60 research outputs found
Эндометриоз послеоперационного рубца после миомэктомии
IMSP Institutul Mamei şi Copilului, Secţia ginecologie chirurgicală, Universitatea de Medicină şi Farmacie “N.Testemiţanu”, Laboratorul de Chirurgie Hepato-Bilio-Pancreatică, IMSP Institutul de Medicină Urgentă, IMSP Institutul Oncologic, Secţia patomorfologieIntroduction: Abdominal wall endometriosis (AWE) is a rare condition, which usually develops in a surgical scar after Caesarean section. AWE following abdominal myomectomy for uterine myomas is extremely rare.
Case presentation: A 27-year-old woman was referred to our clinic for atypical cyclic pain and mass at the left edge of a Pfannenstiel incision scar four years after abdominal myomectomy. Computerized tomographic (CT) scanning of the pelvis with contrast revealed an enhancing mass in the abdominal wall extending from the skin to the muscle layer. The mass was removed completely (R0 resection) and histopathology (with immunohistochemical analysis) of the
surgical specimen revealed endometriosis.
Conclusion: AWE needs to be considered in the differential diagnosis of any woman of reproductive age presenting with a painful abdominal wall mass and a history of uterine surgery via an abdominal incision.Введение: Эндометриоз передней брюшной стенки (ЭПБС) достаточно редкая патология и обычно наблюдается после кесарева сечения. ЭПБС после абдоминальной миомэктомии чрезвычайно редкая ситуация.
Клиническое наблюдение: Пациентка 27 лет направлена с циклическими болями и наличием объемного образования в левом углу разреза по Пфанненштилю после трансабдоминальной миомэктомии. Компьютерная томография с контрастированием выявила образование в передней брюшной стенке от подкожной клетчатки до прямой мышцы живота. Образование иссечено радикально (R0 резекция) и гистологическое исследование с
иммуногистохимией подтвердило наличие эндометриоза.
Вывод: ЭПБС должен рассматриваться в дифференциальном диагнозе у женщин репродуктивного возраста при наличии болезненного опухолевидного образования в области послеоперационного рубца после оперативных вмешательств на матке
Endometriosis of postoperative scar: a report of thirty two cases
Catedra de chirurgie nr. 1 „Nicolae Anestiadi”, Laboratorul de chirurgie hepato-pancreato-biliară, USMF „Nicolae
Testemițanu”, Secţia Ginecologie Chirurgicală, IMSP Institutul Mamei şi Copilului, IMSP Institutul Medicină
Urgentă, Secţia Morfopatologie, IMSP Institutul Oncologic, Chişinău, Republica Moldova,
Conferința stiințifică „Nicolae Anestiadi – nume etern al chirurgiei basarabene” consacrată centenarului de la nașterea profesorului Nicolae Anestiadi 26 august 2016Introducere. Endometrioza cicatricii postoperatorii (ECP) este o afecțiune rară dificilă în diagnostic, provocată
de obicei de chirurgia ginecologico-obstetricală.
Scopul. Aprecierea particularităților de diagnostic și tratament chirurgical.
Material și metode. Au fost analizate 32 cazuri de ECP tratate chirurgical la baza a doua clinici pe parcursul
anilor 1991-2016.
Rezultate. Vârsta medie a pacientelor cu ECP a constituit 30.4±0.9 ani (95%CI:28.41-32.41). Indicele masei
corporale a pacientelor cu ECP a constituit 21.6±0.6 kg. (95%CI:20.28-22.85). Perioada de apariție ECP 44.1±2.8
luni (95%CI:38.39-49.73). În toate cazurile pacientele au prezentat formațiune tumorală (n=32, 100%), în regiunea
cicatricei postoperatorii a peretelui abdominal anterior (n=26, 81%), incizia Pfannenstiel (n=23), mediană
inferioară (n=2), ombilic (n=1), regiunea perineală (n= 6). Au fost determinate particularitățile caracteristice
pentru ECP prevalența: monofocal vs. bifocal (n=29, 90.6% vs. n=3, 9.3%, p<0.0001), unghiul stâng a cicatricei
postoperatorii vs.drept și central (82.6% vs. 17.3%, p<0.0001). La stabilirea diagnosticului au fost utilizate
metode imagistice: USG cu doplerografie, TC și RMN. Intervenit chirurgical cu excizia ECP en bloc depășind
5-10 mm în limitele țesuturilor sănătoase. La examenul histopatologic dimensiunile macropreparatului stabilite
(max.3.3±0.4 și min.2.6±0.3) ce confirmă diagnosticul de ECP. Examenul imunohistochimic demonstrează
expresie difuză la CD10 în regiunea stromei citogene, colorație nucleară a nucleului glandei endometriale și a
celulelor stromale receptori progesteron și receptorii estrogeni (ERα).
Concluzie. Evaluarea clinică în combinație cu metodele imagistice, histologice și imunohistochimice constituie
baza în corectitudinea stabilirii diagnosticului.Introduction. Endometriosis of postoperative scar (ECP) is a rare disorder, difficult to diagnose, usually caused
by gynecologic-obstetric surgery.
Purpose. Appreciation of the particularities of diagnostic and surgical treatment.
Material and methods. We analyzed 32 cases of surgically treated ECP, based on two clinics, during the years 1991-2016.
Results. Mean age of patients with ECP was 30.4 ± 0.9 years (95% CI: 28.41-32.41). Body mass index of patients
with ECP was 21.6 ± 0.6 kg. (95% CI: 20.28-22.85). The period of ECP appearance was 44.1 ± 2.8 months
(95% CI: 38.39-49.73). In all cases the patients showed tumor (n = 32, 100%) in postoperative scar of anterior
abdominal wall (n = 26, 81%), the Pfannenstiel incision (n = 23), median lower incision (n = 2), umbilical
incision (n = 1), in perineal region (n = 6). Were determined the particularities of ECP: prevalence: monofocal
vs. bifocal (n = 29, 90.6% vs. n = 3, 9.3%, p <0.0001), the left angle of postoperative scar vs. right and center
(82.6% vs. 17.3%, p <0.0001). Ultrasound with dopplerography examination, computed tomography (CT) and
magnetic resonance imaging (MRI) has an important value in the diagnosis of scar mass. All patients were
undergone excision en bloc of tumors exceeding 5-10 mm beyond the limits of healthy tissues. Histopathological
examination of excised mass with set size (max.3.3 ± 0.4 and 0.3 ± min.2.6) confirmed the diagnosis of ECP.
Immunohistochemistry examination demonstrated CD10 diffusion in cytogenetic region, nuclear staining of
the nucleus of endometrial gland and of stromal cells, progesterone and estrogen receptors (ERα).
Conclusion. The clinical evaluation in combination with imaging methods, histological and immunohistochemical
examination are basic in the accuracy of diagnosis
An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics
For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types
Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas
This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing
molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin
Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context
Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts
Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas
Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN
Spatial Organization and Molecular Correlation of Tumor-Infiltrating Lymphocytes Using Deep Learning on Pathology Images
Beyond sample curation and basic pathologic characterization, the digitized H&E-stained images
of TCGA samples remain underutilized. To highlight this resource, we present mappings of tumorinfiltrating lymphocytes (TILs) based on H&E images from 13 TCGA tumor types. These TIL
maps are derived through computational staining using a convolutional neural network trained to
classify patches of images. Affinity propagation revealed local spatial structure in TIL patterns and
correlation with overall survival. TIL map structural patterns were grouped using standard
histopathological parameters. These patterns are enriched in particular T cell subpopulations
derived from molecular measures. TIL densities and spatial structure were differentially enriched
among tumor types, immune subtypes, and tumor molecular subtypes, implying that spatial
infiltrate state could reflect particular tumor cell aberration states. Obtaining spatial lymphocytic
patterns linked to the rich genomic characterization of TCGA samples demonstrates one use for
the TCGA image archives with insights into the tumor-immune microenvironment
Driver Fusions and Their Implications in the Development and Treatment of Human Cancers.
Gene fusions represent an important class of somatic alterations in cancer. We systematically investigated fusions in 9,624 tumors across 33 cancer types using multiple fusion calling tools. We identified a total of 25,664 fusions, with a 63% validation rate. Integration of gene expression, copy number, and fusion annotation data revealed that fusions involving oncogenes tend to exhibit increased expression, whereas fusions involving tumor suppressors have the opposite effect. For fusions involving kinases, we found 1,275 with an intact kinase domain, the proportion of which varied significantly across cancer types. Our study suggests that fusions drive the development of 16.5% of cancer cases and function as the sole driver in more than 1% of them. Finally, we identified druggable fusions involving genes such as TMPRSS2, RET, FGFR3, ALK, and ESR1 in 6.0% of cases, and we predicted immunogenic peptides, suggesting that fusions may provide leads for targeted drug and immune therapy
Integrated Genomic Analysis of the Ubiquitin Pathway across Cancer Types
Protein ubiquitination is a dynamic and reversibleprocess of adding single ubiquitin molecules orvarious ubiquitin chains to target proteins. Here,using multidimensional omic data of 9,125 tumorsamples across 33 cancer types from The CancerGenome Atlas, we perform comprehensive molecu-lar characterization of 929 ubiquitin-related genesand 95 deubiquitinase genes. Among them, we sys-tematically identify top somatic driver candidates,including mutatedFBXW7with cancer-type-specificpatterns and amplifiedMDM2showing a mutuallyexclusive pattern withBRAFmutations. Ubiquitinpathway genes tend to be upregulated in cancermediated by diverse mechanisms. By integratingpan-cancer multiomic data, we identify a group oftumor samples that exhibit worse prognosis. Thesesamples are consistently associated with the upre-gulation of cell-cycle and DNA repair pathways, char-acterized by mutatedTP53,MYC/TERTamplifica-tion, andAPC/PTENdeletion. Our analysishighlights the importance of the ubiquitin pathwayin cancer development and lays a foundation fordeveloping relevant therapeutic strategies
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