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Background: Accumulating evidence suggests a relationship between endometrial cancer and ovarian cancer. Independent genome-wide association studies (GWAS) for endometrial cancer and ovarian cancer have identified 16 and 27 risk regions, respectively, four of which overlap between the two cancers. We aimed to identify joint endometrial and ovarian cancer risk loci by performing a meta-analysis of GWAS summary statistics from these two cancers. Methods: Using LDScore regression, we explored the genetic correlation between endometrial cancer and ovarian cancer. To identify loci associated with the risk of both cancers, we implemented a pipeline of statistical genetic analyses (i.e., inverse-variance meta-analysis, colocalization, and M-values) and performed analyses stratified by subtype. Candidate target genes were then prioritized using functional genomic data. Results: Genetic correlation analysis revealed significant genetic correlation between the two cancers (rG = 0.43, P = 2.66 × 10−5). We found seven loci associated with risk for both cancers (PBonferroni < 2.4 × 10−9). In addition, four novel subgenome-wide regions at 7p22.2, 7q22.1, 9p12, and 11q13.3 were identified (P < 5 × 10−7). Promoter-associated HiChIP chromatin loops from immortalized endometrium and ovarian cell lines and expression quantitative trait loci data highlighted candidate target genes for further investigation. Conclusions: Using cross-cancer GWAS meta-analysis, we have identified several joint endometrial and ovarian cancer risk loci and candidate target genes for future functional analysis. Impact: Our research highlights the shared genetic relationship between endometrial cancer and ovarian cancer. Further studies in larger sample sets are required to confirm our findings.

We report a meta-analysis of breast, prostate, ovarian, and endometrial cancer genome-wide association data (effective sample size: 237,483 cases/317,006 controls). This identified 465 independent lead variants (P−8) across 192 genomic regions. Four lead variants were >1Mb from previously identified risk loci for the four cancers and an additional 23 lead variant-cancer associations were novel for one of the cancers. Bayesian models supported pleiotropic effects involving at least two cancers at 222/465 lead variants in 118/192 regions. Gene-level association analysis identified 13 shared susceptibility genes (P−6) in 13 regions not previously implicated in any of the four cancers and not uncovered by our variant-level meta-analysis. Several lead variants had opposite effects across cancers, including a cluster of such variants in the TP53 pathway. Fifty-four lead variants were associated with blood cell traits and suggested genetic overlaps with clonal hematopoiesis. Our study highlights the remarkable pervasiveness of pleiotropy across hormone-related cancers, further illuminating their shared genetic and mechanistic origins at variant- and gene-level resolution.

Accumulating evidence suggests a relationship between endometrial cancer and epithelial ovarian cancer. For example, endometrial cancer and epithelial ovarian cancer share epidemiological risk factors and molecular features observed across histotypes are held in common (e.g. serous, endometrioid and clear cell). Independent genome-wide association studies (GWAS) for endometrial cancer and epithelial ovarian cancer have identified 16 and 27 risk regions, respectively, four of which overlap between the two cancers. Using GWAS summary statistics, we explored the shared genetic etiology between endometrial cancer and epithelial ovarian cancer. Genetic correlation analysis using LD Score regression revealed significant genetic correlation between the two cancers (rG = 0.43, P = 2.66 × 10−5). To identify loci associated with the risk of both cancers, we implemented a pipeline of statistical genetic analyses (i.e. inverse-variance meta-analysis, co-localization, and M-values), and performed analyses by stratified by subtype. We found seven loci associated with risk for both cancers (PBonferroni < 2.4 × 10−9). In addition, four novel regions at 7p22.2, 7q22.1, 9p12 and 11q13.3 were identified at a sub-genome wide threshold (P < 5 × 10−7). Integration with promoter-associated HiChIP chromatin loops from immortalized endometrium and epithelial ovarian cell lines, and expression quantitative trait loci (eQTL) data highlighted candidate target genes for further investigation.

Aim of the study : To present the changes in the incidence of cancers of the head and neck organs in south-eastern Poland and in the whole country in the years 1990-2012. Material and methods : A retrospective analysis the incidence of cancers of the head and neck organs in south-eastern Poland in the years 1990–2012. Statistical methods used for cancers of ICD-10 C00-C14 and C30-C32. Results: For Poland, the absolute number of cases was 123,120 in the years 1990-2012. For males, the number of cases per year increased from 4468 in 1990 to 4953 in 2012, and for females from 816 to 1442. The percentage share of tumours of the head and neck in all malignant tumours decreased from 10.0% to 6.5% for males and from 2.1% to 1.9% for females. In the years 1990–2012 in south-eastern Poland, for males, the absolute number of cases per year decreased from 335 in 1990 to 286 in 2012. For females, a minimal increase in cases was from 63 to 64 cases. The percentage share of tumours of the head and neck in all malignant tumours decreased from 12.2% to 6.7% for males and from 2.7% to 1.8% for females. Conclusions : Incidences of cancers of the head and neck organs in Poland have seen a slight upward trend in the absolute number of cases over the last two decades. In Poland a decrease in the incidence of cancer of the larynx was reported, with an increase in the incidence of oropharyngeal cancer.

Wstep. Rak piersi u mezczyzn uwazany jest za nowotwor rzadki, stanowiący ponizej 1% wszystkich nowotworow u mezczyzn, jak rowniez wystepujący 100-krotnie rzadziej niz u kobiet oraz rozpoznawany u mezczyzn w poźniejszym wieku i wyzszym niz u kobiet stopniu zaawansowania. Celem pracy byla analiza trendow w zachorowaniach na raka piersi u mezczyzn na bazie 192 przypadkow zarejestrowanych w latach 1963–2011 w regionie Polski poludniowo-wschodniej i odniesienie tych danych do problematyki zachorowan na raka piersi u kobiet w „regionie” oraz do zachorowalności u mezczyzn w Polsce i w piśmiennictwie. Material i metody. Retrospektywnej analizie poddano 192 zachorowania na raka piersi u mezczyzn z lat 1963–2011, z terenu Polski poludniowo-wschodniej. Obliczono wspolczynniki surowe i wskaźniki struktury (odsetki). W oparciu o dostepne dane obliczono wspolczynniki zachorowalności wedlug plci dla lat 1963–2011 w regionie Polski pld.-wsch. oraz w oparciu o piśmiennictwo — dla Polski. Dokonano analizy średniego wieku zachorowan w latach 1990–2011 dla kobiet i mezczyzn oraz stopni zaawansowania nowotworu i danych histopatologicznych u chorych pierwszorazo­wych z lat 1999–2011, jak rowniez zastosowanych metod leczenia. Dane te odniesiono do wybranych wskaźnikow zachorowalności na raka piersi w regionie Polski pld.-wsch. i w Polsce tak dla mezczyzn, jak i kobiet. Wyniki. W latach 1963–2011 zarejestrowano w Polsce 3551 pierwszorazowych zachorowan na raka piersi u mezczyzn — w tym w regionie Polski pld.-wsch. — 192. W „regionie” stanowily one 0,18% zachorowan na nowotwory u mezczyzn oraz 0,09% wszystkich zachorowan na nowotwory w latach 1963–2011. W tym samym okresie dla Polski rak piersi u mezczyzn stanowil odpowiednio 0,18% zachorowan na nowotwory u mezczyzn i 0,09% wszystkich zachorowan na nowotwory. W latach 1963–2011 wspolczynnik surowy zachorowalności dla „regionu” wynosil w poszczegolnych latach od 0,12 do 0,86 na 100 tys. mezczyzn — średnio 0,4. Wspolczynnik ten dla Polski w tym samym czasie wyno­sil od 0,18 do 0,66 — średnio 0,42 na 100 tys. mezczyzn. W oparciu o powyzszy material oceniono średni wiek dla mezczyzn z rakiem piersi, ktory wynosil dla „regionu” ogolem 64,5 roku. W latach 1990–2010 średni wiek dla kobiet chorych na raka piersi wynosil w „regionie” 59,4 roku. Wspolczynnik zachorowan w latach 1963–2011 dla „regionu” mezczyźni/kobiety odpowiednio wynosil od 1:33 do 1:327 — średnio 1:86, a dla Polski od 1:23 do 1:167, średnio 1:99 na 100 000 mezczyzn i kobiet. Wnioski. W ciągu 48 lat obserwacji średnia zachorowalnośc na raka piersi u mezczyzn w regionie Polski poludniowo-wschodniej byla nizsza niz średnia zachorowalnośc dla Polski, średni wiek zachorowan na raka piersi dla mezczyzn w regionie Polski poludniowo-wschodniej byl średnio o 5 lat wyzszy niz dla kobiet. W stopniach zaawansowania u mezczyzn dominowal stopien zaawansowania regionalnego, a u kobiet stopien zaawansowania miejscowego. W zakresie oceny histopatologicznej u obu plci dominowal rak przewodowy naciekający, a najczestszą metodą leczenia byla chirurgia, przed chemioterapią i radioterapią.

Kolejne lata dzialalności Wojewodzkiego Szpitala Onkologicznego w Rzeszowie wykazaly, jak wielkie jest na Pod­karpaciu zapotrzebowanie w zakresie lecznictwa onkologicznego. W 1985 r. dr Jozef Malek zglosil kompleksowy plan budowy nowego Szpitala Onkologicznego w Rzeszowie. Wniosek ten, pozytywnie zaopiniowany przez prof. Skolyszewskiego, zostal w 1986 r. przyjety do realizacji. W kwietniu 1988 projekt zakladający budowe szpitala onko­logicznego, planowanego na 300 lozek, w tym 50 dla stanow lekkich, oraz zespolu sal operacyjnych zostal pozytywnie zaopiniowany przez ministra zdrowia. Koncepcja ta nie zostala jednak zrealizowana, i w 1990 r. podjeto decyzje o rozwiązaniu Wojewodzkiego Szpitala Onkologicznego w Rzeszowie oraz wlączeniu jego Oddzialow do Szpitala Wojewodzkiego Nr 1. W lutym 1992 r. rozpoczeto leczenie telegammaterapią w nowym pawilonie bomby kobaltowej, a wkrotce potem curieterapie zastąpiono brachyterapią after-loading LDR, MDR. W latach 1992–1997 dzialające na bazie Oddzialow onkologicznych Stowarzyszenia zorganizowaly szereg konferencji krajowych i miedzynarodowych o tematyce onkologicznej. W 1995 r. utworzono na bazie oddzialow i zakladow onkologicznych Rzeszowski Ośrodek Onkologiczny. W ramach jego rozbudowy uzyskano kolejną bombe kobaltową oraz dwa dwustanowiskowe aparaty Selectron LDR/MDR. W listopadzie 1999 r. Rzeszowski Ośrodek Onkologiczny przeksztalcono w dzialające do dziś w strukturach Wojewodzkiego Szpitala Specjalistycznego Podkarpackie Centrum Onkologii.

The first document referring to the organisation of oncological care in the region of Rzeszow province comes from 1952. The first oncological unit in the Rzeszow region — Provincial Oncological Dispensary started its activities on December 1952. In March 1961, dr Jozef Malek became the Head of the Dispansery. He also directed the organisation of the first roentgenotherapy laboratory, who was ready for work on May, 1962. The Provincial Oncological Centre in Rzeszow was estabilished on 19-th December 1963. The Centre had several sections: general radiotherapy, gynecological radiotherapy, surgery, roentgenotherapy lab, physics lab, radium rooms, docementation section and methodical and organisation section. In 1971, the Centre acquired 550 mg of radium for the curietherapy laboratory. In 1975 and 1976, the named was changed into Provincial Oncological Hospital in Rzeszow. Under above-mentioned name the oncological medical center in Rzeszow was working until 1990.

Contains fulltext : 153959.pdf (Publisher’s version ) (Closed access) Epidemiological studies have demonstrated associations between endometriosis and certain histotypes of ovarian cancer, including clear cell, low-grade serous and endometrioid carcinomas. We aimed to determine whether the observed associations might be due to shared genetic aetiology. To address this, we used two endometriosis datasets genotyped on common arrays with full-genome coverage (3194 cases and 7060 controls) and a large ovarian cancer dataset genotyped on the customized Illumina Infinium iSelect (iCOGS) arrays (10 065 cases and 21 663 controls). Previous work has suggested that a large number of genetic variants contribute to endometriosis and ovarian cancer (all histotypes combined) susceptibility. Here, using the iCOGS data, we confirmed polygenic architecture for most histotypes of ovarian cancer. This led us to evaluate if the polygenic effects are shared across diseases. We found evidence for shared genetic risks between endometriosis and all histotypes of ovarian cancer, except for the intestinal mucinous type. Clear cell carcinoma showed the strongest genetic correlation with endometriosis (0.51, 95% CI = 0.18-0.84). Endometrioid and low-grade serous carcinomas had similar correlation coefficients (0.48, 95% CI = 0.07-0.89 and 0.40, 95% CI = 0.05-0.75, respectively). High-grade serous carcinoma, which often arises from the fallopian tubes, showed a weaker genetic correlation with endometriosis (0.25, 95% CI = 0.11-0.39), despite the absence of a known epidemiological association. These results suggest that the epidemiological association between endometriosis and ovarian adenocarcinoma may be attributable to shared genetic susceptibility loci.

Local staging of malignancy, introduced in the past few decades into clinical practice, is based on the identification of the...