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  • ISSN: 2373-9436
    Volume 3, Issue 2
    Review Article
    Surajo Mohammed Aminu1, Sani Ibrahim2, Ahmed Adamu3, Yawale Iliyasu4, Mohammed Sani Shehu4, John Idoko4, Atara Ntekim5, Khalid Zahir Shah6 and Mohammed Faruk4*
    Abstract: Human Endogenous Retroviruses (HERVs) are remnants of ancient retroviral infections with similarities to exogenous retroviruses and make up 8% of the entire human genome. HERVs are found to play a role in carcinogenesis. We sought to analyze 37HERVs in relation to 16 types of cancers using phylogenetic analysis. HERVs nucleotide sequences were aligned and corrected manually. A neighbor-joining method was used to create a phylogenetic tree using CLUSTAL X2 version algorithm. Two thousand (2000) replications were employed for bootstrap probabilities in creating the tree. The results obtained were systematically analyzed as they relate to different types of cancer. The phylogenetic analysis shows three main branches of HERVs. The first main branch was made up of HERV-H, HER-F, HERV-S71-related, ERV9, MSRV, HERV-K1.1, HERV-E, HERV-R, HERV-I, RTLVH, HERV-S and HRES-1. The second main branch was composed of HERV-T, HERV-P, HERV-FRD, HERV-KHTDV, and HERV-W. The third main branch contains majorly HERV-Ks family, HERV-L, HERV-P-T47D and XMRV. The HERV-Ks family is the most homologous among all the HERVs and also ubiquitous in terms of cancer tissues expression. The youngest sub-class of the HERV-Ks - HERV-K 133, and HERV-KHML 1.1, together with the widely debated XMRV were nested in the same group and present about 60% similarity. HERV-F and HERV-H present 70% similarity. HERV-S-71-Related, ERV9 and MSRV showed 100% similarity. Testing for HERVs, which phylogenetically present high sequence homology with each other, may help further research in the use of HERVs as an agent of immunotherapeutic target in cancer management.
    Ghosal, Gargi and Jason T. Yustein*
    Abstract: Chromosomal translocation of the EWSR1 gene with the members of ETS gene family of transcription factors results in the generation of a chimeric transcription factor that underlies the hallmark signature of Ewing sarcoma family of tumors (EFTs). The most predominant translocation and in-frame gene fusion EWS-FLI1, occurs between the N-terminal trans-activating domain of EWS and the C-terminal DNA binding domain of FLI1 in Ewing Sarcoma. EWS-FLI1 has been extensively characterized as a transcriptional regulator. However, additional roles of EWS-FLI1 in DNA damage response (DDR), cell-cycle checkpoint control and alternative splicing is only being uncovered now. This review article will discuss the functions of EWS and EWS-FLI1 in genotoxic stress and its potential implications in Ewing Sarcoma oncogenesis and targeted therapy.
    Case Report
    Benny Johnson* and Robert Johnson
    Abstract: Hemophagocytic Lymphohistiocytosis (HLH) is a clinical syndrome that develops due to the unregulated activation of the inflammatory system and is considered when a patient presents with a constellation of symptoms and objective findings consisting of fevers, splenomegaly, hepatomegaly, cytopenias, hepatitis, hypertriglyceridemia and/or hypofibrinogenemia, hyperferritinemia, biopsies of the bone marrow, spleen or lymph node demonstrating hemophagocytosis, and elevated soluble CD25 receptor levels. This clinical diagnosis requires a high index of suspicion as well as prompt initiation of therapy. HLH can be classified as primary or secondary. Primary HLH can be categorized into familial HLH due to specific gene mutations or hereditary immune deficiencies. Secondary HLH is often reactive due to malignancy, infection, autoimmunity or suppression of the immune system. We report a case of a 57 year old African American female who presents with secondary HLH in the context of newly diagnosed acute leukemia, specifically Philadelphia positive, CD20 positive, B-ALL. This case highlights the importance of recognizing the rare association of secondary HLH as a presenting feature in a patient with newly diagnosed acute leukemia and further reiterates the need to immediately begin appropriate targeted therapy concurrently for HLH and the underlying malignancy.
    Jyothi Nagraj, Sudeshna Mukherjee and Rajdeep Chowdhury*
    Abstract: Cancer is intricately linked to our evolutionary history. The origin and progression of cancer can hence be better understood when viewed from an evolutionary perspective. In this review, we portray the fundamental fact that within the complex ecosystem of the human body, the cancerous cells also evolve. Just like any organism, they face diverse selective pressure to adapt to the tumor environment. There exists a competitive struggle that eliminates the unfit, leaving the well-adapted to thrive. Sequential acquisition of "driver mutations", chromosomal instability triggering macro-mutations and punctuated bursts of genetic changes can all hypothetically contribute to the origin and evolution of cancer. We further describe that like in any ecosystem, cancer evolution involves not just the cancerous cells but also its interaction with the environment. However, as cancer evolves, individual cells behave more like a uni-cellular organism focused on its own survival. We also discuss evidences where cancer has evolved through transmission between individuals. An evolutionary analogy can open up new vistas in the treatment of this dreadful disease.
    Short Communication
    Omar Ghallab1, Nahla AM Hamed1*, Sahar El Shafei2, Reham Abo Elwafa3 and Shaimaa Sherif2
    Abstract: We investigated the relation between MDR-1 gene single-nucleotide polymorphisms (SNPs) and treatment outcome in chronic myeloid leukemia (CML) patients.2 groups of patients were included: group 1 (resistant group) consists of 29 CML patients andresponsive group (controls, group 2)consists of 25CML patients of matched age and sex.For all patients, we measuredBCR-ABL transcriptspercent at diagnosis and 3 months thereafterand MDR-1 gene SNPs (C3435T and G2677T). All patients were followed up for 6 months We found statistically significant difference inthe frequency of C3435T genotype and combined C3435T and G2677T (CC&GG, CT> and TT&TT) between both groups as well as in the frequency of mutated type (CT> and TT&TT).So, these genotypes may helpin early identification of CML patients not responding optimally to therapy and in planning CML individualized therapy. Larger patient population study is still needed to confirm these findings.
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