCC 11 month later. One of three specimens of adjacent tissue presented activity and a recurrence occurred after 6 months. Out of 10 tissues of distal normal mucosa, 2 demonstrated activity which could also be proved in the corresponding tumor. Detection of telomerase reactivation may be a novel method for early detection of immortalised cell clones and malignant cells in histopathologically normal oral squamous epithelium.

Lipogranulomas as complications of septorhinoplasty.

BACKGROUND: Nasal tumors caused by lipogranulomas are a rare complication of a rhinoplasty; only 1 report of this occurrence was found in the literature. OBJECTIVE: To present a series of 4 patients with subcutaneous nasal tumors after each had undergone a rhinoplasty, together with a review of the literature and the clinical consequences. DESIGN: Case series. SETTING: Hospitalized care at a university ear, nose, and throat department. PATIENTS: Four patients were referred within 6 months from a single department for consultation because of broad nasal pyramids after each patient had undergone a rhinoplasty. The origin of the deformities was not known. INTERVENTIONS: Ear, nose, and throat and ultrasound examinations and computed tomography (ie, bone and soft tissue examinations). Two patients had undergone revision surgery and histological examinations of subcutaneous fibrous tissue. MAIN OUTCOME MEASURE: Search for the origin of the nasal deformity. RESULTS: All 4 patients had wide nasal pyramids. One of the 4 patients also had subcutaneous tumors of the nasal dorsum, glabella, and medial canthus area; this patient had subcutaneous cystic lesions on computed tomography and ultrasound examination and a foreign body reaction around "empty spaces" on histological examination. The tumorlike lesions were the result of displaced ointment from the endonasal packings. Two of the 4 patients with minor deformities did not undergo any surgical revision, and they still had some moderate reduction of the cystic lesions within 1 year after the rhinoplasty. CONCLUSIONS: Lipogranulomas caused by ointments that are used together with nasal packings are most often reported in the orbit after endonasal sinus surgery. The incidence should be more frequent in patients who undergo a rhinoplasty because connections between the endonasal cavity and the extranasal subcutaneous layer are created routinely by osteotomies or removal of a hump. Thus, postoperative deformities (eg, inadequate narrowing of the bony pyramid or supratip thickening [permanent swelling of the nasal tip]) should be examined by use of computed tomography, if lipid ointments were used endonasally. For prevention, no lipid substances should be applied together with pressure from packings. In the case of a lipogranuloma, surgical removal via an open approach is the treatment of choice.

Isolated diffuse hemangiomatosis of the spleen: case report and review of literature.

Small localized hemangiomas are common neoplasms of the spleen. Isolated diffuse splenic hemangiomatosis, however, is very rare. This lesion can be accompanied by severe hypersplenism and other complications. We report on a case with significant splenomegaly caused by diffuse hemangiomatosis, which was an incidental finding without any clinical disorders. After splenectomy, the normal parenchyma was found to be widely replaced by multiple spongy nodules. Histologically, cavernous vessels were distributed throughout the whole organ, with endothelial cells expressing vimentin, factor VIII and CD 31, but not CD8. Splenic sinus lining cells exhibited a strongly positive reaction with CD8, which became faint and disrupted in highly dilated sinuses in the vicinity of cavernous vessels. In some areas, there seemed to be a gradual transition from cystically dilated splenic sinuses to cavernous vessels. The differential diagnosis must consider other splenic vascular tumors, such as littoral cell angioma, lymphangioma, peliosis of the spleen, and hamartoma. The pathogenesis of diffuse splenic hemangiomatosis is controversial, and a malformative or neoplastic origin is under debate. A derivation from splenic sinusoidal cells was suggested by some authors, but was rejected by others. Our findings cannot exclude a neoplastic origin from splenic sinuses but, finally, the etiology and pathogenesis of this vascular lesion remain uncertain.

Decrease of antigastric autoantibodies in Helicobacter pylori gastritis after cure of infection.

H. pylori infection leads to the formation of autoantibodies against canalicular structures with human parietal cells in about 30% of all patients. This type of autoreactivity is associated with gastric mucosa atrophy. This study aimed to analyse the effect of cure of infection on anticanalicular autoantibodies. H. pylori infection was cured in 34 patients. Sera of these patients were screened for anticanalicular autoantibodies using an immunohistochemical method before, 10 weeks after and one year after cure of infection. Prevalence of anticanalicular autoantibodies significantly decreased from 26% before treatment to 9% after one year. The data presented in this study add new information to the possible reversibility of gastric mucosa atrophy.

Suppression of HHV-8 viremia by foscarnet in an HIV-infected patient with Kaposi's sarcoma and HHV-8 associated hemophagocytic syndrome.

Human herpes virus 8 (HHV-8) seems to be involved in the pathogenesis of Kaposi s sarcoma. In vitro, antiviral drugs with activity against herpes viruses also can suppress HHV-8, however, little is known about the antiviral activity against HHV-8 in vivo. In this report we describe the effects of foscarnet on HHV-8 viremia in an HIV-infected patient with disseminated Kaposi s sarcoma and a presumably HHV-8 associated hemophagocytic syndrome. HHV-8 DNA could be detected in this patient by PCR in peripheral blood mononuclear cells (PBMC), in bronchoalveolar fluid and tumor biopsies. After initiation of foscarnet because of a severe hemophagocytic syndrome HHV-8 PCR turned negative in PBMC, but stayed positive in pleural effusions and in a tumor biopsy. After termination of foscarnet therapy HHV-8 DNA in PBMC persistently reappeared. Under treatment with foscarnet the hemophagocytic syndrome dramatically improved, suggesting that HHV-8 had a pathogenetic role in this syndrome.

[Cholesterol, triglycerides and lipoproteins in the serum of healthy, normal weight children between 6 and 12 years of age]. / Cholesterin, Triglyceride und Lipoproteine im Serum gesunder, normalgewichtiger Kinder im Alter zwischen 6 und 12 Jahren.

Serum cholesterol, triglycerides and lipoproteins were investigated in 276 healthy, prepubertal children and adolescents of normal weight aged 6 to 12 years. The results were evaluated on the basis of the guidelines of the Austrian Cholesterol Consensus Conference 1988 and according to the 90th and 95th percentiles of the Lipid Research Clinics (LRC) data. A relatively high percentage of the probands revealed cholesterol concentrations which could be classified as "risk" (50% of the female and 53% male probands) or "high risk" (39% of the girls and 25% of the boys). Classifying the cholesterol data according to the LRC criteria 46% of the girls and 41% of the boys exceeded these "cut off" values of the 90th percentile. Our data show that the mean serum cholesterol concentrations in healthy children and adolescents of normal weight--like in other European countries--are in a region concomitant with the category in adults which is associated with an increased risk for cardiovascular diseases. We assume that apart from genetic factors a high fat intake might play a predominant role in causing these raised levels.

[Hyperferritinemia in Still syndrome in the adult and reactive hemophagocytic syndrome]. / Hyperferritinämie beim Still-syndrom des Erwachsenen und reaktives hämophagozytisches syndrom.

This report describes the fatal outcome of a case of adult onset Still's disease in a 46-year old man. The diagnosis was made according to the 1992 criteria, proposed by Yamaguchi. Nine months after the initial disease manifestations a rapid deterioration with progressive hepatosplenomegaly developed. In parallel, pancytopenia and marked hyperferritinemia could be detected. Transjugular liver biopsy revealed the presence of a hemophagocytic syndrome. The course of the disease was refractory to any form of treatment and the patient died from disseminated intravascular coagulation, hepatic and pulmonary failure. Pathogenetic mechanisms and possible associations between Still's disease and reactive hemophagocytic syndrome are discussed.

[To what extent do patients with coronary heart disease want to be informed?]. / Wie weit wollen Patienten mit koronarer Herzkrankheit aufgeklärt werden?

To what extent do patients suffering from coronary heart disease want to be informed? New legislation on patients' rights, passed in Austria in 1993, laid down what information patients are entitled to received. This raises dilemmas. On the one hand the patient has the right to be fully informed about his condition, on the other hand, disclosure could cause sufficient stress to impair the prognosis. The doctor must balance his duty to inform against the therapeutic reasons not to inform, in his duty to care. The empirical part of this research is concerned with the wish to be informed, of patients with coronary heart disease. A questionnaire was administered to patients after bypass operation. It is hoped that the results will be helpful to doctors. Nurses, who are not legally entitled to give information may, nevertheless, find it helpful to know about patients' individual needs for information, when they deliver professional nursing care.

Primary Burkitt's Lymphoma of the Ovary in Early Weeks of Pregnancy - A Case Report.

Primary ovarian Burkitt's lymphoma is a rare tumour predominantly affecting children and young adults. We report here on a 17-year-old pregnant woman with a Burkitt's lymphoma of the left ovary. After tumour removal and induced abortion, the patient underwent polychemotherapy. Full remission was achieved 7 months after the initial diagnosis.