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  • ISSN: 2373-938X
    Early Online
    Volume 8, Issue 1
    Research Article
    KM Monirul Islam*, Alicia Stevens, and Apar Kishor Ganti
    Background: Small cell lung cancer (SCLC) generally has poor outcomes. The past thirty years have seen some improvement in management options for these patients, but their impact for the general population is unclear.
    Objective: The present study analyzed trends in the diagnosis and survival of SCLC patients between 1988 and 2015.
    Method: The Surveillance, Epidemiology, and End Result (SEER) registry was used to identify SCLC cases from 1988 to 2015. Patients were classified as having either limited stage (LS) or extensive stage (ES) disease. Cox regressions were used to compare overall survival (OS).
    Results: We analyzed 98,281 SCLC patients. Males were diagnosed more ES-SCLC with worse OS compared to females (HR: 1.14 [CI 1.11-1.16]). Although younger patients had higher proportion of ES-SCLC diagnosis, the older patients had worse OS for both stages (LS-SCLC: HR 1.36 [CI 1.32-1.40]; ES-SCLC: HR: 1.34 [CI 1.31-1.36]). Among LS-SCLC, the Blacks had worse OS compared to whites (LS-SCLC: HR 1.06 [CI 1.02-1.10]) and no differences in OS in ES-SCLC among races. Compared to the reference period 1988-1992, patients diagnosed with ES-SCLC during the later periods had improved OS: 1998-2002 (HR: 0.97 [CI, 0.94-1.00]), 2003- 2007 (HR: 0.92 [CI 0.90-0.95]), 2008-2012 (HR: 0.91 [CI 0.88- 0.94]), and 2013-2015 (HR: 0.91 [CI 0.88- 0.94]).
    Conclusion: Females, whites, and younger patients with SCLC had better OS compared to males, blacks, and older patients. The results show increase in OS of SCLC patients over time, particularly for those with LS-SCLC.
    Arnold J Levine*
    Tissue-specific stem cells are the target for selected mutations in oncogenes or tumor suppressor genes that enhance the fitness of these cells, resulting in a self-limited clonal expansion and eventual cancer development. The initial or truncal mutations in the stem cell select for subsequent mutations that enhance their fitness, producing a reproducible order of mutations, selected for in each tissue type, during cancer development. Mutations in stem cells occur randomly, but the selection for increased fitness, occurs non-randomly, conferring a functional order on the selection of mutations. Tissue-specific stem cells are units of natural selection for somatic stem cells throughout life. This is why inherited cancer-causing mutations, which, by definition, are initial or truncal mutations, are observed to cause cancers with limited tissue specificities, even though the mutations are present in stem cells for all tissue types.
    In future studies, we need to understand why the same signal transduction pathways function differently in different tissue-specific stem cells. We also need to understand the truncal mutations for each cancer type, so as to eradicate the stem cell clones for that cancer before they produce a malignant tumor. To accomplish these objectives, we need to carry out new kinds of clinical trials with drugs that target mutations in tissue-specific stem cells.
    Short Note
    Osman Demirhan*
    Every living species has a unique set of chromosomes that carry the necessary and sufficient genetic information to survive and reproduce. In order for living organisms to reproduce, it is very important that they correctly transfer their genetic information to new generations of cells. Here, defects in DNA replication, defects in cell cycle progression and control points, repair of DNA damage, correct and balanced separation of chromosomes are important. An error in any of these genetic pathways can lead to cell death or the formation of cells with altered genetic information. Since this situation changes the expression of genetic information significantly, it causes the development of pathological defects in the embryo or organism. The numerical chromosome abnormalities (NCAs) occurring in the organism are defined as aneuploidy. Cancer-related genetic events; it is unknown how activation of oncogenes and inactivation of tumor suppressors occurs with genes on the X chromosome. The molecular basis for the oncogenic effects of doubling the copy number of the genes that are affected is also unclear. But, the X-chromosome aneusomy is thought to have a possible role in neoplastic transformation. The X-chromosome monosomy provides a unique genetic gain for the expression of common cancer-causing genetic events. In this review, we explain the unique features of X chromosome with the features of cancer biology.
    Case Report
    Minna Kankuri-Tammilehto*
    Today we are increasingly interested in finding out the hereditary variants of moderate risk from a cancer patient. Multigene next generation sequencing (NGS) panel technology, massive parallel sequencing, can efficiently and economically analyze genes in 3 to 6 weeks. There are agreed criteria based on which to suspect hereditary breast cancer and thus to make a referral to clinical genetic unit. The topic research subject is to investigate the cancer risk associated with moderate risk genes. Appropriate follow-up recommendations for persons with moderate genetic susceptibility pathogenic variants to breast cancer are updated regularly as scientific research is published. This is a case report on two CHEK2 families in which pathogenic variant in CHEK2 gene does not alone explain the breast cancer risk of the patients. This is also a mini review of genetic susceptibility of CHEK2 moderate breast cancer gene.
    Review Article
    Minna Kankuri-Tammilehto*
    Multigene next generation sequencing (NGS) panel technology, massive parallel sequencing, can efficiently and economically analyze genes in 3 to 6 weeks. There are agreed criteria based on which to suspect hereditary ovarian and endometrial cancer and thus to make a referral to clinical genetic unit.
    The geneticist interprets the genetic results and the information from pedigree. When a person is diagnosed with pathogenic variant (mutation) with genetic susceptibility to ovarian and endometrial cancer, counseling is provided on the associated cancer risk and appropriate monitoring is organized. Healthy family members with mutation can participate in recommended surveillance. Identifying carriers allows treatment and follow-up to reduce the morbidity and mortality for cancer patients and their healthy relatives.
    This is a case report on gene test results in hereditary breast and ovarian cancer syndrome (HBOC) families who have ovarian cancer in southwestern Finland. And a review of genetic susceptibility to ovarian and endometrial cancer.
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