Objective: Early cardiac structural and functional changes after chemotherapy are significant challenges when treating cancer patients. The aim of this study is the early detection of sub-clinical myocardial systolic depressed functions by echocartography among patients receiving anthracyclines (postoperative chemotherapy).Methods: Early picking up subclinical left ventricular systolic dysfunction by echocardiography (TTE) among patients who had been treated with anthracycline chemotherapy 18 and 3 months before. The study included eighty patients. We reported measurements of left ventricular ejection fractions (LVEF), fractional shortening (FS), mitral annular plane systolic excursion (MAPSE) and global longitudinal strain (GLS). Pre-chemotherapy 3, 6 and 18 months after complete doses of anthracyclines were mearsured.Results: This current prospective cohort study included 80 patients: 8 men (10%), 72 women (90%), with a mean age of 51.95 ± 13.69 years. Number of cycles ranged between 4 and 6 cycles of one of the anthracyclines. Mean heart rate was 76 beats/ minute, mean systolic blood pressure was 118, and mean diastolic blood pressure was 77.5 mmHg. The mean baseline FS was 32.40% ± 5.11%, which significantly decreased to 29.45% ± 5.78% and 26.75% ± 6.85% after 3 and 18 months, respectively. Mean three-dimensional echocardiography measures ejection fraction (3D-EF): Baseline was 61.08% ± 3.62% which was significantly depressed to 58.30% ± 5.54% after 3 months. The mean baseline MAPSE was 13.35 ± 1.35 mm, but it was reduced to 12.69 ± 1.92 mm and 12.60 ± 2.46 mm after 3 and 6 months, respectively. Mean baseline GLS was –17.62 ± 1.32% but reduced to –16.54 ± 2.42%, –15.35 ± 2.64% after 3 and 6 months respectively. By univariate analysis, significant parameters that showed abnormal outcome after 18 months were: gender, ejection fraction (EF), end-diastolic volume of the left ventricle (EDV), end-systolic volume of the left ventricle (ESV), 3D-EF (%), but by multivariate analysis, only EF (%) was significantly correlated with the outcome.Conclusions: Evaluation of myocardial deformation and functional capacity improved early sub-clinical diagnosis of chemotherapyinduced cardiac toxicity. GLS and MAPSE are much more sensitive as predictors for early deterioration of left ventricular functions.
Hypoxia, a characteristic of the tumor microenvironment caused by abnormal blood vessels and rapid cellular growth, enhances tumor aggressiveness and leads to resistance against conventional therapies. Unlike normal cells, hypoxic tumor cells activate adaptive survival mechanisms, prominently mediated by hypoxia-inducible factors (HIFs). HIF-1α is the most studied member of the HIF family, and the stability of its alpha subunit (HIF-1α) is a crucial determinant of the overall activity of the HIF-1α complex. HIF-1α stabilization under low oxygen occurs via oxygen-dependent and oxygen-independent pathways: in the oxygen-dependent pathway, HIf-1α is normally degraded by the von Hippel–Lindau protein (pVHL) when oxygen is present. Under hypoxia, hydroxylation is inhibited, allowing HIF-1α to accumulate. In the oxygen-independent pathway, growth factor signals activate cascades like PI3K/Akt/mTOR and MAPK/ERK, stabilizing HIF-1α regardless of oxygen levels. Stabilized HIF-1α translocates to the nucleus, promoting transcription of proangiogenic genes such as vascular endothelial growth factor (VEGF), thereby facilitating angiogenesis, tumor invasion, and progression. Dysregulation of these signaling pathways underpins the pathogenesis of many cancers, making HIF and its associated cascades critical targets for innovative cancer therapies. This review focuses on the pivotal role of HIF in tumor angiogenesis and emphasizes the therapeutic potential of targeting HIF signaling in cancer treatment.
Chimeric antigen receptor-T (CAR-T) therapy has been an effective treatment for leukemia and lymphoma. Unlike hematological cancers, solid tumors like prostate cancer utilize a dynamic microenvironment to evade the host immune defenses. We aimed to systematically review preclinical and clinical studies to evaluate how CAR-T therapies in prostate cancer modify the tumor microenvironment and influence patient outcomes. PubMed, Embase, and Scopus were screened for published, peer reviewed preclinical and clinical studies in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. The CAR-T antigen, tumor eradication rates, change in prostate–specific antigen (PSA) expression, and tumor tissue infiltration were compared across studies. Nineteen preclinical trials examining xenograft mice models and 3 phase I clinical trials with 32 total patients were included in this review. Tumor eradication rates in mice treated with armored CAR-T therapy were significantly greater than that of mice treated with unarmored CAR-T cells (p–value < .05). Ten of 32 clinical trial patients had a minimum of 30% PSA decline. Patients receiving higher doses of lymphocyte depletion (LD) therapy had higher peaks of CAR-T expansion, and those receiving LD therapy before CAR-T infusion experienced reduced dose–limiting toxicities. Immunohistochemistry staining of biopsied tumor tissue suggests CAR-T increased T cell proliferation markers and upregulated cytokines. CAR-T cells can modify the tumor microenvironment when armored or paired with LD therapy. Future studies should include expanded clinical investigations, particularly using armored CAR-T cells with LD regimens, to determine its safety and efficacy profiles in prostate cancer.
Objective: Glioblastoma (GBM) is the most common and malignant brain tumor, with a ~14.5 months median survival rate without disease-modifying curative treatment. After surgical resection, radiation, and adjuvant temozolomide (TMZ) chemotherapy is the first-line treatment of GBM with adverse effects, including bone marrow suppression, genotoxicity, and teratogenicity. Here, we report a synthetic quinazoline derivative that inhibits the growth of GBM cells as a new therapeutic approach.Methods: A potent quinazoline derivative (6-Pyridin-2-yl-5,6-dihydro-benzo[4,5] imidazo[1,2-c] quinazoline) was synthesized by one chemical step with 90% yield, followed by in vitro testing in GBM and neuroblastoma cells.Results: The in vitro studies showed that the quinazoline derivative is highly specific by decreasing GBM cell invasion while inducing cell death and inhibiting the cellular invasion in the three-dimensional Matrigel matrix. This compound is highly specific to GBM cell death compared with other cells. Synthetic quinazoline derivative is non-toxic to normal non-tumorigenic cells but toxic to cancerous cells. Under these experimental conditions, quinazoline derivatives caused inhibition of beta-1 integrin, which is an important cell adhesion molecule required for tumor cell invasion and metastasis, with extracellular matrix-mediated interactions. Furthermore, a synthetic quinazoline derivative decreases oncogenic PKC-epsilon activity in neuroblastoma cells.Conclusions: These studies suggest that a synthetic quinazoline derivative may treat GBM effectively alone or combined with other chemotherapeutic/immunotherapeutic agents.
Objective: In most countries of the world, breast cancer ranks first in the structure of oncological morbidity in women. The etiology of this disease remains largely unclear, although it is known that disturbances in the elemental homeostasis of somatic cells play a certain role in oncogenesis. The purpose of this study was to identify changes in the content of chemical elements during malignant transformation of breast tissue.Methods: For this purpose, we used the previously developed method of sample preparation, which allows determining the content of Al, Ba, Ca, Cu, Fe, K, Mg, Mn, Na, P, S, Si, Sr, Ti, and Zn in micro samples of breast tissue by using atomic emission spectrometry with inductively coupled plasma. Samples of cancerous and visually unchanged breast tissue adjacent to the tumor were examined using the developed technique.Results: A significantly higher content of all the chemical elements studied, except for Si, was found in cancerous tissue compared to their content in intact tissue.Conclusions: The detected multiple increase in the content of many minor and trace elements in cancer tissue compared to adjacent intact breast tissue can be used to develop new methods for in vitro and in vivo cancer diagnostics, in which the ratios of chemical elements levels in these tissues will act as tumor markers. Further, more in-depth study and understanding of the discovered phenomenon will allow the development of new methods for the prevention and treatment of breast cancer.
Objective: Exosome (Exo)-based therapies have attracted considerable interest due to their potential as carriers for therapeutic molecules and their capacity to elicit anti-tumor immune responses. The objective of this study was to engineer TC-1 tumor cell line-derived exosomes with GFP-tagged heat shock protein (Hsp) 27-human papillomavirus (HPV)16 E7 fusion protein and evaluation of cytokine secretion from antigen-presenting cells (APCs: macrophages and dendritic cells) exposed to the engineered exosomes in vitro.Methods: In this study, different in silico methods were employed to evaluate the Hsp27-E7 and Hsp27-E7-GFP fusion proteins as potential vaccine candidates. Regarding to the in silico data, the Hsp27-E7-GFP fusion gene was subcloned into pCDH lentiviral vector for production of lentivirions harboring the Hsp27-E7-GFP fusion protein in eukaryotic cells. Subsequently, the TC-1 tumor cells were transduced with these lentivirions to isolate the engineered exosomes (i.e., Exo-Hsp27-E7-GFP) using the ExoQuick-TCTM kit and their characterization using physicochemical methods. Finally, the secretion of key cytokines (IFN-γ, TNF-α, and IL-10) was evaluated through incubation of antigen-presenting cells (APCs) with the engineered Exo-Hsp27-E7-GFP using enzyme-linked immunosorbent assay (ELISA).Results: Our in silico data showed that both the Hsp27-E7 and Hsp27-E7-GFP constructs were soluble and non-allergenic, and exhibited strong interaction with TLR4. Indeed, the linkage of GFP did not affect the physicochemical properties, and interaction of Hsp27-E7 with the immune receptors. Moreover, western blot analysis confirmed the presence of Hsp27-E7-GFP fusion protein in the isolated exosomes. The Exo-Hsp27-E7-GFP could significantly enhance the secretion of TNF-α and IL-10 from APCs compared to Exo and Exo-GFP, as well.Conclusions: These engineered vesicles derived from tumor cells demonstrate the capacity to induce effective immunity, suggesting their potential as a promising strategy in the development of cell-free vaccine candidates.
Objective: Hepatocellular carcinoma (HCC) incidence has increased dramatically over the previous two decades and is anticipated to rise further in some countries, notably the United States, by 2030. HCC is most widespread in Asia and Africa, where hepatitis B and C are ubiquitous and lead to the development of chronic liver disease and, finally, HCC. In this study, we examined changes in the characteristics and prognosis of HCC patients, as well as the risk of developing HCC after direct-acting antiviral (DAA) medication.Methods: The study enrolled all individuals who attended the Clinical Oncology and Nuclear Medicine Department, Suez Canal University Hospital, Ismailia, Egypt, with a proven diagnosis of HCC in the period between January 2020 and December 2021. HCC is diagnosed based on radiographic appearance (arterial enhancement phase and delayed washout phase) or compatible histology.Results: This retrospective cohort included 254 HCC patients, separated into three groups. Kaplan-Meier curves with log-rank analysis revealed that hepatitis C virus (HCV) treatment therapy considerably reduced the time to HCC development following hepatitis diagnosis (p < .001). HCV therapy had a substantial impact on progression-free survival and overall survival in HCC patients (p < .001).Conclusions: The emergence of DAA medication has greatly altered the management of HCV patients in the context of HCC. DAAs have been shown to be both safe and beneficial in these individuals, particularly in terms of lowering the risk of hepatic decompensation. DAAs have been reported to enhance overall survival in patients with cirrhotic HCV-related HCC, most likely due to decreased hepatic decompensation.
Objective: In many countries, including Russia, breast cancer ranks first in the incidence of cancers in women. The etiology of this disease remains largely unclear, but there is evidence indicating that disturbances in the somatic homeostasis of trace elements may be involved in the process of oncogenesis. Therefore, this study was aimed at identifying changes in the content of trace elements during malignant transformation of breast tissue.Methods: For this purpose, an effective method of small sample analysis by means of inductively coupled plasma mass spectrometry was developed. The method makes it possible to determine the content of 35 trace elements in microsamples (with mass ≥ 10 mg) of breast tissue obtained by puncture biopsy. With the help of this technique, the samples of cancerous (n = 43) and normal (n = 38) breast tissue were studied.Results: In malignant breast tissue, the content of Al, As, B, Cd, Co, Cs, Cu, Mg, Mn, Mo, Ni, Rb, Se, Sr, Ti, Tl, U, V, Zn, and Zr was higher, while the content of Ge, Pb, Sb and Th was lower than in healthy gland tissue. All the identified differences were statistically significant.Conclusions: The significant disruption of somatic homeostasis of trace elements resulting from malignant transformation of breast tissue has been described, but its cause has not been determined, so additional research is required. Further the method we employ, which we have developed and described here, requires tissue samples weighing only a few milligrams, so it is possible to use it with tissue obtained from puncture tissue biopsies.
The aryl hydrocarbon receptor (AhR) plays a crucial role in cellular responses to various environmental pollutants, including several known carcinogens. As a ligand-activated transcription factor, AhR activation modulates the expression of genes involved in critical cellular processes, including detoxification pathways, cell proliferation and differentiation, and immune system regulation. The AhR exhibits pleiotropic effects under normal physiological conditions, contributing to the development and function of various organ systems. AhR activity is important in angiogenesis, cardiomyocyte differentiation, oocyte maturation, oculomotor nerve formation, and hematopoietic stem cell maintenance. Additionally, AhR plays a role in regulating immune cell differentiation and function, maintaining the integrity of the intestinal epithelium and its associated immune system, and mediating UVB-induced DNA damage repair responses in the skin. It acts as a critical environmental sensor, mediating cellular responses to various exogenous ligands. Importantly, activation or inhibition of AhR affects distinct signaling pathways depending on the specific ligand and cellular context. Ligands for the AhR are divided into exogenous or endogenous and have agonistic or antagonistic activity. Recently, the AhR role was determined in cancer development. It can exert both tumor-promoting and tumor-suppressive effects depending on factors such as the specific ligand, cell type, and tissue microenvironment. Emerging evidence suggests that AhR may represent a promising target for immunotherapy and serve as a potential biomarker for cervical cancer. AhR interacts with apoptotic pathway, immune checkpoint system, steroid hormones, and immune cell regulation process in cervical cancer. Despite its potential significance, the precise role of AhR in cervical cancer development and progression is still unknown. In this review, we describe significant roles of AhR in gynecological cancers; e.g., in cervical cancer.
Pancreatic cancer is a significant public health concern, with increasing incidence rates and limited treatment options. Recent studies have highlighted the role of the human microbiome, particularly the gut microbiota, in the development and progression of this disease. Microbial dysbiosis, characterized by alterations in the composition and function of the gut microbiota, has been implicated in pancreatic carcinogenesis through mechanisms involving chronic inflammation, immune dysregulation, and metabolic disturbances. Researchers have identified specific microbial signatures associated with pancreatic cancer, offering potential biomarkers for early detection and prognostication. By leveraging advanced sequencing and bioinformatics tools, scientists have delineated differences in the gut microbiota between pancreatic cancer patients and healthy individuals, providing insights into disease pathogenesis and potential diagnostic strategies. Moreover, the microbiome holds promise as a therapeutic target in pancreatic cancer treatment. Interventions aimed at modulating the microbiome, such as probiotics, prebiotics, and fecal microbiota transplantation, have demonstrated potential in enhancing the efficacy of existing cancer therapies, including chemotherapy and immunotherapy. These approaches can influence immune responses, alter tumor microenvironments, and sensitize tumors to treatment, offering new avenues for improving patient outcomes and overcoming therapeutic resistance. Overall, understanding the complex interplay between the microbiome and pancreatic cancer is crucial for advancing our knowledge of disease mechanisms and identifying innovative therapeutic strategies. Here we report phylogenetic analysis of the 16S rDNA microbial sequences of the pancreatic cancer mice microbiome and corresponding age matched healthy mice microbiome. We successfully identified differentially abundant microbiota in pancreatic cancer.
Background: Ventricular tachycardia (VT) is a potentially life-threatening arrhythmia which remains a major contributor to cardiac morbidity and mortality worldwide. Recently the use of stereotactic radiation has demonstrated efficacy, although standardization of methodology is lacking and variations in technique exist. In this paper, we discuss our outcomes as well as the various options available and the proposed indications for each.Methods: 12-lead EKGs and device-obtained tracings were used to approximately localize the arrhythmogenic origin and to define the arrhythmic mechanism. When feasible, electrophysiology studies (EPS) with 3-D electroanatomic (EA) mapping during which a 3-D electroanatomic substrate map was created to delineate cardiac structures, identify areas of low voltage scar and confirm arrhythmic circuits. A 4-D cardiac magnetic resonance imaging (cMRI) or cardiac computed tomography (cCT) was performed to delineate cardiac geometry and structures. The Stereotactic arrhythmia radioablation (STAR) treatment plans delivered a total dose of 25 Gy in a single treatment fraction covering the entire arrhythmogenic target.Results: Six of the nine patients showed a reduction in VT events at 6 weeks post STAR. One patient underwent cardiac transplantation two weeks following STAR. Excluding this patient from the analysis, all but one patient had a dramatic diminution in VT events (to 0) at 6 months post-procedure, including both patients with an LVAD. Six of the nine patients survived at least 4 months post procedure event free and 6 patients survive to date. The lone patient who did not respond died 13 months post procedure, however he had no further defibrillator discharges. Another patient died two months post procedure from uncontrolled multiple myeloma. One patient developed an asymptomatic pleural effusion, but no serious STAR-induced postoperative complications occurred.Conclusions: STAR appears to be an effective therapy for refractory ventricular tachycardia, although long term data are still developing. Additional clinical trials and techniques are in development and STAR programs should be encouraged for additional well-equipped centers with experienced multidisciplinary clinicians.
Background: Recently, peripheral blood inflammatory biomarkers such as neutrophil-lymphocyte ratio (NLR) have been identified for their prognostic role in many types of cancers. Elevated NLR was associated with poor prognosis & increased mortality rates. This study assessed the predictive value of pretreatment NLR in non-metastatic breast cancer.Objective: To assess the role of pretreatment NLR in non-metastatic breast cancer and their effect on prognosis in terms of 5 years disease-free survival and overall survival.Methods: This retrospective cross-sectional study was conducted in Suez Canal University Hospitals in Ismailia, Egypt. 105 patients with pathologically proven breast cancer were recruited from January 2015 to December 2016. Patients & tumor characteristics were collected from medical records. Five-year overall survival & disease-free survival were analyzed.Results: Mean patients’ ages were 47.82 ± 11.65. The age ranges were between 25 & 78 years. There was no statistical significance between patients with low & high pretreatment NLR in terms of patients’ characteristics & tumor variables. With the ROC curve, the cut-off points for NLR were 1.65 & 1.55 for DFS and OS, respectively. In terms of patients’ DFS & OS, no statistically significant difference was found between non-metastatic breast cancer patients with low & high NLR (plog-rank = .357 and .236, respectively). No statistically significant difference was found between patients with low & high pretreatment NLR in the period of five years OS & DFS.Conclusions: Pretreatment NLR is an inflammatory biomarker that might affect patient prognosis and survival. Further research is required to confirm the prognostic significance.
Background: One of the most common cancers all over the world is Head and Neck cancers, with higher mortality rates among developing countries. Squamous cell carcinomas (SCCs) represent more than 90%. SCCs arise commonly from the mucosal lining of the upper aerodigestive tract.Objective: To Compare between Concurrent Chemoradiation following Neoadjuvant Chemotherapy versus Concurrent Chemoradiation alone in Locally Advanced Larynx & Nasopharynx Cancer (stage III or IVA,B) regarding efficacy, toxicity, progression free survival, disease free survival and organ preservation (in laryngeal cancer).Methods: A Retrospective study was conducted to Compare between Concurrent Chemoradiation following Neoadjuvant Chemotherapy versus Concurrent Chemoradiation alone in Locally Advanced Larynx & Nasopharynx Cancer (stage III or IVA,B) in the Clinical Oncology Department, Suez Canal University Hospital, Ismailia, Egypt between 1/2017 & 12/2018, with follow up 2 years (from 1/2019 to 12/2020).Results: Results of our study show a statistic significance in progression free survival in Concurrent chemoradiation following neoadjuvant chemotherapy compared with concurrent chemoradiation alone.Conclusions: Neoadjuvant chemotherapy by TPF or PF is a wise choice in the locally advanced squamous cell carcinoma of the nasopharynx and larynx (non-metastatic cases). Better results were detected in radiological assessment post radiation therapy in laryngeal cancer cases and progression free survival in both treatment groups.
This small prospective pilot study of 17 patients evaluated the efficacy of PECS block in preventing both immediate and long term post-operative pain after mastectomy. It describes the technique for performing a PECS blockade and demonstrated very low pain scores in both the peri-operative period and at 6 months.
Background: Ameloblastoma is a common benign aggressive odontogenic tumor with a tendency for high recurrence rate. Ameloblastic Carcinoma is the malignant counterpart of Ameloblastoma. However, they are usually difficult to be distinguished from one another. Therefore, using Immunohistochemical markers might be beneficial for diagnosing them accurately.Objective: Evaluation of SOX2 and GPC3 expressions as well as evaluating their roles in the tumorigenesis and the biological behavior of Ameloblastoma and Ameloblastic Carcinoma.Methods: Tissue samples are composed of 34 archived histopathologically confirmed cases of (19 Conventional Ameloblastomas, and 15 Ameloblatic Carcinomas). Sections were subjected to Immunohistochemical staining according to a standard protocol by applying antibodies to SOX2, and GPC3.Results: SOX2 and GPC3 expressions in recurrent Ameloblastoma were significantly higher than non- recurrent cases. Ameloblastic Carcinoma showed the highest immune-reactivity to SOX2 and GPC3 compared to the Conventional Ameloblastoma. Desmoplastic Ameloblastoma showed the highest scores of SOX2 and GPC3 compared to the other subtypes.Conclusions: SOX2 and GPC3 can be used as a panel for diagnosing the aggressive and the malignant odontogenic tumors accurately. Desmoplastic Ameloblastoma behaves more aggressively than other Conventional Ameloblastoma subtypes.
Background and aim: Tumor-stroma ratio (TSR) is the proportion of tumor cells to surrounding stroma. TSR was reported in many carcinomas as an independent strong, prognostic parameter, and could be applied routinely in diagnostic pathology. This study aimed to clarify the association between prognosis and TSR of oral squamous cell carcinoma (OSCC) and to evaluate its correlations with the clinical stages and histological grades of the studied cases.Materials and Methods: One hundred thirty-nine anti-vimentin stained slides were digitized and analyzed for TSR scoring. TSR was classified as stroma rich (< 50%) and stroma poor (≥ 50%). Correlations between clinicopathological variables and TSR were assessed.Results: Microscopical examination of the studied cases revealed that 67 (48.2%) were stroma-rich and 72 (51.8%) were stroma-poor. Overall findings explained that stroma rich group had larger size, higher clinical stage, higher recurrence rate with a low disease free survival (DFS) and worse overall survival (OS) than the stroma poor.Conclusion: The clinical outcomes of stroma rich OSCC is poor as it is associated with decreased OS and DFS of patients. Hence, TSR may be used as a prognostic independent factor for OSCC and thus, TSR can be considered as an important, low cost and valuable parameter that could be used in addition to the TNM status. Moreover, TSR might be helpful for the judgment of prognosis and for the determination of OSCC high-risk patients to treat them individually.
We are presenting an evaluation of Allele Specific Multiplex Sequencing (ASMS) to detect two EGFR somatic mutations (L858R, T790M). Late stage lung cancer samples were tested for both EGFR mutations and were compared to either pyrosequencing or TruSeq. The analytical lower limit of detection (LLOD) for the ASMS-L858R assay was found to be 36 copies, and 72 copies for the ASMS-T790M assay. The forty-one FFPE samples that were tested for T790M showed 100% concordance with the respective comparative method. The forty-five FFPE samples tested previously by Truseq for L858R showed 100% concordance with ASMS. Out of the twenty L858R samples previously tested by pyrosequencing, there was 95% concordance with ASMS. Additionally, twenty-one normal blood samples were tested by ASMS were found to be negative for L858R and T790M. In conclusion, the detection of L858R and T790M by ASMS are in acceptable concordance with both pyrosequencing and TruSeq in detecting EGFR mutations from late stage lung cancer. Further, ASMS was able to detect EGFR (L858R) with 10 picograms (3 copies gDNA) of FFPE extracted DNA, and hence could be used to detect mutations from samples carrying low copy numbers.
Plexiform neurofibromatosis is an autosomal dominant and is frequently seen at birth. Surgical excision is asociate to facial nerve damage and profussal bleeding. Sequential multi-layered hemostatic sutures is a technique frequently used in our practice for Arterio-veous malfromations (AVM). 15 patiets with facial plexiform neurofibroma were treated from 2004 to 2020 with surgical excision, in all patients the hemifacial area was affected. Although preoperative embolization is well known as a safe technique to reduce intraoperative bleeding, low rates of serious complications were reported as stroke, ischemic attack and necrosis. The multi-layered hemostatic sutures permit to remove piecewise the tumor avoiding dramatically bleeding in all our procedures, and is based on vessel collapse after mechanical ligation. The sequential multi-layer suture and the retrograde disection of the facial nerve in our practice has decresed the average of iatrogenic damage of nerve, and massive bleeding during the excision of the plexiform neurofibroma.
Objective: The current study was carried out to assess the prognostic value of androgen receptor expression in urothelial carcinoma of the bladder and correlate it to the disease outcome.Methods: Histologically confirmed cases of bladder urothelial carcinoma were studied. Clinical, pathological, and radiological data were collected. Paraffin embedded tissue sections were submitted for hematoxylin and eosin staining, as well as immunohistochemical staining for androgen receptor in tumor cells.Results: Nuclear androgen receptor expression was positive in 75% of the studied histopathological specimens. Additionally, a significant positive association between androgen receptor expression and tumor grade, muscle invasion & tumor size were noticed.Conclusions: There is a significant association between large tumor size, high grade, deep invasion, and expression of Androgen receptor in urothelial bladder carcinoma. Antiandrogen could be an effective chemo preventive or therapeutic approach in treatment of urothelial bladder carcinoma.
Background: Renal cell carcinoma is a rare tumor and till recently few treatment options were available. It is poorly understood why people develop RCC since only a few etiologic factors have been clinically identified as risk factors for RCC.Purpose: To analyze our experience at Ain Shams University Clinical Oncology department in Egypt with patients presenting with advanced renal cell carcinoma to provide a correlations between clinic-pathological factors, treatment and survival outcomes.Methodology: Retrospective review of the data of 54 patients who were diagnosed as RCC and presented to Ain Shams University Clinical Oncology department in Egypt from 1 May 2013 till 1 May 2015. Descriptive and clinic-pathological data were described using simple and relative frequencies. Survival outcome for the patients will be described using Kaplan Meier curves stratified according to morphology, age group and treatment received.Results: The sample included 54 patients (53.7% were males) of whom 14.3% were less than 40 years and 3.7% were elderly (≥ 70 years old). The median age was 55.5 years (SD ± 13.6 , range 19-71). Median PFS was 6.5 months (SD ± 12.3846 Range 43) while the median OS was 13 months (SD ± 12.161 Range 46). PFS in patients aged below 55.5 years was 9 months (95% CI=6.509-11.491) compared to 4 months (95% CI=2.704-5.296) in older patients (p = .004). PFS in patients who achieved PR after sunitinb was 17 months (95% CI=6.916-27.084) compared to 5 months (95% CI=3.699-6.301) in patients who didn’t achieved PR (p < .001). OS in patients aged below 55.5 years was 15 months (95% CI=9.131-20.869) compared to 11 months (95% CI=8.947-13.053) in older patients (p = .012). Favorable pathology status was associated with prolonged OS of 14 months (95% CI= 9.403-18.597) versus 11 months (95% CI=8.363-13.637) for unfavourable pathology status (p = .11). Low grades histopathogy was associated with prolonged OS of 44 months (95% CI= 38.456-49.544) versus 12 months (95% CI=10.077-13.923) for higher grades (p = < .001).Conclusion: Multivariate analyses supported a conclusion that younger age was an independent prognostic factor for survival along with other known risk factors such as tumor grade and pathology status.
