{"id":866,"date":"2018-08-31T10:08:25","date_gmt":"2018-08-31T14:08:25","guid":{"rendered":"https:\/\/www.bumc.bu.edu\/genetics\/?page_id=866"},"modified":"2019-12-16T14:29:49","modified_gmt":"2019-12-16T19:29:49","slug":"news-and-announcements-from-the-genetics-program","status":"publish","type":"page","link":"https:\/\/www.bumc.bu.edu\/genetics\/news-and-announcements-from-the-genetics-program\/","title":{"rendered":"News"},"content":{"rendered":"

August 2018<\/b><\/span><\/p>\n

Dr. Sam Thiagalingam receives Boston University Clinical and Translational Science Institute (BU-CTSI) Integrated Pilot Grant<\/b><\/span><\/a><\/p>\n

Colon cancer is the second leading cause of cancer deaths in non-smoking men and women, and because surgery has limited therapeutic role with metastatic colon cancer, chemotherapy is widely used as the first-line therapy. However, several studies have indicated that patients harboring SMAD4 mutations corresponding to chromosome 18q deletions that frequently occur during advanced stages of colon cancer exhibit resistance to chemotherapy. Dr. Thiagalingam has been awarded a BU-CTSI Integrated Pilot grant entitled “Sensitization of chemotherapy resistant metastatic colon cancer” to initiate the identification of molecular mediators that promote colon cancer metastasis and resistance to common chemotherapeutic agents correlating to the loss of function of SMAD4 for precision targeting to restore sensitivity to chemotherapy. In the long-term, this award will help Dr. Thiagalingam to generate critical preliminary data to tap into funds to undertake comprehensive understanding of resistance to chemotherapy in colon cancer.<\/span><\/p>\n

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July 2018<\/b><\/span><\/span><\/p>\n

Dr. Huiping Zhang receives BU CTSI grant to study the epigenetic mechanism of cocaine use disorders (CUDs)<\/span><\/strong><\/p>\n

Dr. Huiping Zhang receives BU CTSI grant to study the epigenetic mechanism of cocaine use disorders (CUDs). He and his collaborator Dr. Vidhya Kumaresan will investigate cocaine use\/withdrawal induced microRNA (one type of epigenetic markers) expression alterations in the brain’s reward circuit (e.g., the nucleus accumbens) using a translational rat model of incubated drug craving (i.e., extended access to cocaine with prolonged abstinence and consequent increased craving). It is expected that cocaine withdrawal responsive microRNAs (or their target genes) could be potential biomarkers for CUDs and novel therapeutic targets.”<\/p>\n

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May 2018<\/span><\/strong><\/p>\n

Shoumita Dasgupta Elected to Association of Professors of Human and Medical Genetics<\/strong><\/a><\/p>\n

Shoumita Dasgupta, PhD<\/a><\/span>,<\/strong> associate professor of medicine, was recently elected president-elect of the Association of Professors of Human and Medical Genetics (APHMG). Dr. Dasgupta, who also serves as assistant dean of admissions, will serve as president-elect from 2018-2020 and president from 2020-2022.<\/p>\n

The mission of the APHMG is to advance education in human and medical genetics among medical students, residents, lab directors and providers. During her time in office, Dasgupta\u00a0\u00a0 hopes to engage inter-professional communities in this mission. \u201cI also hope to further expand the scope of our work in helping to advocate for engaging genomic medicine curricula through projects bridging the National Human Genome Research Institute (NHGRI) <\/span>and the Association of American Medical Colleges,\u201d said Dr. Dasgupta.<\/p>\n

Dr. Dasgupta is the past chair of the Medical Genetics Course Directors Special Interest Group of the APHMG. In this position she directed national initiatives of significance for educators of medical genetics in North America. She is also an affiliate scientist of the American College of Medical Genetics, has implemented educational initiatives at the American Society of Human Genetics\u2019 2016 international meeting and serves on the National Institutes of Health\u2019s (NIH) Inter-Society Coordinating Committee for Practitioner Education in Genomics and the NHGRI\u2019s Genomic Literacy, Education and Engagement Initiative.<\/p>\n

The Association of Professors was incorporated in 1995 to promote human and medical genetics educational programs of human and medical genetics in North American medical and graduate schools.<\/p>\n

<\/span>January 2018<\/span><\/strong><\/span><\/p>\n

2018 Wing Tat Lee Awards<\/strong><\/p>\n

Xiaoling Zhang, MD, PhD, Assistant Professor of Medicine in Biomedical Genetics<\/strong> is one of the recipients of the 2018 Wing Tat Lee awards<\/strong>, funded to establish cooperative research programs between BUSM and Chinese universities (with a preference for Hong Kong).<\/p>\n

\"XiaolingDr Zhang <\/strong>will examine how disease severity in Alzheimer’s Disease (AD) correlates with retinal and brain neurodegeneration. She will work with Zhigang Fan, MD, PhD, Sun Yat-sen University, to identify gene biomarkers and imaging markers in patients with mild cognitive impairment and AD to improve early diagnosis of AD. Dr. Zhang received her MD from Hubei University of Chinese Medicine and her PhD from Boston University.<\/span><\/p>\n

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January 2016<\/span>
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Fighting the Darkness<\/a>
\n<\/span><\/strong>Study offers insight on genetics of age-related macular degeneration<\/em><\/span><\/span><\/p>\n

The disease can start with blurry or fuzzy vision, or with the weird sense that straight edges\u2014like doorframes or windowsills\u2014actually curve. Eventually, it can lead to a total loss of sharp, central vision, leaving those affected legally blind. The disease, age-related macular degeneration (AMD), is a leading cause of blindness among the elderly worldwide, affecting more that 15 percent of people aged 65 and older, approximately 150 million people globally. More than 10 million Americans have AMD, more than those who suffer from cataracts and glaucoma combined, according to the American Macular Degeneration Foundation<\/a>. While some treatments exist, there is currently no way to cure or prevent the disease.<\/p>\n

Now, a sweeping study has identified 52 common and rare genetic variants distributed across 34 genomic regions\u2014including 13 previously unknown\u2014that play a role in AMD. The findings, published online in the December 21, 2015, issue of Nature Genetics<\/em><\/a>, offer clues to the onset and progression of the disease that may eventually lead to better treatments or a cure. \u201cWe think of these variants as potential targets for new drug development, or biomarkers that could identify people who are at very high risk, so we could potentially intervene early, even before the disease becomes apparent,\u201d says Lindsay A. Farrer<\/em><\/strong><\/a>, chief of the biomedical genetics<\/a>\u00a0section at Boston University School of Medicine<\/a> (MED) and a co-leader of the study. \u201cThat\u2019s the hope.\u201d
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\n<\/span>*Please click on the title above for the full article.<\/em><\/span><\/span><\/strong><\/span><\/p>\n

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Discovery of a novel metastasis suppressor gene in breast cancer.<\/strong><\/a><\/p>\n

Metastatic dissemination of cancer cells represents a significant clinical obstacle to curative therapy and it is the major cause of death of patients affected by cancers. Despite the advent of advanced technologies, the discovery of new metastasis suppressor genes that prevent the spread of breast cancer to distal sites using genomic efforts has been slow potentially due to their primary mode of regulation by epigenetic mechanisms. The team led by Dr. Sam Thiagalingam report that the serum deprivation response (SDPR<\/em>) is a novel metastasis suppressor gene localized to 2q32-33, a region associated with significant loss of heterozygosity in breast cancer. \u00a0SDPR<\/em> is regulated by epigenetic rather than genetic mechanisms enabling the cancer cells to readily adapt to new microenvironments at distal sites away from the initial sites at which the cancer cells form. Interestingly, analysis of gene expression data sets indicated that loss of SDPR occurs in multiple tumor types including breast, bladder, colorectal, kidney, lung, pancreatic and ovarian cancers as well as in sarcomas. Follow up studies of this research may help with better prognosis and in the development of precision cancer therapies of metastatic cancer.<\/p>\n

Ozturk S, Papageorgis P, Lambert AW, Wong CK, Thiagalingam A, Abdolmaleky HM, Cohen HT, and Thiagalingam S, 2016. SDPR functions as a metastasis suppressor in breast cancer by promoting apoptosis. SDPR functions as a metastasis suppressor in breast cancer by promoting apoptosis. Proc. Natl. Acad. Sci.<\/em> USA. 113(3): 638-643. http:\/\/www.pnas.org\/content\/113\/3\/638.full.pdf?with-ds=yes<\/a><\/p>\n

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Editors\u2019 choice: Science\u00a0 22 Jan 2016:Vol. 351, Issue 6271, pp. 351<\/em>. http:\/\/science.sciencemag.org\/content\/351\/6271\/twil<\/a><\/strong><\/p>\n

http:\/\/www.bumc.bu.edu\/busm\/2016\/01\/08\/epigenetic-regulation-of-metastatic-breast-cancer-progression-could-guide-prognosis-and-future-therapies\/<\/a><\/p>\n

http:\/\/medicalxpress.com\/news\/2016-01-epigenetic-metastatic-breast-cancer-prognosis.html<\/a><\/p>\n

http:\/\/health-innovations.org\/2016\/01\/11\/major-epigenetic-metastasis-supressor-identified-for-breast-cancer\/<\/a><\/p>\n

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November\u00a02015<\/strong><\/span><\/p>\n

New breast cancer stem cell clues may help develop therapeutics<\/strong> <\/a> Basal-like breast cancer is an aggressive subtype of breast cancer that is often enriched with cancer stem cells, which may drive metastasis, resistance to chemotherapy, and disease recurrence.\u00a0 The team led by Dr. Sam Thiagalingam<\/em> <\/strong><\/span>found that periostin, a matricellular protein, secreted by many basal-like breast cancer cells regulates key cytokines that maintain the stem cell state.\u00a0This work suggests that tumor cell-derived factors may allow basal-like breast cancer cells to establish their own functional niche, which acts to maintain a population of cancer stem cells.<\/p>\n

Stem Cell News<\/span>: http:\/\/tinyurl.com\/zhzxykr<\/strong><\/a><\/p>\n

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EurekaAlert<\/span>: http:\/\/tinyurl.com\/njj3w7z<\/strong><\/a><\/p>\n

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The Daily Free Press<\/span>: http:\/\/tinyurl.com\/jle2qzy<\/strong><\/a><\/p>\n

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Oncology Central<\/span>: http:\/\/tinyurl.com\/hwuld7d<\/strong><\/a><\/p>\n

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Specialty Pharmacy Times<\/span>: http:\/\/tinyurl.com\/grhk2jw<\/strong><\/a><\/p>\n

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Science Daily<\/span>: http:\/\/tinyurl.com\/jnxj8hf<\/strong><\/a><\/div>\n
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Lambert AW, Wong CK, Ozturk S, Papageorgis P, Raghunathan R, Alekseyev YO, Gower A, Reinhard BM, Abdolmaleky HM, and Thiagalingam S. 2016. Tumor cell derived periostin regulates cytokines that maintain breast cancer stem cells. Mol. Cancer Res. <\/em>14:1 103-113. http:\/\/mcr.aacrjournals.org\/content\/14\/1\/103.long<\/a>; \u00a0<\/em>Highlights: http:\/\/mcr.aacrjournals.org\/content\/14\/1\/1.full.pdf+html<\/a> <\/span><\/p>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n

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Panos Papageorgis, Ph.D. receives<\/span> Cyprus Research Award \u2013 Young Researcher 2015 in Life Sciences<\/span><\/a><\/strong><\/p>\n

Dr\u00a0Panagiotis Papageorgis<\/strong><\/span>, Assistant Professor of Molecular Biology\u00a0at the European University Cyprus has been awarded the prestigious \u201cCyprus Research Award \u2013 Young Researcher 2015\u201d of the Research Promotion Foundation of the Republic of Cyprus in the thematic section \u201cLife Sciences\u201d.\u00a0He received this award from the Minister of Finance Mr. Harris Georgiades during a special ceremony held on Monday Nov 23rd<\/sup>, 2015 at the Hilton hotel Cyprus, Nicosia. Dr. Papageorgis was formerly a Genetics and Genomics graduate student (2004-2009) in the Biomedical Genetics Section with Dr. Sam Thiagalingam and he continued to work as a joint-post doctoral fellow with him on breast cancer metastasis (2010-2014).<\/p>\n

\"Sam<\/a> <\/strong><\/p>\n

*Please click on the title above for the full article.<\/span><\/strong><\/span><\/em><\/p>\n

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August 2015<\/strong><\/span><\/p>\n

Dr. Sam Thiagalingam<\/strong><\/a><\/span> is a recipient of a pilot grant from the BU Clinical and Translational Science Institute and the Department of Medicine. The award was provided for the grant entitled \u201cTargeting IL13R\u03b12 to suppress basal-like breast cancer metastasis\u201d<\/em>.\u00a0 <\/strong>The goal of the proposed studies is to examine the clinical utility of IL13R\u03b12 as prognostic biomarker and to decipher novel therapeutic targets. This work is a follow up recent studies reported in Breast Cancer Research<\/em> by the Thiagalingam (BUSM) and the Constantinou (University of Cyprus) laboratories (see<\/em> http:\/\/www.bumc.bu.edu\/busm\/2015\/08\/05\/novel-prognostic-marker-and-potential-therapeutic-target-for-triple-negative-breast-cancer-identified\/<\/a>)<\/p>\n

A novel prognostic biomarker and therapeutic target for triple negative breast cancer identified<\/strong><\/span><\/p>\n

– Basal-like breast cancer (BLBC), commonly known as the triple negative breast cancer is among the most aggressive tumors with a prevalence of 15-20% of all cases of breast cancer irrespective of the ethnicity or method of analysis. A cell surface receptor, IL13R\u03b12 (IL13R alpha2) abundant in metastatic or late-stage BLBC has been identified by a team led by Dr. Sam Thiagalingam at the Biomedical Genetics\/Boston University School of Medicine and by Dr. Constantinou at the University Cyprus.\u00a0 These researchers are hopeful that their discovery may lead to breakthroughs in diagnosis and therapy of breast cancer.<\/p>\n

Please click on the following links for more information:<\/strong><\/em><\/span><\/p>\n

Boston University School of Medicine:<\/strong> http:\/\/tinyurl.com\/pflox4o<\/a><\/strong><\/p>\n

Consumer Affairs<\/strong>: http:\/\/bit.ly\/1IewVGW<\/a><\/strong><\/p>\n

NewsMax Health: http:\/\/ow.ly\/QmDRX<\/a><\/span><\/strong><\/p>\n

Science World Report:<\/strong> http:\/\/tinyurl.com\/o5pjb5o<\/strong><\/a><\/p>\n

Mammary Cell News:<\/strong> http:\/\/tinyurl.com\/nevhv3q<\/a><\/strong><\/p>\n

OncoTherapy Network:<\/strong> http:\/\/tinyurl.com\/o2c9net<\/a><\/strong><\/p>\n

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July 2015<\/strong><\/span><\/p>\n