Objective: To determine the role of the hormone hCG in pregnancy, choriocarcinoma and cancer cell growth and invasion. Methods: Third trimester placenta cytotrophoblast primary cultures, two choriocarcinoma cell lines, and one trophoblastic cancer and 5 non-trophoblastic cancer cell lines. Results: Hyperglycosylated hCG promotes growth and invasion of normal pregnancy, 2 of 2 choriocarcinoma cell lines and 6 of 6 cancer cell lines. The hormone hCG attenuates or blocks growth and invasion in normal pregnancy, 2 of 2 choriocarcinoma and 6 of 6 cancer cell lines. Discussion: Cancer cells seemingly have adopted the hCG/LH receptor system. All cancers may be treated with hormone hCG to block and attenuate cancer growth, invasion and progression.

The proposal that carcinogenesis results from the somatic inheritance of defective epigenetic transmission is consistent with the establishment of genetic instability and the generation of a clonally divergent population of cells expressing anomalous structural and functional characteristics. The majority of these uncoordinated properties would be expected to be deleterious, thus placing cancer cells at a proliferative disadvantage. To compensate for this the malignant phenotype requires a property that enables the deviant cells to survive proliferative competition. This question is explored using a competitive growth model based on viewing cell populations as existing in microenvironmental domains subject to a barrier to migration. The model demonstrates that the ability to penetrate this migratory barrier is sufficient to permit otherwise less competitive cells to proliferate and expand the anomalous population. The possible nature of the domain barrier is briefly discussed.

Local recurrence and lymphnode (LN) metastasis are the most significant risk factors for morbidity and mortality for oral squamous cell carcinoma (OSCC) patients. In the current study, we aimed to evaluate the clinical significance of SCCAg mRNA expression in OSCC patients having histopathologically negative lymphnodes (HNLNs) and pretherapeutic peripheral blood samples (PPBs.). SCCAg mRNA was evaluated in total N=123 samples using nested RT-PCR technique. SPSS statistical software was used and p value <0.05 was considered as significant. The analysis revealed that in HNLNs, the mean ? SE for SCCAg mRNA expression was 1794.98 ? 106.67 with a median of 1488.0 while in PPBS it was 2308.27 ? 196.10 with a median of 1985.0. The frequency of SCCAg mRNA in HNLNs and in PPBs was 27% (15/55) and 29% (8/28), respectively. SCCAg mRNA expression in HNLNs and in PPBs showed a significant positive correlation with tumor size and lymphatic permeation. Multivariate survival analysis for RFS demonstrated that only SCCAg mRNA expression in HNLNs (p=0.001) and PPBs (p=0.001) were the most significant independent prognostic factors. However, for OS, multivariate analysis showed that SCCAg mRNA of HNLNs emerged at step 2 after tumor size and for PPBs it remained as single most significant independent prognostic marker. Thus, SCCAg mRNA may represent a useful tool for more accurate staging, which could improve disease management and help to obtain maximal therapeutic benefit from adjuvant therapies. Hence, SCCAg mRNA transcript could serve as a useful independent predictor of disease relapse, suggesting an increased risk of silent metastasis.

Metastatic castration-resistant prostate cancer (mCRPC) remains a therapeutic challenge. As a result of advances in genomic sequencing technology, “next-generation sequencing” (NGS) is increasingly incorporated into clinical trials and routine oncology clinical practice. Molecular profiling of mCRPC can be a valuable way of defining molecular alterations that might contribute to optimal treatments while reduce risk of adverse effects. To effectively apply cutting edge research to daily patient care, oncologists must grasp the fundamentals of genomic oncology, molecular testing and interpretation. There is an urgent need for health professional education to allow implementation of these novel precision medicine tools.

Growing teratoma syndrome (GTS) is a rare disease occurring in patients with non-seminomatous germ cell tumors (NSGCT), which is characterized by enlarging masses in the presence of normal tumor markers either during or after completion of chemotherapy. The disease is chemo-resistant and radio-resistant and complete surgical removal offers the best chance of long-term survival. GTS was first described by Logothetis et al. in 1982, who designated criteria to diagnose this rare entity [1]. The fact that GTS is not common leads to delays in diagnosis and surgical intervention. This case report refers to a testicular growing teratoma with its first clinical manifestation being a gigantic forearm mass.

With the advent of next-generation sequencing technologies, tremendous progress has been made in the understanding of the genomic landscape of several tumor types. Clinicopathologically bladder carcinoma is classified into non-muscle invasive bladder cancer and muscle invasive bladder cancer. Patients are often diagnosed with bladder carcinoma at an advanced stage, owing to a lack of early clinical symptoms and effective biomarkers for early detection. Failure of chemoradiotherapy at an advanced stage usually results in a poor outcome. Currently, there are limited targeted therapies available for bladder carcinoma. Thus, there is an immediate need to identify alternative strategies and novel therapeutic targets for the treatment of bladder carcinoma. The genomic underpinnings of bladder carcinoma may lead to the better understanding of this disease and improved targeted therapy. A large number of genomic alterations including somatic mutations, copy number alterations and fusion genes were identified to be involved in the pathogenesis of bladder carcinoma. A high mutational burden was observed in bladder carcinoma as compared to other tumors. Recurrent somatic mutations in genes such as TP53, KMT2D, RB1, FGFR3, KDM6A, STAG2 and PIK3CA were identified. Multiple signaling pathways such as the cell cycle pathway, DNA repair pathway, chromatin remodeling and histone modifications were found to be altered. Most likely, targeting mutated genes of these altered pathways could provide opportunities for personalization of bladder carcinoma therapy. This review discusses the molecular alterations, altered identified genes and the molecular pathways involved in bladder carcinoma.

Vaginal malignant melanoma is a rare and aggressive neoplasm of the genital tract. It is associated with early dissemination and metastasis. It presents a diagnostic dilemma as it is often confused with squamous cell carcinoma of the vagina and/or cervix, hence, resulting in late diagnosis and poor prognosis. We present a case of malignant melanoma of vagina which was extensively metastatic at diagnosis. It was initially diagnosed after a frontal craniotomy done for a space-occupying lesion in the brain. Subsequently, multiple nodes were detected in axillary and inguinal regions. She was treated with palliative whole brain radiotherapy. Then, she received 6 cycles of adjuvant chemotherapy, paclitaxel and carboplatin. Her disease progression is stable and her KPS has improved with the treatment. Prompt detection of metastasis followed by adjuvant chemotherapy, radiotherapy and immunotherapy can control disease progression in metastatic disease.

Background: Pemetrexed is a newer antifolate drug that has multiple intracellular targets. Clinical trials of Pemetrexed in advanced nonsmall cell lung carcinoma (NSCLC) setting have demonstrated beneficial outcomes. This study evaluated the efficacy and safety of Pemetrexed and Cisplatin combination as first line in advanced stage NSCLC adenocarcinoma patients. Methods: This was a prospective study conducted on previously untreated 50 patients with NSCLC (adenocarcinoma) of stage III B and IV disease. Patients received Pemetrexed 500 mg/m2 and Cisplatin 75 mg/m2 on day 1 of every 21-day cycle for a total of 6 cycles. Tumor response was calculated after 3 cycles and 6 cycles as per RECIST criteria version 1.1. Toxicity and adverse events (AEs) were assessed as per Common Terminology Criteria for Adverse Events (CTCAE) version 3. Results: The tumor response rate after 6 cycles of chemotherapy was as follows: 12% (6) patients had complete response, 48% (24) had a partial response, and 22% (11) stable disease. The overall response rate was 60% and the clinical benefit rate was 82%. Out of total patients, hematological toxicity in the form grade 3/4 granulocytopenia was seen in 20 (40%) patients, followed grade 3/4 leukopenia 12 (24%), grade 3/4 anaemia in 5 (10%) and grade 3/4 thrombocytopenia in 5(10%). Whereas nonhematological toxicity was comparatively less in the form of grade 3 vomiting in 2 (4%) patients. Over all this combination was well tolerated. Conclusion: Pemetrexed and Cisplatin chemotherapy combination was found to be efficacious and was well tolerated in advanced NSCLC adenocarcinoma patients.

Background: Cancer patients have a high risk of new or recurrent venous thromboembolism. Thrombosis decrease 1 year life expectancy of malignant lymphoma patients. In the last 10 years, it has been continuosly developed a method to detect early venous thrombosis by combining Modified Wells (MW), D-dimer and Doppler ultrasonography level but only 25% are detected early. Objective: We analyzed the association between MW score and D-dimer level. Method: It is an analytic observational study of LNH and LH patients based on clinical and histopathological diagnosis who had never received chemotherapy. The subjects were 35 patients with malignant lymphoma consisting of 30 LNH patients and 5 LH patients. D-dimer was measured using immunochromatography method. Result: There was a positive linear relationship between MW score and D-dimer level with p=0.001 and r=0.462. However, there was no association in LH patients (p=0.215). Conclusion: There was a moderate positive correlation between MW scores and D-dimer levels in naive LNH patients.