International Journal of Cancer Management
Volume:15 Issue: 8, Aug 2022

Gestational trophoblastic disease (GTD) is a general term that includes several types of pathologically different diseases, which range from hydatidiform mole to choriocarcinoma. Early differentiation of these types is important to determine treatment strategy and prognosis.

Genetic markers such as TP53 and HER-2/neu expression are recently shown to have diagnostic and prognostic values. The aim of this study was to evaluate its significance.

We enrolled 62 patients diagnosed with GTD referred to Imam Hossein Hospital in Tehran, Iran between 2012 and 2017. Endometrial pathologic specimens were stained, using the immunohistochemistry (IHC) method for the expression of TP53 and HER-2/neu genes. Expression levels determined by IHC were compared between final pathologic diagnoses, using one-way ANOVA test (analysis of variances), which detects significant differences between the means of 3 or more independent groups.

Out of 62 participants, 32 and 24 cases were diagnosed as partial and complete hydatidiform mole, respectively. Four cases had invasive hydatidiform mole and only 2 cases were diagnosed as choriocarcinoma. Analysis using ANOVA demonstrated that expression levels of both TP53 and HER-2/neu genes are significantly higher among patients with invasive form and choriocarcinoma compared with non-invasive hydatidiform mole (P < 0.05 for both genes). The receiver operating characteristic (ROC) curve for each gene showed that more than 55% positive staining for the TP53 gene can differentiate non-invasive hydatidiform mole from invasive form and choriocarcinoma with 100% sensitivity, and 92.9% specificity.

TP53 expression might serve as a potential diagnostic aid to differentiate benign and malignant GTDs and a future target for adjusting treatment based on the expression levels.

The rate of childhood cancer death has dropped steadily over the past 50 years. The pediatric cancer risk has remained under investigation.

This study aims at investigating the associated factors with the survival of pediatric patients with retinoblastoma, sarcoma, brain tumor, and leukemia cancer.

The cohort study of 1879 children with retinoblastoma, sarcoma, brain tumor, and leukemia aged < 1, 1 - 5, 6 - 10, 11 - 15, and > 15 years in Mahak Hospital and Rehabilitation Complex from 2007 to 2016 were enrolled in the study. Median survival time was reported for each cancer. Parametric survival models including Gompertz, Weibull, lognormal, and log-logistic models were fitted. Then, the model with almost minimum Akaike information criterion (AIC) was chosen. The hazard ratio (HR) and the analysis were performed by R3.5.1.

Totally, 270 (14.37%) patients with Retinoblastoma, 667 (35.5%) with leukemia, 625 (33.26%) with a Brain tumor, and 317 (16.87%) with Sarcoma were included in this study; 815 (43.37%) patients were female. Gompertz’s model was chosen to fit the data due to the minimum AIC. The associated factors with the survival of childhood cancers were as follows: age < 1 year, parental relation, locoregional relapse and chemotherapy alone (HR: 7.63, 1.56, 4.61, 1.12) in leukemia, other nationalities, metastasis or metastasis and loco-regional relapse and chemotherapy alone (HR = 3.74, 5.75, 2.12) in retinoblastoma, loco-regional relapse and metastasis (HR = 2.40, 3.71) in brain tumor, other ages except for 5 - 10 years, parental relation, chemotherapy alone, and metastasis (HR = 33.3, 1.80, 3.57, 3.8) in sarcoma.

Age, parental familial relationships, combination therapy, and metastasis of primary cancer were the risk factors for survival of children with 4 common cancers of leukemia, retinoblastoma, brain tumors, and sarcoma, using the Gompertz model.

Endometrial cancer (EC) is known as the most common malignancy of the female reproductive system, suggested to be associated with hereditary nonpolyposis colorectal cancer (HNPCC) or Lynch syndrome (LS).

Therefore, the aim of the present study was to screen for LS in patients with EC using immunohistochemistry (IHC).

In this retrospective cross-sectional study, the patients with EC, referred to Qaem Hospital, Mashhad, Iran, from 2015 - 2019, were enrolled. Paraffin-embedded tissue blocks were then examined via IHC for the expression of four mismatch repair (MMR) proteins, including MLH1, MSH2, MSH6, andPMS2. The demographic and tumor-related data were also extracted from medical records and pathology reports. The data were consequently analyzed at the significance level of P < 0.05.

A total number of 100 patients with EC were evaluated using IHC, and 12 (12%) cases were found suspected. As well, no significant relationship was observed between LS and age, tumor site, tumor histology, tumor size, tumor grade, tumor-infiltrating lymphocytes (TILs), and a family/personal history of malignancies.

The prevalence of LS based on the IHC expression of the MMR proteins (MLH1, MSH2, MSH6, and PMS2) was 12% in the patients with EC. There was also no significant relationship between the cases suspected and the demographic and tumor-related data

Hepatocyte growth factor (HGF) protein regulates cell growth, motility, and morphogenesis in a variety of cells and tissues by binding to the HGF receptor. The rs5745687 SNPs in the introns of the HGF gene could affect the splicing and expression of HGF mRNA.

In this study, the genotype frequency of rs5745687 in breast cancer (BC) and gastric cancer (GC) (positive helicobacter) patients has been investigated and compared with the healthy controls in the Isfahan population.

Firstly, initial bioinformatics studies were done. Then, according to the results, bioinformatics High-Resolution Melt (HRM) and Real-Time PCR were recruited to determine genotypes rs5745678 for 432 participants in the case-control analysis (84 GC with 126 healthy control samples, as well as 111 BC cases with 111 normal controls). The conditional logistic regression model was used to measure odds ratios (OR) and 95% confidence intervals (CI) to produce these cancers based on genotype frequency.

The homozygote genotype of the mutant (G) allele of rs5745678 has a significant association with the lower risk of gastric cancer (P-value < 0.0001) and this allele can increase the risk of GC in a co-dominant model (OR: 5.541, P-value < 0.0001). Also, the rs5745678 SNP had a significant association with the clinicopathological features (age, smoking, H. Pylori infection) in GC patients.

The presence of a single G allele in rs5745678 heterozygote (AG/AA) and co-dominant (AG/AA+GG) models could significantly impact GC pathogenicity in different ways. There was no significant correlation between the rs5745678 polymorphism and BC (P-value: 0.671) in the studied sample size.

Among the primary bone tumors, osteosarcoma accounts for a malignant tumor with a high rate of progression and poor prognosis. Despite the achievement of combined therapy regimens in improving patients’ overall survival, patients with osteosarcoma confront the chemoresistance obstacle.

This study aimed at determining the expression pattern of autophagy and necroptosis pathways mediators in osteosarcoma tumors.

The expression level of autophagy main mediators such as autophagy-associated protein 5 (ATG5), Beclin 1 (BECN1), and microtubule-associated protein 1A/1B-light chain 3 (LC3), necroptosis biomarkers such as receptor-interacting protein kinases (RIPK1 and RIPK3), and mixed lineage kinase domain-like (MLKL) were evaluated in 80 bone tissues including 60 bone tumors (40 malignant tumors and 20 benign tumors) and 20 margin tissues, using real-time PCR. The correlations of gene expression levels with the patient’s clinical and pathological features were considered.

Based on our data, ATG5, BECN1 and LC3 expression were down-regulated in osteosarcoma tumors compared to margin tissues. Also, malignant osteosarcoma tumors showed a significant decrease in the expression level of RIPK1 and MLKL as necroptosis regulators, which revealed a correlation with tumor malignancy. In addition, the higher expression levels of BECN1, LC3, RIPK1, and MLKL were observed in tumor tissues of patients under the chemotherapy regimen, indicating the relevance of autophagy and necroptosis pathways with the patient’s response to therapy.

Reduction in the expression level of autophagy and necroptosis mediators in high-grade osteosarcoma tumors indicates the possible impact of these pathways on the rate of proliferation and growth of osteosarcoma tumor cells and can emphasize the importance of cell death alternative pathways for treatment when apoptosis machinery is mutated and cause chemoresistance.