Subject(s)
Carcinoma, Squamous Cell/secondary , Hernia, Umbilical/diagnostic imaging , Jejunal Neoplasms/secondary , Uterine Cervical Neoplasms/pathology , Carcinoma, Squamous Cell/surgery , Female , Hernia, Umbilical/pathology , Humans , Jejunal Neoplasms/surgery , Middle Aged , Neoplasm Staging , RadiographyABSTRACT
Chronic abdominal pains caused by peritoneal tuberculosis - two case reports. The diagnosis of a peritoneal tuberculosis could be a demanding task for even an experienced Physician, because of the unspecific symptoms. We report on two patients, who as a result of therapy refractory chronic abdominal pains, weight loss and ascites were admitted to our hospital. The excisional biopsy taken from the peritoneum and the omentum major during an exploratory laparotomy resulted in the histopathologic diagnosis of peritoneal tuberculosis being made. Both patients were given tuberculostatic therapy with isoniazid, rifampicin, pyracinamide and streptomycin and both have since recovered. The symptoms, the difficulties encountered in making the diagnosis and the therapy of the peritoneal tuberculosis are discussed using these two case reports.
Subject(s)
Pelvic Pain/etiology , Peritonitis, Tuberculous/diagnosis , Adult , Antitubercular Agents/therapeutic use , Biopsy , Combined Modality Therapy , Diagnosis, Differential , Drug Therapy, Combination , Female , Humans , Laparoscopy , Omentum/pathology , Pelvic Pain/diagnostic imaging , Pelvic Pain/surgery , Peritoneum/pathology , Peritonitis, Tuberculous/pathology , Peritonitis, Tuberculous/surgery , UltrasonographyABSTRACT
We report on a 24 years old patient with an acute abdominal pain and an unknown intact tubal pregnancy in the 8th gestation week. The sonographic examination confirmed an intact tubal pregnancy. Shortly after the diagnosis, it ruptured with a massive intraabdominal bleeding. Thereafter, the patient collapsed. We carried out a laparoscopy and performed salpingotomy. Because of the persistent bleeding a salpingectomy was performed. We also report on a second patient 34 years old, who was referred to our Department on suspicion of a ruptured ectopic pregnancy with acute abdominal pains and a positive pregnancy test. The transvaginal sonography revealed massive intraabdominal fluid, adnexal tumor and endometriumhyperplasia without a sign of a gestational sac or an embryo.We carried out a laparoscopy, which revealed a ruptured tubal pregnancy with a life, fetus lying in the abdominal cavity. As a result of the massive and persistent intraabdominal bleeding, we carried out laparotomy and performed salpingectomy. Using these two case reports, the etiology, symptoms, clinical course, diagnosis, as well as surgical and drug therapy are discussed.
Subject(s)
Embryo, Mammalian/diagnostic imaging , Pregnancy, Tubal/diagnosis , Abdominal Pain/diagnostic imaging , Adult , Female , Humans , Laparoscopy , Pregnancy , Pregnancy Tests , Pregnancy Trimester, First , Pregnancy, Tubal/diagnostic imaging , Pregnancy, Tubal/pathology , Pregnancy, Tubal/surgery , Rupture, Spontaneous , Salpingostomy , Treatment Outcome , Ultrasonography, PrenatalABSTRACT
We analyzed tumor tissues from 14 patients with invasive squamous cell carcinoma of the cervix for aberrations of chromosome 17 and p53 expression. All but 3 patients were negative for p53 protein expression, the protein being detected in 2 International Federation of Obstetrics and Gynecology stage IIa cancers and 1 stage Ib G3 carcinoma. Significant cytogenetic aberrations in the form of losses and gains of chromosome 17 were diagnosed in 9 and 7 patients, respectively. There was no correlation with tumor prognosis, clinical stage or histologic grade. According to most reports, almost all cervical carcinomas contain integrated human papilloma virus (HPV) and express E6 oncoproteins. Increasing evidence suggests that E6 protein interaction leads to p53 mutation in HPV-infected cervical epithelium. Since most cervical tumors are infected with HPV, and the tumors originate through p53 gene mutation caused by the said interaction, which leads subsequently to the overexpression of p53 oncoprotein, lack of the latter in the remaining 11 cervical tumors may either be the result of technical shortcomings, or the tumor may arise in such circumstances through a p53-independent pathway. On the other hand, 2 of 3 stage IIa cancers and 1 Ib G3 carcinoma were found to be p53 positive, thus supporting the notion that p53 inactivation is a relatively late event in the progression of cervical cancer.
Subject(s)
Carcinoma, Squamous Cell/pathology , Chromosome Aberrations , Chromosomes, Human, Pair 17 , Gene Expression , Genes, p53/genetics , Uterine Cervical Neoplasms/pathology , Carcinoma, Squamous Cell/genetics , Female , Humans , In Situ Hybridization, Fluorescence , Neoplasm Invasiveness , Neoplasm Staging , Prognosis , Uterine Cervical Neoplasms/geneticsABSTRACT
Sertoli-Leydig cell tumors (SLCTs) represent a rare group of sex-cord stromal tumors of the ovary of unknown pathogenesis. We report a SLCT of intermediate differentiation with peritoneal recurrence and lymph node metastasis 12 months after removal, including cytogenetic analysis by comparative genomic hybridization and fluorescence in situ hybridization, which showed trisomy 8 as sole unbalanced karyotypic aberration. Our results provide evidence that a simple numeric chromosomal abnormality in SLCT may be associated with a malignant phenotype and suggest that the molecular pathogenesis of SLCT may be different from ovarian granulosa-stromal cell tumors.
Subject(s)
Chromosomes, Human, Pair 8 , Neoplasm Metastasis/genetics , Ovarian Neoplasms/genetics , Sertoli-Leydig Cell Tumor/genetics , Trisomy , Adolescent , Fatal Outcome , Female , Humans , In Situ Hybridization, Fluorescence , Karyotyping , Lymphatic Metastasis , Neoplasm Recurrence, Local , Nucleic Acid Hybridization , Ovarian Neoplasms/pathology , Ovarian Neoplasms/surgery , Peritoneum/pathology , Sertoli-Leydig Cell Tumor/pathology , Sertoli-Leydig Cell Tumor/surgeryABSTRACT
Preeclampsia is associated with an increased platelet activation; however, there are few studies concerning platelet activation of the newborn. The aim of our study was to compare platelet activation in newborns of preeclamptic mothers to newborns of healthy mothers by using whole blood flow cytometry. Blood samples were obtained from 20 newborns (10 healthy controls, 10 cases of preeclampsia/HELLP [hemolysis, elevated liver enzymes, and low platelet count] syndrome) during cesarean section. Antibodies against the following antigens were used as markers for platelet activation: CD 41, CD62P, CD 63, and platelet-bound fibrinogen. In addition to the basal platelet activation, the ability of platelets to undergo activation as a result of in vitro incubation with a weak agonist (adenosine diphosphate) was evaluated. A significant difference between the groups concerning basal platelet activation could only be seen for platelet-bound fibrinogen; the control group showed a higher extent of platelet activation (16.6 +/- 11.3 vs. 6.1 +/- 4.9; p = 0.03). Incubation with adenosine diphosphate in the control group resulted in minor increases of platelet activation, which was significant only for platelet-bound fibrinogen (16.6 +/- 11.3 vs. 42.5 +/- 22.1; p = 0.02). However, the preeclamptic group showed significantly increased levels of platelet activation for all used markers after in vitro activation (CD 41: 115.6 +/- 18.2 vs. 163.2 +/- 29.6; p = 0.002; CD62P: 2.4 +/- 0.4 vs. 3.9 +/- 0.3; p < 0.001; CD 63: 2.7 +/- 0.5 vs. 3.7 +/- 0.6; p = 0.002; platelet-bound fibrinogen: 6.1 +/- 4.9 vs. 55.1 +/- 9.1; p < 0.001). Preeclampsia or HELLP syndrome is therefore associated with an increased susceptibility to neonatal platelets, even against weak activators such as adenosine diphosphate. Whether this results from peculiarities in the fetal vascular environment or maternal influences is yet uncertain.
Subject(s)
Infant, Newborn/blood , Platelet Activation , Pre-Eclampsia/blood , Adenosine Diphosphate/pharmacology , Antigens, CD/blood , Biomarkers/blood , Female , Fibrinogen/metabolism , Flow Cytometry , HELLP Syndrome/blood , HELLP Syndrome/etiology , Humans , Male , Platelet Activation/drug effects , Platelet Activation/physiology , Pre-Eclampsia/etiology , PregnancyABSTRACT
Infiltrating ductal (DC) and lobular carcinoma (LC) of the breast represent the most frequently observed varieties of invasive breast cancer, characterized by differences in their histological and clinical properties. Although comparative genomic hybridization (CGH) of invasive breast carcinomas has revealed a complex and consistent pattern of DNA copy number changes, the data with regard to type specific aberrations are limited. A comprehensive study was therefore performed on 19 LCs and 29 DCs to ascertain type-specific differences of unbalanced DNA copy number changes by CGH. Statistical analysis revealed significantly higher frequencies for underrepresentation of chromosomes 16q (p<0.01), 22 (p<0.05), and 17q (p<0.05), and a lower frequency for overrepresentation of chromosome 8q (p<0.01) in LC. Similar frequencies of non-random chromosomal changes in LC and DC were obtained for gain of 1q (74%/59%) and loss of 19p (53%/52%), parts of 1p (42%/41%) and 11q (21%/24%). Less frequently, gains mainly involving parts of chromosomes 20q, 20p, 3q, and 5p and partial losses of chromosomes 17p and 13 were observed in both groups of tumours. Minimal regions of overlapping amplifications were mapped to 17q23 exclusively in DC (17%) and 11q13-q14 in both DC and LC (21% and 11%, respectively). High occurrences of DNA copy number decreases were detected at the distal part of chromosomes 1p, 19 and 22, but further analysis is required to confirm these imbalances. It is suggested that the observed differences are involved in the development of type-specific properties of DC and LC.
Subject(s)
Breast Neoplasms/genetics , Carcinoma, Ductal, Breast/genetics , Carcinoma, Lobular/genetics , Chromosome Aberrations , Adult , Aged , Aged, 80 and over , Breast Neoplasms/pathology , Carcinoma, Ductal, Breast/pathology , Carcinoma, Lobular/pathology , DNA, Neoplasm/genetics , Female , Humans , Image Processing, Computer-Assisted/methods , In Situ Hybridization , Middle Aged , Neoplasm InvasivenessABSTRACT
AIMS: Cytogenetic data on solitary fibrous tumours (SFT) are very limited. We studied a benign pleural SFT for its ultrastructural and immunohistochemical details, and made cytogenetic analyses for comparison with other genetic and ultrastructural studies of SFT. RESULTS: Immunohistochemistry showed strong positivities for CD34 and vimentin, but no reactions with anti-cytokeratins and epithelial membrane antigens. Electron microscopy revealed primitive desmosomes in our SFT. The results thus evinced fibroblast-like cells with intermediate epithelial-mesenchymal character. Comparative genomic hybridization of the tumour revealed losses of 1p33-->pter, 17pter q21, entire copies of chromosomes 19 and 22, and gains of 1p21-p22, 2q23-q32.3, 3pl2-q13.2, 4p14-q28, 6p12-q21, 9p21-->pter and 13q21-q31. Furthermore, there was loss of 20q, as was previously reported elsewhere in a case of benign and a case of malignant SFT. CONCLUSIONS: The results furnish further evidence of the involvement of -20q in SFT. In addition, they show that SFT may have complex genomic imbalances and primitive features, despite having a benign appearance.
Subject(s)
Chromosome Deletion , Chromosomes, Human, Pair 20/genetics , Neoplasms, Fibrous Tissue/genetics , Pleural Neoplasms/genetics , Desmosomes/ultrastructure , Epithelium , Female , Humans , Karyotyping , Middle Aged , Neoplasms, Fibrous Tissue/pathology , Pleural Neoplasms/pathologyABSTRACT
To demonstrate associations of certain chromosomal aberrations with defined renal cell tumour (RCT) subtypes, we analysed 239 tumour nephrectomy cases for specimens with multicentric tumours. Chromosomal in situ hybridization was then performed on 15 cases with 34 foci (16 conventional renal cell carcinomas (RCCs), and 18 papillary RCTs (11 carcinomas and seven adenomas) for specific chromosomal aberrations, using alpha-satellite probes for chromosomes 3, 7 or 17. Particular preference was given to cases which had separate foci with different cytomorphologies. Furthermore, we compared aberrations in relation to tumour size, stage, grade and between different foci in a specimen. Thirty-four cases had multiple tumours. Forty-seven per cent of the multicentric tumours were conventional RCCs and 53% papillary RCTs (against 83% solitary conventional RCCs and 5% solitary papillary RCTs). Three conventional RCCs sized 8 mm (G3), 13 cm (pT2, G2) and 15 cm (pT3b, G3), respectively, revealed monosomy 3, and 13 were disomic. Seventeen papillary RCTs (11 carcinomas and six adenomas) displayed trisomy 17, irrespective of size or grade. Four papillary carcinomas and six papillary adenomas had trisomy 7, and the rest (seven papillary carcinomas and one papillary adenoma) revealed disomy 7. In conclusion, papillary RCTs were tendentially multicentric. Although specific for conventional RCCs heedless of size, monosomy 3 was only observed in high-grade and/or advanced tumours. Trisomy 17 was only detectable in papillary RCTs irrespective of tumour state, showing increased copies with tumour growth. Papillary RCTs also appeared to lose some copies of chromosome 7 with tumour progress, possibly reflecting malignancy.
Subject(s)
Carcinoma, Renal Cell/genetics , Carcinoma, Renal Cell/pathology , Chromosome Aberrations , Chromosomes, Human, Pair 17 , Chromosomes, Human, Pair 3 , Chromosomes, Human, Pair 7 , Kidney Neoplasms/genetics , Kidney Neoplasms/pathology , Carcinoma, Papillary/genetics , Carcinoma, Papillary/pathology , Carcinoma, Papillary/surgery , Carcinoma, Renal Cell/surgery , Chromosome Mapping , Female , Humans , In Situ Hybridization , Interphase , Kidney Neoplasms/surgery , Male , Middle Aged , Monosomy , Neoplasm Staging , NephrectomyABSTRACT
We evaluated the in vitro cytotoxicity of topotecan (TPT), versus cisplatin, etoposide (VP-16) and paclitaxel (PTX) in four squamous cell cancer cell lines of the cervix uteri and vulva. Four established human squamous cancer cell lines from the cervix uteri (A-431, Ca Ski and C-33) and vulva (CAL-39) were used. The cytotoxic effects of the agents were examined using the ATP-Tumor Chemosensitivity Assay (ATP-TCA). In addition to the single agents, the following combinations were tested: TPT+cisplatin, TPT+VP-16 and TPT+PTX. Three cell lines (C-33, Ca Ski and CAL-39) were highly sensitive to TPT, but one cell line (A-431) was less sensitive. Furthermore, the cytotoxic activity of TPT was superior to that of cisplatin in Ca Ski and C-33 cells, but inferior in CAL-39 and A-431. TPT was also more active than VP-16 in CAL-39 and Ca Ski. On the other hand, the cytotoxic activity of TPT was weaker than PTX in C-33, CAL-39 and A-431. TPT increased the cytotoxic activity of cisplatin and VP-16 in C-33, Ca Ski and A-431. However, synergistic features were observed only in A-431 cells. TPT also enhanced the cytotoxic activity of PTX in A-431 and Ca Ski. In CAL-39 and C-33, however, increased cytotoxic activity occurred only at higher drug concentrations, whereas antagonism was observed at lower drug concentrations. In conclusion, our results suggest that TPT has a significant cytotoxic effect on most squamous cell cancer cell lines which may be superior to cisplatin, VP-16 and PTX in some instances. Furthermore, TPT is likely to potentiate the cytotoxic activity of these agents in individual cell lines tested.
Subject(s)
Antineoplastic Agents/toxicity , Antineoplastic Combined Chemotherapy Protocols/toxicity , Carcinoma, Squamous Cell/drug therapy , Topotecan/toxicity , Uterine Cervical Neoplasms/drug therapy , Vulvar Neoplasms/drug therapy , Adenosine Triphosphate/analysis , Cisplatin/administration & dosage , Cisplatin/toxicity , Drug Screening Assays, Antitumor , Enzyme Inhibitors/toxicity , Etoposide/administration & dosage , Etoposide/toxicity , Female , Humans , Luminescent Measurements , Paclitaxel/administration & dosage , Paclitaxel/toxicity , Topotecan/administration & dosage , Tumor Cells, CulturedABSTRACT
A 6-y-old girl with right atrial myxoma presented with remittent fever attacks, general arthralgia and laboratory investigations mimicking rheumatic or autoimmune disease. Interleukin-6 (IL-6) serum concentration was markedly elevated before and normal after tumour resection, whereas myxoma cells stained negatively for IL-6. IL-6 should be considered a myxoma marker: overproduction by myxoma cells and consecutive systemic passage are assumed to cause immunological features.
Subject(s)
Heart Atria/surgery , Heart Neoplasms/diagnosis , Interleukin-6/blood , Myxoma/diagnosis , Rheumatic Diseases/diagnosis , Biomarkers, Tumor/blood , Child , Echocardiography , Female , Heart Neoplasms/surgery , Humans , Immunohistochemistry , Myxoma/surgeryABSTRACT
AIMS: To resolve the conflicting diagnoses of five pathologists (which included well-differentiated neuroendocrine carcinoma, malignant carcinoid, undifferentiated small-cell carcinoma, primitive neuroectodermal tumour, metastases of small-cell lung carcinoma (SCLC) and Merkel cell carcinoma (MCC)), and tumour-free lungs after necropsy, we investigated an alarmingly metastasizing MCC in a 32-year-old Caucasian man using chromosomal in-situ hybridization (CISH). Differences in incidence and course in males and females also prompted targeted analyses for chromosomes X and Y. The lesion was also analysed for p53 gene mutations. METHODS AND RESULTS: Paraffin sections of the thorax, buccal lymph nodes and scalp tumours were stained with haematoxylin and eosin. Immunohistochemistry was performed with antibodies against pancytokeratin, keratin 20, neuron-specific enolase (NSE), chromogranin, neurofilaments and vimentin, among others. Sections (5-6 microm) of the tumours were analysed with alpha-satellite probes for chromosomes 1, 6, 7, 11, 12, 17, 18, X and Y using CrSH; and exons 5-9 of the p53 gene were examined by polymerase chain reaction and single strand conformation polymorphism (PCR-SSCP) methods. Although positive for pancytokeratin, keratin 20, chromogranin, NSE, synaptophysin and vimentin, the similarity in antigen profiles expressed by SCLC and MCC prevented a definitive tumour diagnosis. Chromosomal in-situ hybridization, however, revealed trisomies 1 and 11, two frequent aberrations in MCC, and trisomy 18. Moreover, 71% of the tumour cells had two to three copies of X, whereas 98% of the cell nuclei in the hair follicles and normal epidermis (purported Merkel cell origins) displayed one X chromosome. No mutations were detected in the five exons of the p53 gene examined. CONCLUSIONS: Had CISH been performed earlier, treatment may have been tailored specifically to suit MCC, since MCC and SCLC have different therapeutic strategies. Finally, chromosome X may be of prognostic relevance in MCC, which apparently predominates in females and yet shows poorer prognosis in males, and hence be worthy of further investigation.
Subject(s)
Carcinoma, Merkel Cell/genetics , Scalp , Skin Neoplasms/genetics , Adult , Carcinoma, Merkel Cell/pathology , Chromosomes, Human , Genes, p53/genetics , Humans , Immunohistochemistry , In Situ Hybridization , Interphase , Male , Sex Chromosomes , Skin Neoplasms/pathologyABSTRACT
AIMS: To determine by cytogenetic analysis the origins of two clear cell tumours in a 70-year-old Caucasian woman, one in the thyroid gland, and the other in the skin, 16 and 20 years, respectively, after tumour nephrectomy. We sought a conclusive distinction between primary clear cell thyroid carcinoma and its cutaneous metastasis, and between thyroid and cutaneous metastases of clear cell renal carcinoma (RCC). METHODS AND RESULTS: Paraffin sections of the previously formalin-fixed thyroid tumour, and the fresh cutaneous tumour were stained with haematoxylin and eosin (H & E) and periodic acid-Schiff (PAS). Additionally, samples of both tumours were examined electron microscopically. Immunohistochemistry was performed with antibodies against thyroglobulin, pancytokeratin, keratin 7, 8, 18 and 19, chromogranin, calcitonin, CEA, vimentin and EMA. Five to six micrometre sections of both tumours were analysed with alpha-satellite probes of chromosomes 3, 7 and 17 using chromosomal in-situ hybridization (CISH). The cutaneous tumour was also cultured and analysed cytogenetically. The thyroid tumour displayed some follicle-like structures that stained positive with both PAS and antithyroglobulin, giving evidence of possibly entrapped thyroid follicles in metastatic RCC. The cutaneous tumour was negative for both stains. The tumours were ultrastructurally completely devoid of neurosecretory granules. Classical cytogenetical analysis of the cultured cutaneous tumour cells revealed monosomies 3 and 14, well-known specific primary and secondary aberrations, respectively, in clear cell RCC, and hitherto not reported in thyroid carcinomas. CISH of both tumours revealed monosomy 3, indicating a cytogenetical correlation between them. There was no evidence of typical chromosomal aberrations for thyroid carcinomas like structural changes on 10q, structural rearrangements or translocations of chromosome 7. CONCLUSION: Although neither histological sections, nor paraffin blocks of the original nephrectomy specimen were available for review, the original tumour was on record as clear cell RCC. Therefore the two tumours' renal origin was confirmed.
Subject(s)
Carcinoma, Renal Cell/genetics , Kidney Neoplasms/genetics , Skin Neoplasms/genetics , Thyroid Neoplasms/genetics , Aged , Carcinoma, Renal Cell/pathology , Carcinoma, Renal Cell/ultrastructure , Chromosome Aberrations , Chromosome Disorders , Diagnosis, Differential , Female , Humans , Immunoenzyme Techniques , In Situ Hybridization , Karyotyping , Kidney Neoplasms/pathology , Skin Neoplasms/secondary , Skin Neoplasms/ultrastructure , Thyroid Neoplasms/secondary , Thyroid Neoplasms/ultrastructureABSTRACT
The short arm isochromosome of chromosome 12 and trisomy 12 are well-established chromosomal alterations in human ovarian germ cell tumors. However, numerical aberrations of chromosome 12 in epithelial ovarian tumors (EOTs) are highly controversial; both trisomy 12 and monosomy 12 have been observed. We performed chromosomal in situ hybridization in paraffin-embedded and formalin-fixed tissue sections of 31 EOTs. Twenty-five EOTs could be evaluated statistically (2 mucinous, 11 serous, 5 endometrioid, 3 borderline, and 4 other epithelial-type tumors) to examine the copy number of chromosome 12 and 15. The frequency distribution of hybridization signals with alpha-satellite centromeric DNA probes for chromosome 15 revealed disomy in all cases. However, we found the loss of chromosome 12 in 16 of 25 tumor samples. No correlation was found between the presence of monosomy 12 and the clinical stage of the tumors. Frequent loss of chromosome 12 may indicate that this chromosome is involved in the tumorigenesis of EOTs. Further studies are needed to clarify whether loss of chromosome 12 is an early or late event in ovarian carcinogenesis.