HCC_Awareness_Campaign

🔬 Excited to share the publication "Novel Gene-Correction-Based Therapeutic Modalities for Monogenic Liver Disorders". 🥼 Authored by Mahsa Ghasemzad, Mahdieh Hashemi, Zohre Miri Lavasani, Nikoo Hossein-khannazer, Haleh Bakhshandeh, Roberto Gramignoli, Hani Keshavarz Alikhani, Mustapha Najimi, Saman Nikeghbalian and Massoud Vosough, MD, Ph.D. 🚀 The majority of monogenic liver diseases are autosomal recessive disorders, with few being sex-related or co-dominant. Herein, this paper highlighted the most common monogenetic liver disorders, followed by proposed genetic engineering approaches, offered as promising therapeutic modalities. Welcome to access the full article freely here 👉 https://lnkd.in/gxrSvZ82. And welcome to follow our LinkedIn account: https://lnkd.in/grPNkBrg. 👏 #liver #gene_therapy #gene_editing #viral #nonviral #vectors

This is our national day for medical doctors to recognize their sincere contributions in health services. I would like to extend this recognition to medical professionals all over the world. You deserve all the best.

📌فقط ۲ روز تا سمپوزیوم پزشکیبازساختی و چشمانداز آینده این بحث پرطرفدار جهان! 📝هنوز برای ثبتنام دیر نشده و میتونید از لینک زیر اطلاعات بیشتر رو مطالعه بفرمایید 👇 https://lnkd.in/dSjVnvCv 😍🌱🧬🙏🏻

#rAj_Tspin, a soluble recombinant peptide from Apostichopus japonicus, can inhibit the integrin β1 (ITGB1)/FAK/AKT signaling pathway in #hepatocellular_carcinoma (HCC) via cell #epithelial_mesenchymal_transition (EMT) and #apoptosis. #Zyxin (ZYX) is a focal adhesion protein that is considered a novel mediator of EMT and apoptosis. However, the inhibitory mechanisms of rAj-Tspin in HCC and whether it is related to ZYX are unclear. In this study, results revealed that rAj-Tspin strikingly reduced the viability promoted the apoptosis of Huh7 cells, and inhibited HCC tumor growth in nude mice. rAj-Tspin inhibited ITGB1 and ZYX protein expression in vivo and in vitro in a dose-dependent manner. Mechanistically, the FAK/AKT signaling pathway and the proliferation and invasion of #HCC cells were suppressed upon ITGB1 and ZYX knockdown. Moreover, the effect of ITGB1 overexpression on the growth of HCC cells was inhibited by rAj-Tspin. In contrast, the promoting effect of ITGB1 overexpression could be inhibited by ZYX knockdown. ZYX knockdown did not affect ITGB1 expression. These findings suggest that ZYX is required for the indispensable role of ITGB1 in rAj-Tspin-alleviated HCC and provides an important therapeutic target for HCC. In summary, the anti-HCC effect of #rAj_Tspin potentially involves the regulation of the #ITGB1/ZYX/FAK/AKT pathway, which in turn impacts #EMT and #apoptosis. REF: https://lnkd.in/dDXA4Jg7 #rAj_Tspin #Epithelial_mesenchymal_transition #apoptosis #Zyxin #Non_alcoholic_fatty_liver_disease #NAFLD #Hepatocellular_Carcinoma #HCC_Awareness #liver

https://lnkd.in/dhnuiA49

✅ #Non_alcoholic_fatty_liver_disease (#NAFLD) and #metabolic_syndrome (#MetS) are intricately linked, sharing many pathophysiological mechanisms. ⁉ How are they contributing to each other's progression??? 📝 Fat distribution significantly impacts #metabolic health. Subcutaneous adipose tissue (#SAT) is more metabolically benign than visceral adipose tissue (#VAT), closely associated with metabolic disturbances. The "adipose tissue expandability hypothesis" suggests that when the capacity of #SAT to store fat is exceeded, fat is deposited in ectopic sites such as the liver and muscles, leading to IR and #NAFLD. 📝 #Genetic predisposition also plays a role in the variability of #NAFLD among individuals. Genome-wide association studies have identified variants in genes such as #PNPLA3 and #TM6SF2, which are strongly associated with #NAFLD severity but do not necessarily correlate with #metabolic_syndrome components. 📝 #Oxidative_stress and #inflammation are key mechanisms linking #NAFLD to #MetS. Increased production of #reactive_oxygen_species (#ROS) and lipid peroxidation contribute to liver damage and further exacerbate IR. Inflammation, marked by elevated cytokines like #IL_6 and #TNF_α, also promotes IR and atherosclerosis, establishing a vicious cycle that deteriorates metabolic health. Early diagnosis and intervention in #NAFLD are crucial. Non-invasive diagnostic tools such as serum biomarkers and imaging techniques can help identify and monitor the disease. Therapeutic strategies include lifestyle modifications like diet and exercise, and in some cases, pharmacological treatments targeting IR and lipid metabolism. Understanding the interplay between #NAFLD and #MetS is vital for developing effective prevention and treatment strategies, ultimately reducing the burden of cardiovascular and #liver_related_diseases. #Non_alcoholic_fatty_liver_disease #NAFLD #metabolic_syndrome #MetS #Hepatocellular_Carcinoma #HCC_Awareness #Oxidative_stress #ROS #liver REF:  https://lnkd.in/dJgpsnFH

The complexity of life is far from our computational knowledge to model its details. Please take a look at the recent paper in "Frontiers in Cell and Developmental Biology". https://lnkd.in/dKigrxGM This paper cited our recent paper entitled, " A Shadow of Knowledge in Stem Cell Science". https://lnkd.in/d-s6_mAy

#Non_alcoholic_fatty_liver_disease (#NAFLD) and #metabolic_syndrome (#MetS) are intricately linked, sharing many pathophysiological mechanisms and contributing to each other's progression. #MetS is characterized by a cluster of conditions including #insulin_resistance (IR), central #obesity, #dyslipidemia, and #hypertension, all of which are major risk factors for #cardiovascular disease and type 2 #diabetes. The primary driver of #MetS is insulin resistance, often linked to visceral adiposity, which also plays a crucial role in developing NAFLD. #NAFLD represents a spectrum of liver conditions ranging from simple steatosis (fat accumulation) to non-alcoholic steatohepatitis (#NASH), which can progress to #cirrhosis and #liver_cancer. Fat distribution significantly impacts metabolic health. Subcutaneous adipose tissue (#SAT) is more metabolically benign than visceral adipose tissue (#VAT), closely associated with metabolic disturbances #Non_alcoholic_fatty_liver_disease #metabolic_syndrome #insulin_resistance #liver_cancer #cirrhosis #NAFLD REF: https://lnkd.in/dgDnP_S4 https://lnkd.in/dJgpsnFH

🙌 🙌 Original Article: #Glioma-associated #oncogene (GLI)-specific decoy oligodeoxynucleotide induces apoptosis and attenuates proliferation, colony formation, and #migration in #liver #cancer cells 👨⚕️ Authors: Zahra Hajilou, Roya Solhi, Bahare Shokouhian, Shukoofeh Torabi,  Zahra Heydari, Zahra Farzaneh, Sadaf Bahadori, Abbas Piryaei,  Moustapha Hassan, Andreas K. Nussler, Massoud Vosough 📝 The transfection efficiency of GLI-specific decoy ODN was measured using fluorescent microscopy. Then, the effects of GLI-specific decoy ODN on apoptosis, viability, proliferation rate, colony formation, and migration capacities of Huh-7 cells were assessed. Furthermore, the expression of genes associated with the alteration of SHH was assessed. ✔ Full text: https://lnkd.in/gGdDSUGT ✔ Cite This Article: Hajilou Z, Solhi R, Shokouhian B, Torabi S, Heydari Z, Farzaneh Z, Bahadori S, Piryaei A, Hassan M, Nussler AK, Vosough M. Glioma-associated oncogene (GLI)-specific decoy oligodeoxynucleotide induces apoptosis and attenuates proliferation, colony formation, and migration in liver cancer cells. Hepatoma Res 2024;10:32. https://lnkd.in/gGTFc9Vq Don't miss it! Massoud Vosough, MD, Ph.D Zahra Hajilou Roya Solhi Bahare Shokouhian Shukoofeh Torabi, PhD Zahra Heydari Roya Solhi Sadaf Bahadori Abbas Piryaei Moustapha Hassan Andreas Nüssler Emily Kooner Remco van Dijk Michael Klemt-Kropp Kristel Hunt George Therapondos Kiran Rao, MD Monica Tincopa MD MSc Quentin M. Anstee Niloufar Safinia

#Hepatocellular_carcinoma (HCC) is the most prevalent form of primary liver cancer. Transforming growth factor-beta (#TGF_β) is abundantly expressed in the #liver_tumor #microenvironment and is known to suppress immune cell function. This research utilized human #induced_pluripotent_stem_cells (iPSCs) to generate natural killer (#NK) cells with enhanced #anti_HCC capabilities. The #iPSC-NK cells were engineered with either a knockout of the TGF-β receptor 2 (TGFBR2-KO) or a dominant negative (DN) form of the #TGF_β receptor 2 (TGFBR2-DN), along with chimeric antigen receptors (CARs) targeting GPC3 or AFP. These TGFBR2-KO and TGFBR2-DN #iPSC_NK cells are resistant to TGF-β inhibition and exhibit improved anti-HCC activity. However, the expression of anti-HCC CARs on iPSC-NK cells alone did not result in effective anti-HCC activity unless TGF-β activity was also inhibited. The findings indicate that blocking #TGF_β_signaling is essential for effective NK cell function against HCC and potentially other cancers with high TGF-β expression. Consequently, #cell_based #immunotherapies, such as #CAR_T or #CAR_NK cells, are promising new treatments for #solid_tumors. #HCC_Awareness_Campaign #Hepatocellular_carcinoma #iPSC #cell_based_immunotherapies #solid_tumors #CAR_T_cell #CAR_NK_cells #TGF_β REF: https://lnkd.in/dJHBAGFr