The latest news in the ever evolving universe of CRISPR gene technology is that the editing tool has been used for the first time in humans to cure aggresive lung cancer by a team of Chinese researchers. Read about it :
Teaching parents of children with autism how to interact more effectively with their offspring brings the children benefits that linger for years, according to the largest and longest-running study of autism interventions. The training targeted parents with 2–4-year-old children with autism. Six years after the adults completed the year-long course, their children showed better social communication and reduced repetitive behaviours, and fewer were considered to have “severe” autism as compared to a control group, according to results published on 25 October in The Lancet. Child psychiatrist Jonathan Green of the University of Manchester, and an investigator on the study said that even though it is not a cure, yet it does have a sustained and substantial reduction in severity and that’s important in families. Although the therapy benefited communication skills and decreased repetitive behaviours, it did not lessen anxiety.
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The normal human genome contains about 54 mutations that might sicken or even kill their bearer, but they don’t. Recently, medical genetics has been evolving, as the fast pace of genomic research has packed the literature with thousands of gene mutations associated with disease and disability. Many such associations are solid, but many others once suggested to be dangerous or even lethal are turning out to be not so through the Exome Aggregation Consortium, or ExAC.
ExAC combines sequences for the protein-coding region of the genome — the exome — from more than 60,000 people into one database, allowing scientists to compare and understand how variable they are. The resource is having tremendous impacts in biomedical research, by helping scientists to eliminate bogus disease–gene links, and generating new discoveries. By looking more closely at the frequency of mutations in different populations, researchers can gain insight into what many genes do and how their protein products function. ExAC has turned completely revised how we look at genetics, as instead of starting with a disease or trait and working backwards to find its genetic underpinnings, researchers can start with mutations that look like they should have an interesting effect and investigate what might be happening in the people who harbour them.
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Macrophages play critical role in acute and chronic inflammation and cancer. In response to pathogens or injury, inflammatory macrophages express cytokines that stimulate cytotoxic T cells. Macrophage PI(3)Kinase γ controls a critical switch between immune stimulation and suppression during inflammation and cancer. PI3KC signaling through Akt and mTor inhibits NFκB activation while stimulating C/EBPβ activation. This induces a transcriptional program that promotes immune suppression during inflammation and tumor growth. However, selective inactivation of macrophage PI3Kγ stimulates and prolongs NFκB activation and inhibits C/EBPβ activation, thus promoting an immunostimulatory transcriptional program that restores CD8+ T cell activation and cytotoxicity and synergizes with checkpoint inhibitor therapy to promote tumor regression and extend survival. The therapeutic targeting of intracellular signaling pathways that regulate the switch between macrophage polarization states can control immune suppression in cancer and other disorders.
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The Snippet : HER2 Expression and its Dynamic Functional States within Circulating Breast Cancer Cells
A research published in Nature recently identified some dynamic functional states in the breast cancer cells of HER2 breast cancer. The research postulates that women who have advanced oestrogen-receptor (ER)-positive/human epidermal growth factor receptor 2 (HER2)-negative breast cancer, are prone to acquire a HER2-positive subpopulation after multiple courses of therapy. This acquired heterogeneity during the cancer evolution was previously unknown, and to find out the same the researchers evaluated women with ER+/HER2− primary tumours. The results show that the HER2− circulating tumour cells have shown activation of Notch and DNA damage pathways, which results in resistance to cytotoxic chemotherapy. HER2+ and HER2− circulating tumour cells are able to convert among themselves and produce daughter cells that are opposite within four cell doublings. Even though both HER2+ and HER2− tumour cells found in circulation were comparable in tumour initiating potential, differential proliferation favours the HER2+ state, while oxidative stress or cytotoxic chemotherapy enhances transition to the HER2− phenotype. Thus, these results point to some very distinct yet interconverting phenotypes present within patient population and also contributes in the progression of breast cancer and acquisition of drug resistance.
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Cancer has gripped the world in its clutches, and the grip hasn’t loosened for the past 3 decades. Research into cancer prognosis and treatment has many hurdles, and these hurdles keep on increasing with increasing insight to the disease itself. In terms of glioblastoma as well, the researchers have not had much success in curing patients, as this cancer inflicts the brain, leading to death in more than 70% of patients within the first 18 months. Conventional therapies have failed to make any difference due to the blood brain barrier.
However, a groundbreaking research from Dr. Shawn Hingtgen’s laboratory at the UNC-Chapel Hill Eshelman School of Pharmacy, may well be the answer to this complicated cancer enigma. The research carried out in this lab progresses from the Nobel winning cell reprogramming research, and Hingtgen’s team has successfully reprogrammed skin cells into cancer killing machines. They first genetically converted patient’s skin cells into induced neural stem cell, and later provided these stem cells with optical reporters and tumor-killing proteins to actively seek out and destroy cancer cells.
For more information on this spectacular and innovative cancer research, click on the link below to read the full story.