Endometrioza i mięsakorak – hipotetyczny związek czy udowodniona wspólna ścieżka patogenetyczna? Opis przypadku mięsakoraka jelita grubego wychodzącego z ogniska endometriozy

We present the first case of a patient with a synchronic occurrence of three neoplasms: non-small cell lung cancer, serous cancer of the ovary, and carcinosarcoma of the colon. Moreover, the possible origin of the carcinosarcoma is an endometriotic focus, which is an extremely rare occurrence, especially in women with no history of endometriotic treatment. Immunohistochemical staining of the carcinosarcoma was positive for CD10, estrogen receptors and desmin – typical markers for endometriotic foci. The growth of endometriosis depends on estrogen, which is produced at reduced levels after menopause. However, in some cases endometriosis could be diagnosed de novo in postmenopausal women. On the basis of the reported patient we discuss possible correlations between endometriosis and carcinosarcoma, as well as treatment methods of carcinosarcoma.Prezentujemy pierwszy na świecie przypadek pacjentki, u której rozpoznano synchroniczne występowanie trzech nowotworów: niedrobnokomórkowego raka płuc, raka surowiczego jajnika oraz mięsakoraka jelita grubego. Co więcej, najbardziej prawdopodobnym punktem wyjścia mięsakoraka jelita grubego jest ognisko endometriozy. Niesłychanie rzadko opisuje się karcynogenezę związaną z endometriozą u pacjentek, które wcześniej nie leczyły się z powodu endometriozy. Badanie immunohistochemiczne mięsakoraka ujawniło ekspresję CD10, desminy oraz receptorów dla estrogenów – typowych markerów endometriozy. Aktualnie uznaje się, że endometrioza – mająca podłoże estrogenne, może być diagnozowana de novo nawet po menopauzie. Na podstawie przedstawionego opisu przypadku przedyskutowaliśmy możliwy związek endometriozy i mięsakoraka oraz dostępne opcje terapeutyczne mięsakoraków

Immunoekspresja białek związanych z apoptozą i proliferacją w surowiczych nowotworach jajnika

Introduction: Ovarian cancer takes fourth place as a cause of death from all cancers and first place fromgynaecological malignancies in Poland. Recent investigations have noted the prognostic significance of proteinslinked with proliferation (Ki-67) and apoptosis (CAS – cellular apoptosis susceptibility protein).The aim of the study was to evaluate the immunoexpression of CAS and Ki-67 proteins in metastatic andnon-metastatic serous ovarian tumours, as well as to find possible relationships between this immunoexpressionand tumour proliferation activity. Material and methods: The analysis comprised 43 women diagnosed and treated for malignant epithelialovarian tumours. The immunoexpression of CAS protein was assessed semiquantitatively, whereas immunoexpressionof Ki-67 was performed using a computer image analysis system. Results: The immunoexpression of both CAS and Ki-67 proteins was significantly increased in the metastaticgroup as compared with patients without metastases. Also, a positive correlation was found between immunoexpressionof Ki-67 and CAS protein, but this correlation was not significant. Conclusions: In conclusion, our data suggest that increased immunoexpression of CAS and Ki-67 proteins inserous ovarian tumours may be helpful in identifying cases of higher metastatic potential

Effects of Helicobacter pylori Infection on Ghrelin and Insulin-like Growth Factor 1 Secretion in Children with Idiopathic Short Stature

Background: A diagnosis of "idiopathic short stature" (ISS) in a child means that the cause of the disease has not been established, although there are certainly some unknown factors that contributed to its occurrence. Ghrelin and leptin are important in controlling food intake; ghrelin is also a growth hormone (GH) stimulator. Both enterohormones are produced in the stomach and their secretion may be affected by a Helicobacter pylori (H. pylori) infection. Methods: Our study included a group of 61 children (53 prepubertal and 8 peripubertal) with ISS, without any gastrointestinal tract symptoms but in whom the histopathological evaluation of stomach tissue was made during gastroscopy to diagnose H. pylori infection. In each child, fasting ghrelin, leptin and IGF-1 concentrations, and GH levels in two stimulation tests were assessed. Results: H. pylori infection was confirmed in 24.6% of the children. Ghrelin and IGF-1 concentrations were significantly lower in H. pylori-positive than H. pylori-negative children (this was more noticeable in prepubertal subgroups), however there was not a discrepancy in regards to GH concentrations in stimulation tests, leptin levels or the nutritional state between groups. Conclusions: Short children, infected by H. pylori seem to have lower ghrelin and IGF-1 concentrations than children without infection, this may be the reason for a worse growth rate in this subgroup

Immunoregulation of antigen presenting and secretory functions of monocytic cells by Helicobacter pylori antigens in relation to impairment of lymphocyte expansion

The role of Helicobacter pylori (H. pylori) antigens in driving a specific immune response against the bacteria causing gastroduodenal disorders is poorly understood. Using a guinea pig model mimicking the natural history of H. pylori infection, we evaluated the effectiveness of immature and mature macrophages in promoting the blastogenesis of splenocytes from H. pylori infected and uninfected animals, in response to H. pylori antigens: glycine acid extract (GE), cytotoxin associated gene A protein (CagA), urease A (UreA) and lipopolysaccharide (LPS). Lymphocyte expansion was assessed in 72 h cell cultures, containing: immature or mature macrophages derived from bone marrow monocytes, unstimulated or stimulated with H. pylori antigens for 2 h. The proliferation was expressed as a ratio of [3H]-thymidine incorporation into DNA of antigen-stimulated to unstimulated cells and the DNA damage was determined by DAPI cell staining. TGF-β and IFN-γ were assessed immunoenzymatically in cell culture supernatants. Lymphocytes of control and H. pylori-infected animals proliferated intensively in response to phytohaemagglutinin (PHA) and in co-cultures with immature or mature macrophages treated with CagA or UreA (significantly) and GE (slightly) exluding the cultures containing H. pylori or E. coli LPS. This lymphocyte growth inhibition was related to DNA damage of monocytic cells in response to H. pylori or E. coli LPS and secretion of regulatory TGF-β, but not proinflammatory IFN-γ. Impaired homeostasis of monocytic cell function related to DNA damage and TGF-β release, in response to H. pylori LPS may lead to the suppression of adaptive immune response against the bacteria and development of chronic infection

Immunoregulation of antigen presenting and secretory functions of monocytic cells by Helicobacter pylori antigens in relation to impairment of lymphocyte expansion

The role of Helicobacter pylori (H. pylori) antigens in driving a specific immune response against the bacteria causing gastroduodenal disorders is poorly understood. Using a guinea pig model mimicking the natural history of H. pylori infection, we evaluated the effectiveness of immature and mature macrophages in promoting the blastogenesis of splenocytes from H. pylori infected and uninfected animals, in response to H. pylori antigens: glycine acid extract (GE), cytotoxin associated gene A protein (CagA), urease A (UreA) and lipopolysaccharide (LPS). Lymphocyte expansion was assessed in 72 h cell cultures, containing: immature or mature macrophages derived from bone marrow monocytes, unstimulated or stimulated with H. pylori antigens for 2 h. The proliferation was expressed as a ratio of [3H]-thymidine incorporation into DNA of antigen-stimulated to unstimulated cells and the DNA damage was determined by DAPI cell staining. TGF-β and IFN-γ were assessed immunoenzymatically in cell culture supernatants. Lymphocytes of control and H. pylori-infected animals proliferated intensively in response to phytohaemagglutinin (PHA) and in co-cultures with immature or mature macrophages treated with CagA or UreA (significantly) and GE (slightly) exluding the cultures containing H. pylori or E. coli LPS. This lymphocyte growth inhibition was related to DNA damage of monocytic cells in response to H. pylori or E. coli LPS and secretion of regulatory TGF-β, but not proinflammatory IFN-γ. Impaired homeostasis of monocytic cell function related to DNA damage and TGF-β release, in response to H. pylori LPS may lead to the suppression of adaptive immune response against the bacteria and development of chronic infection