Genetic and histological subtypes of gastric cancer reviewed, particularly emphasising on microsatellite instability and E-cadherin gene mutation

Almost one million new cases of gastric cancer (GC) were estimated globally in 2012, (i.e. 952,000, representing 6.8% of the total cancer burden), making it the fifth most common malignancy in the world. GC represents a biologically and genetically diverse group of tumours with multifactorial aetiologies; both environmental and genetic. The vast majority of GCs are adenocarcinomas, which can be further subdivided into intestinal and diffuse histological subtypes according to the Lauren classification published in 1965. The molecular classification of GC according to the Cancer Genome Atlas (TCGA) divides GC into four subtypes: tumours positive for the EBV virus (9%), microsatellite unstable tumours (22%), genomically stable tumours (20%) and tumours with chromosomal instability (CIN) at 50%. Most GCs are sporadic by nature, where approximately 10% appear to possess a familial predisposition of which around half can be attributed to hereditary germline mutations i.e. those of the E-cadherin (CDH1) or mismatch repair (MMR) genes. Histopathological characteristics of the tumour type and analysis of potential genetic changes have substantial clinical significance, as they determine the choice of treatment. In this review, we consider the molecular pathogenesis, phenotype and testing of GC placing particular emphasis on microsatellite instability (MSI) and the CDH1 mutation

Genetic and histological subtypes of gastric cancer reviewed, particularly emphasising on microsatellite instability and E-cadherin gene mutation

Almost one million new cases of gastric cancer (GC) were estimated globally in 2012, (i.e. 952,000, representing 6.8% of the total cancer burden), making it the fifth most common malignancy in the world. GC represents a biologically and genetically diverse group of tumours with multifactorial aetiologies; both environmental and genetic. The vast majority of GCs are adenocarcinomas, which can be further subdivided into intestinal and diffuse histological subtypes according to the Lauren classification published in 1965. The molecular classification of GC according to the Cancer Genome Atlas (TCGA) divides GC into four subtypes: tumours positive for the EBV virus (9%), microsatellite unstable tumours (22%), genomically stable tumours (20%) and tumours with chromosomal instability (CIN) at 50%. Most GCs are sporadic by nature, where approximately 10% appear to possess a familial predisposition of which around half can be attributed to hereditary germline mutations i.e. those of the E-cadherin (CDH1) or mismatch repair (MMR) genes. Histopathological characteristics of the tumour type and analysis of potential genetic changes have substantial cli­nical significance, as they determine the choice of treatment. In this review, we consider the molecular pathogenesis, phenotype and testing of GC placing particular emphasis on microsatellite instability (MSI) and the CDH1 mutation

Debarya glyptosperma (De Bary) Wittrock 1872 (Zygnemataceae, Chlorophyta) as a possible airborne alga : a contribution to its palaeoeocological interpretation

This paper reports the fi nding of Debarya glyptosperma zygospores in xeric grasslands far from the natural habitat of algal species. This fact suggests that this species is an airborne alga and this has not been reported before. What is more the discoidal shape of the zygospores may dispose this taxon among the Zygnemataceae family towards air dispersion. This new information may assist in assessing it as an indicator of limnic conditions. However, the simple discovery of Debarya without any accompanying algal taxa and/or other water plants should not be conclusively interpreted as proof of the existence of water bodies because the zygospores might originate from distant transport

Photocatalytic Decolourization of Direct Yellow 9 on Titanium and Zinc Oxides

The photodecolourization of Direct Yellow 9, a member of the group of azo dyes which are commonly used in the various branches of the industry, was investigated. The photostability of this dye was not previously examined. Photocatalytic degradation method was evaluated. Solar simulated light (E=500 W/m2), titanium dioxide, and zinc oxide were used as irradiation source and photocatalysts, respectively. Kinetic studies were performed on a basis of a spectrophotometric method. Degradation efficiency was assessed by applying high performance liquid chromatography. Disappearance of a dye from titanium dioxide and zinc oxide surfaces after degradation was confirmed by thermogravimetry and Raman microscopy. Direct Yellow 9 was found to undergo the photodegradation with approximately two times higher efficiency when zinc oxide was applied in comparison with titanium dioxide. A simple and promising way to apply the photocatalytic removal of Direct Yellow 9 in titanium dioxide and zinc oxide suspensions was presented

Chłoniak MALT dwunastnicy. Opis przypadku i przegląd literatury

Przedstawiono przypadek 69-letniego mężczyzny  skierowanego do poradni gastrologicznej, po przebytym epizodzie krwawienia z przewodu pokarmowego, z łagodną anemią mikrocytarną. Na podstawie wykonanych badań, w których kluczową rolę odegrała ultrasonografia jamy brzusznej, postawiono rozpoznanie chłoniaka MALT opuszki dwunastnicy. Nie stwierdzono zakażenia Helicobacter pylori. W leczeniu zastosowano radioterapię radykalną i uzyskano remisję choroby (czas obserwacji 9 miesięcy). Dotychczas w literaturzepisano 45 chorych z chłoniakiem MALT dwunastnicy, u 19 chorych zmiany zlokalizowane były w opuszce dwunastnicy, u połowy chorych stwierdzono zakażenie H. pylori. U 16 chorych zastosowano leczenie eradykacyjne, z czego u 9 chorych uzyskano remisję. Pozostali chorzy leczeni byli chemioterapią, radioterapią, operacyjnie lub stosowano kombinacje wyżej wymienionych  metod. U większości chorych uzyskano remisję choroby (czas obserwacji od 3 tygodni do 12 lat); zgon wystąpił jedynie u 3 chorych.  Chłoniak MALT dwunastnicy jest nowotworem o dobrym rokowaniu, a związki pomiędzy zakażeniem H. pylori  i skuteczność leczenia eradykacyjnego są mniejsze niż w przypadku chłoniaka MALT żołądka

Is FLT3 internal tandem duplication an unfavorable risk factor for high risk children with acute myeloid leukemia? : Polish experience

According to the AML-BFM 2004 Interim, a treatment protocol used in Poland since 2005, presence of FLT3 internal tandem duplication (FLT3/ITD) qualifies a patient with acute myeloid leukemia (AML) to a high-risk group (HRG). The present study was aimed to identify the prevalence of FLT3/ITD in children with AML in Poland and to evaluate its prognostic significance in the HRG patients. Out of 291 children with de novo AML treated in 14 Polish centers between January 2006 and December 2012, samples from 174 patients were available for FLT3/ITD analysis. Among study patients 108 children (61.7%) were qualified to HRG. Genomic DNA samples from bone marrow were tested for identification of FLT3/ITD mutation by PCR amplification of exon 14 and 15 of FLT3 gene. Clinical features and treatment outcome in patients with and without FLT3/ITD were analyzed in the study. The FLT3/ITD was found in 14 (12.9%) of 108 HRG children. There were no significant differences between children with and without FLT3/ITD in age and FAB distribution. The white blood cells count in peripheral blood at diagnosis was significantly higher (p <0.01) in the children with FLT3/ITD. Over 5-year overall survival rate for FLT3/ITD positive children was worse (42.4%) comparing to FLT3/ITD negative children (58.9%), but the statistical difference was not significant. However, over 5-year survivals free from treatment failures were similar. The FLT3/ITD rate (12.9%) observed in the study corresponded to the published data. There was no significant impact of FLT3/ITD mutation on survival rates, although further studies are needed on this subject

Outcome of refractory and relapsed acute myeloid leukemia in children treated during 2005-2011 : experience of the Polish Pediatric Leukemia/Lymphoma Study Group (PPLLSG)

AIM OF THE STUDY: Recent studies showed relatively better outcome for children with refractory (refAML) and relapsed acute myeloid leukemia (relAML). Treatment of these patients has not been unified within Polish Pediatric Leukemia/Lymphoma Study Group (PPLLSG) so far. The goal of this study is to analyze the results of this therapy performed between 2005–2011. MATERIAL AND METHODS: The outcome data of 16 patients with refAML and 62 with relAML were analyzed retrospectively. Reinduction was usually based on idarubicine, fludarabine and cytarabine with allogenic hematopoietic stem cell transplant (alloHSCT) in 5 refAML and 30 relAML children. RESULTS: Seventy seven percent relAML patients entered second complete remission (CR2). Five-year OS and disease-free survival (DFS) were estimated at 16% and 30%. The outcome for patients after alloHSCT in CR2 (63%) was better than that of those not transplanted (36%) with 5-year OS of 34% vs. 2-year of 7% and 5-year DFS of 40% vs. 12.5%. Second complete remission achievement and alloHSCT were the most significant predictors of better prognosis (p = 0.000 and p = 0.024). The outcome of refAML children was significantly worse than relAML with first remission (CR1) rate of 33%, OS and DFS of 25% at 3 years and 53% at 2 years, respectively. All survivors of refAML were treated with alloHSCT after CR1. CONCLUSIONS: The uniform reinduction regimen of the documented efficacy and subsequent alloHSCT in remission is needed to improve the outcome for ref/relAML children treated within PPLLSG. The focus should be on the future risk-directed both front and second line AML therapy