Combined left hepatectomy with fenestration and using a harmonic scalpel, fibrin glue and closed suction drainage to prevent bile leakage and ascites in the management of symptomatic polycystic liver disease: a case report

<p>Abstract</p> <p>Introduction</p> <p>Surgical treatment is the usual therapy for patients with polycystic liver disease and with severe symptoms, yet the results of surgery are often disappointing and the optimal surgical approach is uncertain.</p> <p>Case presentation</p> <p>We present the case of a 41-year-old Greek woman who underwent combined left hepatectomy with fenestration for symptomatic polycystic liver disease using ultrasound scalpel, fibrin glue and closed suction drain to prevent bile leakage, haemorrhage and ascites. Liver resection using the ultrasound scissors allowed quick parenchyma dissection under haemostatic conditions with safe coagulation of small vessels and bile ducts. Moreover, the ultrasound scalpel was applied to the cyst cavities exposed on the peritoneum to ablate the fluid-producing epithelial cyst lining. We also covered the cut cystic cavities exposed to the peritoneum surface of the liver with fibrin glue. Instead of allowing the opened cysts to drain into the abdominal cavity, we used two wide bore closed suction fluted drains. We did not observe excessive fluid loss through the drainage after the second postoperative day. The drain tubes were removed on the third postoperative day.</p> <p>Conclusion</p> <p>In our patient, effective treatment of ascites and prevention of bile leakage and bleeding indicate that this new approach is promising and may become a useful surgical technique for polycystic liver disease.</p

Adrenalectomy for solitary adrenal metastasis from colorectal cancer: A case report

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Prognostic evaluation of epidermal growth factor receptor genotype and phenotype parameters in triple-negative breast cancers

Epidermal growth factor receptor (EGFR) aberrations have been implicated in the pathogenesis of triple-negative breast cancer (TNBC) but their impact on prognosis and, therefore, druggability, remain controversial. Herein, we studied EGFR aberrations at different molecular levels and assessed their prognostic impact in patients with operable TNBC treated with adjuvant anthracycline-based chemotherapy. We evaluated the prognostic impact of EGFR gene status by fluorescent in situ hybridization (FISH), EGFR coding mutations by Sanger and next-generation sequencing, relative EGFR messenger RNA (mRNA) levels by qPCR (upper quartile) and EGFR and p53 protein expression by immunohistochemistry (IHC), in 352 centrally-assessed tumors from an equal number of TNBC patients. Approximately 53.5% of the tumors expressed EGFR, 59.3% p53 and 35.9% both EGFR and p53 proteins; 4.1% showed EGFR gene amplification and 4.4% carried EGFR mutations. The latter were located outside the druggable kinase domain region and presented at low frequencies. Amplification and mutations overlapped only in one case of glycogen-rich clear cell breast carcinoma. EGFR and CEN7 copies were higher in tumors from older patients (p=0.002 and p=0.003, respectively). Patients with amplified tumors (n=11) had excellent prognosis (0 relapses and deaths). Upon multivariate analysis, high EGFR copies conferred significantly favorable disease-free survival (HR=0.57, 95% CI 0.36-0.90, Wald's p=0.017) and high CEN7 copies favorable overall survival (HR=0.49, 95% CI=0.29-0.83, Wald's p=0.008). Patients with EGFR-/p53+ and EGFR+/p53- tumors had significantly higher risk for relapse than those with EGFR-/p53- and EGFR+/p53+ tumors (HR=1.73, 95% CI=1.12-2.67, Wald's p=0.013). EGFR gene amplification and mutations are rare in TNBC, the latter of no apparent clinical relevance. Surrogate markers of EGFR-related chromosomal aberrations and combined EGFR/p53 IHC phenotypes appear to be associated with favorable prognosis in patients with operable TNBC receiving conventional adjuvant chemotherapy.Οι αλλαγές του υποδοχέα του επιδερμικού αυξητικού παράγοντα (EGFR) έχουν εμπλακεί στην παθογένεια του τριπλά αρνητικού καρκίνου του μαστού (ΤΑΚΜ) αλλά η επίπτωσή τους στην πρόγνωση και ως εκ τούτου, η δυνατότητα να αποτελέσουν στόχο φαρμάκων, παραμένει διφορούμενη. Στην παρούσα μελέτη, διερευνήθηκαν οι αλλαγές του EGFR σε διαφορετικά μοριακά επίπεδα και εκτιμήθηκε η προγνωστική τους επίπτωση σε ασθενείς με εγχειρήσιμο ΤΑΚΜ οι οποίες θεραπεύτηκαν με συμπληρωματική χημειοθεραπεία που βασίστηκε στην ανθρακυκλίνη. Πιο αναλυτικά, εκτιμήθηκε η προγνωστική επίπτωση της κατάστασης του γονιδίου του EGFR με τη μέθοδο του φθορίζοντα in situ υβριδισμού (FISH), οι μεταλλάξεις κωδικοποίησης στο γονίδιο του EGFR με αλληλούχιση του γονιδίου χρησιμοποιώντας την τεχνολογία Sanger και την αλληλούχιση της νέας γενιάς (NGS), τα σχετικά επίπεδα του αγγελιοφόρου RNA (mRNA) του EGFR με τη μέθοδο της qPCR (άνω τεταρτημόριο) και η ανοσοϊστοχημική έκφραση της πρωτεΐνης του EGFR και της p53, σε 352 κεντρικά επιβεβαιωμένα καρκινώματα από ίσο αριθμό ασθενών με ΤΑΚΜ. Περίπου 53.5% των καρκινωμάτων εξέφραζαν την πρωτεΐνη EGFR, 59.3% την p53 και 35.9% και τις δυο πρωτεΐνες, ενώ 4.1% εμφάνιζε γονιδιακή ενίσχυση του EGFR και 4.4% έφερε μεταλλάξεις στο γονίδιο του. Οι μεταλλάξεις εντοπίζονταν εκτός της περιοχής του τμήματος της κινάσης που αποτελεί στόχο φαρμάκων και παρουσιάζονταν σε χαμηλές συχνότητες. Η ενίσχυση και οι μεταλλάξεις συνυπήρχαν σε μια μόνον περίπτωση ενός διαυγοκυτταρικού καρκινώματος του μαστού πλούσιου σε γλυκογόνο (glycogen-rich clear cell breast carcinoma). Τα αντίγραφα του EGFR και του CEN7 ήταν περισσότερα στους όγκους μεγαλύτερης ηλικίας ασθενών (p = 0.002 και p = 0.003, αντίστοιχα). Οι ασθενείς με όγκους που εμφάνιζαν ενίσχυση (n = 11) παρουσίαζαν εξαιρετικά καλή πρόγνωση (0 υποτροπές και θάνατοι). Από την πολυπαραγοντική ανάλυση διαπιστώθηκε ότι τα υψηλά αντίγραφα του EGFR προσέδιδαν σημαντικά καλύτερο διάστημα ελεύθερο νόσου (DFS) (HR = 0.57, 95% CI 0.36-0.90, Wald's p = 0.017) και τα υψηλά αντίγραφα του CEN7 σημαντικά ευνοϊκότερη συνολική επιβίωση (HR = 0.49, 95% CI=0.29-0.83, Wald's p = 0.008). Οι ασθενείς με EGFR- / p53+ και EGFR+ / p53- καρκινώματα παρουσίαζαν σημαντικά υψηλότερο κίνδυνο εμφάνισης υποτροπής από τις ασθενείς με EGFR- / p53- και EGFR+ / p53+ καρκινώματα (HR = 1.73, 95% CI=1.12-2.67, Wald's p = 0.013). Οι μεταλλάξεις και η ενίσχυση του γονιδίου του EGFR είναι σπάνιες στον ΤΑΚΜ, με τις πρώτες χωρίς εμφανή κλινική σημασία. Οι "υποκατάστατοι" δείκτες των χρωμοσωμικών αλλαγών που σχετίζονται με τον EGFR και ο συνδυασμός του ανοσοφαινότυπου EGFR / p53 φαίνεται να σχετίζονται με ευνοϊκότερη πρόγνωση στις ασθενείς με εγχειρήσιμο ΤΑΚΜ οι οποίες έλαβαν την καθιερωμένη συμπληρωματική χημειοθεραπεία

Positron emission tomography in breast cancer: 18F- FDG and other radiopharmaceuticals

Abstract Background Breast cancer heterogeneity reflects the complex biology of this disease. Breast cancer subtypes, as identified either by immunohistochemistry (IHC) or by gene expression analysis, present different molecular characteristics and prognosis. In this context, molecular imaging techniques providing functional information, contribute in evaluating response to treatment and long-term prognosis among different subtypes. Nuclear imaging diagnosis modalities play an important role for conducting research on cancer biology and developing new treatment approaches. Positron Emission Tomography (PET) is a radionuclide based imaging method that has the potential to locate the tumor, define its staging, and monitor its response to treatment. Results In the current study, we will review the utility of the most widely used molecular imaging technique, 18F-fluorodeoxyglucose (18F-FDG) PET, in order to determine the relationship between standardized uptake values (SUVs) and immunohistopathological factors, as well as to clarify whether PET is able to predict breast cancer phenotypes. Moreover, we will discuss the rising development of new radiopharmaceuticals in PET imaging, such as 18F-fluoro-17-estradiol (FES), 18F-fluoro-l-thymidine (FLT), 18F-fluoromisonidazole (FISO), and 89Zr-immuno-PET, which give more information about tumor characteristics. Conclusions In order to improve clinical decision making, enabling hereafter more successful individualized therapies, it is imperative to combine PET radiopharmaceuticals and imaging techniques of critical biologic and pathologic phenomena, including ER, PR and HER2 expression, angiogenesis, hypoxia, apoptosis and metabolic changes in the microenviroment of breast tumors

The evolving role of PARP inhibitors in advanced ovarian cancer

The field of ovarian cancer has been revolutionized with the use of poly (ADP-ribose) polymerase (PARP) inhibitors, which present greater inhibition effect in epithelial subtype due to high rates of homologous recombination deficiency. PARP inhibition exploits this cancer pitfall by disrupting DNA repair, leading to genomic instability and apoptosis. Three PARP inhibitors (olaparib, niraparib, and rucaparib) are now approved for use in women with epithelial ovarian cancer, while others are under development. Among women with BRCA1/2 mutations, maintenance PARP therapy has led to a nearly fourfold prolongation of PFS, while those without BRCA1/2 mutations experience an approximately twofold increase in PFS. Differences in trial design, patient selection and primary analysis population affect the conclusions on PARP inhibitors. Limited OS data have been published and there is also limited experience regarding long-term safety. With regard to toxicity profile, there are no differences in serious adverse events between the experimental and control groups. However, combining adverse event data from maintenance phases, a trend towards more events in the experimental group, compared with controls, has been shown. The mechanisms of PARP-inhibitor resistance include restoration of HR through reversion mutations in HR genes, leading to resumed HR function. Other mechanisms that sustain sufficient DNA repair are discussed as well. PARP inhibitors play a pivotal role in the management of ovarian cancer, affecting the future treatment choices. Defining exactly which patients will benefit from them is a challenge and the need for HRD testing to define ‘BRCA-ness’ will add additional costs to treatment

Synchronous colorectal adenocarcinoma and gastrointestinal stromal tumor in Meckel's diverticulum; an unusual association

Abstract Background Coexistence of gastrointestinal stromal tumor with synchronous or metachronous colorectal cancer represents a phenomenon with increasing number of relative reports in the last 5 years. Synchronous occurence of GISTs with other gastrointestinal tumors of different histogenesis presents a special interest. We herein report a case of GIST in Meckel's diverticulum synchronous with colorectal adenocarcinoma. Case presentation A 69 year old man, presented with abdominal distension and anal bleeding on defecation. Colonoscopy revealed colorectal cancer and a low anterior resection was performed, during which a tumor in Meckel's diverticulum was discovered. Histologic examination revealed GIST in Meckel's diverticulum and a rectosigmoid adenocarcinoma. Conclusion Whenever GIST is encountered, the surgeon should be alert to recognize a possible coexistent tumor with different histological origin. Correct diagnosis of synchronous tumors of different origin is the cornerstone of treatment.</p