Chondrosarcomatous differentiation in metastatic deposit of serous papillary cystadenocarcinoma

A rare case of serous papillary cystadenocarcinoma of the ovary showing chondrosarcomatous differentiation in a metastatic deposit late in the clinical course is reported. A 49-year-old female underwent a total abdominal hysterectomy with bilateral salpingo-oophorectomy for bilateral ovarian tumors. Histological diagnosis was serous papillary cystadenocarcinoma of both ovaries with lymph node metastasis. After six courses of chemotherapy, she was confirmed to be in complete remission following a second laparotomy. Following additional chemotherapy, a third laparotomy disclosed swollen left inguinal lymph nodes. In one of these nodes, approximately 5.0 cm in greatest diameter, the predominant histological features were: chondrosarcoma of the bone and soft tissue, with small foci of serous papillary adenocarcinoma and squamous epithelium. A histological transition between mesenchymal and epithelial areas was identified. Immunohistochemical positivity for broad-spectrum cytokeratin (AE1/AE3), vimentin, epithelial membrane antigen, and S-100 protein was observed in both chondrosarcomatous and epithelial areas. The current evidence may suggest that the chondrosarcomatous differentiation was derived from the metastatic epithelial component.     

Localisation of CEA, β-HCG,SP1, and keratin in the tissue of lung carcinomas

Summary One hundred and twenty seven cases of lung tumors were studied by the immunoperoxidase technique for the presence of CEA and-HCG. Twenty-nine of these tumors were additionally stained for keratin and SP1. CEA and SP1 could be demonstrated in 80% of the studied cases, while-HCG was found in only 9%. SP1 revealed an almost identical staining pattern to CEA and keratin was found only in squamous cell carcinomas. The tissue positivity of none of these three markers correlated with tumor size, lymphnodal involvement or histological type.This study was supported by Deutsche Stiftung für Krebsforschung - Dr. Mildred Scheel-Stiftung     

Fate of the type II pneumocyte following tracheal occlusion in utero: a time-course study in fetal sheep

 Tracheal occlusion in utero has been shown to cause accelerated fetal lung growth and is now being considered as a therapeutic modality for pulmonary hypoplasia. We report the effects of tracheal ligation on the surfactant-producing type II pneumocyte population. Three groups of fetal lambs underwent tracheal ligation of 2 weeks’, 4 weeks’ and 6 weeks’ duration, respectively, and all were sacrificed at 136 days’ gestation (9 days pre-term). Nonoperated twins served as controls. The type II pneumocyte population was studied morphometrically using a combination of anti-surfactant protein B immunohistochemistry and computer-assisted stereologic morphometry at light and electron microscopic levels. Single-factor ANOVA was used for statistical analysis. Two weeks of tracheal ligation resulted in doubling of the total lung volume as a result of airspace distension and, to lesser extent, growth of the tissue compartment. With increasing duration of tracheal ligation, there was no additional lung growth. However, more prolonged tracheal occlusion was found to result in significant reduction of the surfactant system, as reflected in the marked decrease of total pneumocyte type II volume (3.14 cm³, 0.95 cm³, and 0.46 cm³, after 2, 4, and 6 weeks of ligation, compared with 5.96 cm³ for controls) and total pneumocyte type II number (13.9 × 10⁹, 3.8 × 10⁹, and 2.4 × 10⁹, compared with 53.2 × 10⁹ for controls). Ultrastructural analysis of the type II cells in obstructed lungs showed vacuolar degenerative changes that, after 6 weeks of ligation, were apparently irreversible. In utero tracheal ligation causes fetal lung hyperplasia, but results in reduction of and injury to the surfactant-producing cell population. Before tracheal occlusion can find widespread clinical application, its pathophysiology needs to be further elucidated. Received: 30 April 1997 / Accepted: 10 July 1997     

Immunohistochemical expressions of cytokeratins, mucin core proteins, p53, and neuroendocrine cell markers in epithelial neoplasm of appendix

Epithelial neoplasms of appendix are infrequent, and their pathological features are not fully characterized. We collected 33 cases of appendiceal tumors and examined immunohistochemically the expression of cytokeratins (CK, CK7, and CK20), mucin core protein (MUC1, MUC2, MUC5AC, and MUC6), E-cadherin, chromogranin A, and p53 protein. Gene analysis of TP53 was also conducted on exons 5 to 8. Clinically, mucinous tumors were predominant in females. Immunohistochemically, all the tumors expressed CK20, whereas CK7 was positive in one third of the cases. Similarly, MUC2 was expressed in all the tumors, whereas MUC1 and MUC5AC were detected in about a half of the cases. Although chromogranin A-positive cells are generally sparse in normal appendix, they were more common in mucinous tumors than in nonmucinous tumors. Contrary to the previous data reported (Mod Pathol 2002;15:599-605), mucinous carcinoma exhibited a higher frequency of p53-positive cells (mean 29%) compared with mucinous adenoma (2.8%) (P < .001), whereas nonmucinous tumors showed high levels of p53-positive cells to similar extent (51%-67%) in both adenoma and carcinoma. The high expression of p53 protein coincided with the presence of mutations in multiple sites of TP53 gene in mucinous tumors. This is the first report that characterized the immunophenotypic profile of appendiceal epithelial neoplasms with an emphasis of a higher frequency of p53 positivity in mucinous carcinoma cases compared with mucinous adenoma in the appendix.     

Diagnosis of squamous-cell carcinoma of the lung by sputum cytology: with special reference to correlation of diagnostic accuracy with size and proximal extent of resected tumor

Sputum cytology was performed in 179 cases of squamous-cell carcinoma of the lung; 134 cases were diagnosed as positive. There were no significant differences in diagnostic accuracy of sputum cytology between tumors sizes. In cases with tumors extending proximally into the main, lobar, or segmental bronchi, the diagnostic accuracy of sputum cytology was significantly higher than in cases where the proximal invasion of tumor was limited to the peripheral bronchi. In cases with tumors 3 cm or less in diameter, when tumors extended proximally into main, lobar, or segmental bronchi, the diagnostic accuracy of sputum cytology was significantly higher than in cases with tumors extending proximally into subsegmental or subsubsegmental bronchi. In peripherally located squamous-cell carcinoma, in cases in which the tumor arose in subsegmental or subsubsegmental bronchi, carcinoma could be detected by sputum cytology even when it was roentgenographically occult.     

Argyrophilic nucleolar organizer regions in colorectal malignancy: application of typing by their density

Colorectal neoplasms obtained at colonoscopy were examined by argyrophilic nucleolar organizer region (AgNOR) staining to evaluate the usefulness of AgNOR as a discriminant for malignancy. AgNOR dots were divided into two kinds: 'structures' (larger and less-densely stained) corresponding to the nucleolus, and 'units' (smaller and densely stained) presumed to be true AgNOR within the structure. The number of structures per nucleus did not differ between the adenoma and carcinoma groups, whereas the number of units per nucleus showed a significant difference. However there were several cases showing an overlap between the adenoma and carcinoma groups, leading to a difficulty in deciding whether any given case was benign or malignant. Three types of AgNOR patterns were categorized based on the ratio of units to structure. Type I was defined as the unit being indistinguishable from the structure, Type II as each structure having one to five units, and Type III as at least one structure having six or more units, irrespective of total number of units per nucleus. The colorectal lesions in which more than half of the neoplastic cells showed Type III coincided well with carcinomas histologically diagnosed, with the exception of adenomas with severe atypia. Labeling index of proliferating cell nuclear antigen (PCNA LI) differed between the adenoma and carcinoma groups with a considerable extent of overlap, and correlated to some extent with the AgNOR values. These results showed that the AgNOR staining was useful for determining malignancy and its usefulness appeared superior to PCNA LI.     

Polymorphisms in the human CYP1A1 gene as susceptibility factors for lung cancer: exon-7 mutation (4889 A to G), and a T to C mutation in the 3′-flanking region

Genetic differences in the metabolism of carcinogens may codetermine individual predisposition to cancer. Cytochrome P-4501A1 (CYP1A1) metabolically activates precarcinogens in cigarette smoke, such as benzo(a)pyrene, which is also an inducer of CYP1A1. Two point mutations have been reported, m1 in the 3-flanking region (6235T to C), and m2 within exon 7 (4889A to G), the latter leading to an isoleucine to valine exchange. In the Japanese population ml and m2 are correlated with lung cancer, suggesting an increased susceptibility to cigarette smoking related lung cancer. We studied 142 lung cancer and 171 reference patients in an ethnically homogeneous German group for m1 and m2 mutations by restriction fragment length polymorphism and allele-specific polymerase chain reaction, respectively. No statistically significant difference was found in the distribution of m1 alleles between lung cancer and controls; the frequency was 8.5% and 7.3% of the alleles, respectively (odds ratio = 1.17). A trend to an overrepresentation of ml alleles was observed among 52 squamous cell carcinoma patients (odds ratio = 1.65). In contrast, the frequency of m2 alleles in lung cancer patients was twofold higher (6.7%) than in the reference group (3.2%; odds ratio = 2.16; 95% confidence limits 0.96–5.11, P = 0.033); the odds ratio of m2 alleles in squamous cell carcinoma was 2.51 (95% confidence limits 0.85–7.05, P = 0.05). There was a close genetic linkage of m2 to m1 (10 of 11 reference patients), but a significantly higher number of cancer patients showed no linkage compared to the controls (odds ratio = 8.89, 95% confidence limits 0.83–433, P = 0.04). Thus no association was found between presence of ml alleles and lung cancer, but, in contrast, m2 alleles proved as a hereditary risk factor, especially if not linked with m1 alleles.Abbreviations Ah aryl hydrocarbon - CYP1A1 cytochrome P4501A1 - CYP1A1 CYP1A1 gene - PCR polymerase chain reaction - PY pack years - RFLP restriction fragment length polymorphism Correspondence to: N. Drakoulis     

Protein 1 and Clara cell 10-kDa protein distribution in normal and neoplastic tissues with emphasis on the respiratory system

Thirty-six different normal tissues and 13 different malignant epithelial tumours, were examined immunohistochemically for the presence of protein 1 (P1) and Clara cell 10-kDa protein (CC10). Adenocarcinomas of the lung were also examined for the expression of pulmonary surfactant apoprotein using a monoclonal antibody (PE-10). The staining results of P1 and CC10 were almost identical both in normal tissues and in malignant tumours. In normal lung, Clara cells were strongly positive for both P1 and CC10. In addition, some goblet cells and non-ciliated non-mucus cells in the upper airways were moderately positive for both proteins. In the malignant tumours, some lung cancers were positive for P1 and CC10, both of which were positive in the same tumour cells on sequential sections. In 117 lung cancers, P1 and CC10 were positive in 10.2% of adenocarcinomas, 20.5% of squamous cell carcinomas, and 12.5% of large cell carcinomas. PE-10 stained positively in 65.3% of adenocarcinomas, a frequency significantly higher than that of P1 and CC10 (P<0.01). These results suggest that P1 and CC10 are nearly identical proteins, that both are useful markers of Clara cells, and that many pulmonary adenocarcinomas express surfactant apoprotein rather than Clara cell proteins.     

Sonic phase delay from trachea to chest wall: spatial and inhaled gas dependency

A parametric phase delay estimation technique is used to determine the spatial and inhaled gas composition dependencies of sound propagation time through an intact human lung at frequencies of 150–1200 Hz. Noise transmission measurements from the mouth to the extrathoracic trachea and six sites on the posterior chest wall are performed in 11 healthy adult subjects at resting lung volume after equilibration with air, an 80% helium-20% oxygen mixture, and an 80% sulfurhexafluoride-20% oxygen mixture. The phase delay, τ(f), exhibits a bilateral asymmetry with relatively decreased delays to the left posterior chest as compared with the right. The phase delay to lower lung sites is greater than to upper sites at frequencies below 300 Hz; yet the opposite is found at higher frequencies, indicating changing propagation pathways with frequency. There is no measurable effect of inhaled gas composition on τ(f) below 300 Hz. At higher frequencies, changes in τ(f) that reflect the relative sound speed of the particular inhaled gas are observed. These findings support and extend previous measurements and hypotheses concerning the strong frequency dependence of the acoustical properties of the intact respiratory system.