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  • ISSN: 2373-9436
    Volume 6, Issue 3
    Review Article
    O'Shea J* and Vernimmen F
    Schwannomas being benign tumours of the nerve sheath are usually treated with surgery. For intracranial schwannomas, especially acoustic neuromas, the role of stereotactic radiotherapy is well established as a viable alternative. For other sites the role of stereotactic irradiation is less well established, however based on experience in the successful use of dose/fractionation schedules in the management of acoustic neuromas there may be merit in their application to extracranial sites when lesions are deemed irresectable. Given the carcinogenic nature of radiation, care must be applied, when treating benign conditions, where the ultimate goal is to maintain a normal life expectancy. This risk of a secondary malignancy is low and can be further reduced by the use of proton therapy which has a lower integral dose. The increasing number of proton therapy facilities worldwide should allow better access to this advantageous radiation modality.
    Luis Miguel Guamán-Ortiz*
    Cancer is known as a set of diseases that, when the prognosis is not favorable for the patients, it ends in death. Clinically three phases of cancer have been described: initiation, promotion and progression. In this context, the molecular involvement in these phases is described: first, the single or multiple mutations at DNA trigger cell transformation; the second step refers to the process of tumor growth, and the latter to the invasive process. Although these terms are well known, molecular processes following a specific order within each of these three phases are explained: mutagenesis, carcinogenesis, tumorigenesis, angiogenesis, and metastasis. Severe mutations commit a healthy cell to transformation, becoming therefore in a cancerous cell with altered metabolism and being able to proliferate unlimitedly to form a tumor mass. This tumor increases its size and stimulates the vascularization for nutrition. At the end of the process, individual cancerous cells escape towards new tissues, making it difficult their localization and compromising vital functions.
    Research Article
    Khedr R*, Emad A, Hamed AA, and Hafez HA
    Background: Survival in childhood acute lymphoblastic leukemia (ALL) has steadily improved with increasing attention to the importance of reducing infection-related mortality. This study investigates the frequency and mortality rates of treatment-related toxicity and its impact on the timely application of chemotherapy regimens during induction and consolidation therapy in pediatric patients with ALL.
    Procedure: This retrospective cohort study analyzed patients below the age of 18 years with ALL, receiving chemotherapy for remission induction and consolidation therapy. We evaluated the frequency of infectious complications and invasive fungal infection, treatment given and outcome. Treatment delay due to fungal infection was reported.
    Results: During the study period, 96 patients were reported. Infection was reported in 42 patients (43.7 %), 19 patients (19.8%) had probable fungal infection, 13 (13.5%) with documented bacterial sepsis, and 10 (10.4%) with soft tissue infections. The total deaths during induction and consolidation were 16 patients (16.70%) (All of them died during induction), the most common cause of death was sepsis (9.4%), followed by fungal infection (3.1%). The median duration of treatment delay during induction and consolidation therapy was 31 days in patients with invasive fungal infection compared to 8 days without IFI (P.<0.001).
    Conclusion: Infectious complications during induction therapy are still a major problem affecting the outcome of the childhood ALL. The high incidence and the mortality rate of fungal infections during ALL induction as well as their impact on chemotherapy schedule may call for the antifungal prophylaxis during this phase of treatment.
  • Current Issue Highlights
  • BRAT1 was originally identified as a BRCA1 interacting protein [1], however, subsequent studies showed that it also binds to ATM, DNA-PK, and SMC1,

    Mechanisms of detecting and repairing damaged DNA are conserved and controlled through the DNA damage response (DDR).

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