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HCG Near Me. #1 Online or Local U.S. HCG Diet Clinic. We ship HCG fast.

Posted: July 11, 2022 at 1:55 am

HCG Diet InformationWhat is Human Chorionic Gonadotropin or HCG?HCG stands for Human Chorionic Gonadotropin & is a very safe & mild hormone present in both males & females. This glycoprotein is composed of 244 amino acids.

Welcome to HCG Near Me, where access to a quality HCG Diet is always near you! If you do not live near the lovely Miami, FL area, no worries, we can ship your entire HCG Diet kit to you after a simple 10 to 15-minute telemedicine phone consultation. HCG Near Me is owned and operated by a licensed Health Care Clinic Establishment in Miami, Florida, and employs certified health professionals to ensure a quality medical weight loss program for all to benefit from.

The use of HCG for weight loss is not a new fly by night fad diet. This diet dates to the 1950s and has helped millions of people since then. It was created by a British endocrinologist named Albert Simeons. Dr. Simeons was studying pregnant women in third world countries and was absolutely fascinated at how these women, who were often malnourished, would give birth to regular sized babies. These women also had to work to survive and often walked everywhere burning plenty of calories.

Therefore, Dr. Simeons wanted to research how these women, who burned high calories and ate fewer calories, would still give birth to regular sized babies that Dr. Simeons assumed would be born malnourished. His research and observations led to the discovery of high levels of HCG in the bloodstream of pregnant women. Further research then led to the discovery of how the HCG helps the body to release adipose fatty acid into the bloodstream for immediate use and consumption. This means the fetus was being nourished by the mothers adipose body fat.

Dr. Simeons then tried using HCG injections with obese or overweight boys in India to see if the HCG injections together with a very low-calorie diet would help the boys lose adipose body fat. His studies concluded that while taking HCG injections and undergoing a low-calorie diet, specifically low in fats, his patients would lose high amounts of unwanted body fat and maintain lean muscle mass.

After many years of research and trial and error with many users of the HCG Diet, this magnificent diet has evolved. The internet is loaded with plenty of good information, but unfortunately, its also filled with plenty of bad and misleading information. The main things wed like to address briefly here is that this diet originally called for 500 calories per day. Our modern program advocates for higher calories that are consistent with a persons body mass index and body metabolic rate. We customize each persons daily caloric allowance!

Also, you may read online that the FDA does not approve or has made the HCG Diet illegal. This is not true; the FDA has made the sale of FAKE homeopathic HCG drops illegal. Yes, there are people out there selling fake drops of HCG and trying to claim its the real hormone. So, remember, the fake HCG drops are illegal, not the real prescription injections or oral tablets you can get through a licensed Health Care Clinic with certified physicians like the ones youll find at HCG Near Me.

HCG mobilizes the bad fat which we all know as adipose fatty tissue (abnormal fat). Basically, mobilizing bad fat is when the body releases fatty acid into the bloodstream as a mechanism to protect from starvation. There are 3 types of fat:

As mentioned earlier, pregnant females produce extremely high amounts of HCG, over 1 million IUs (International Units) to be exact. Note: this is way higher than the amount of HCG you receive for a 30-day weight loss program (6,000 IU). Everyone, male or female, will receive safe doses for their weight loss program. What the HCG actually does is mobilize the abnormal fat full of nutrients, vitamins, and minerals to nourish the unborn fetus.

Dr. Simeons states, In pregnancy, it would be most undesirable if the fetus was offered ample food only when there is a high influx from the intestinal tract. Ideal nutritional conditions for the fetus can only be achieved when the mothers blood is continually saturated with food, regardless of whether she eats or not, as otherwise, a period of starvation might hamper the steady growth of the embryo.

So how does the HCG work for someone taking injections? Basically, a person taking HCG injections and undergoing a low-calorie diet will lose weight because the presence of HCG in their system will cause the body to mobilize adipose body fat and release fatty acid into the bloodstream. HCG does this in a pregnant female to protect the fetus. If you were to do the HCG Diet, since you are now eating a low-calorie diet, you become like the fetus that the HCG is protecting. The HCG ensures you do not starve while you are undergoing a low caloric daily intake. It is for this reason HCG also controls hunger for those taking the injections. Even though you are eating much less, the release of this adipose body tissue into the bloodstream helps keep you nourished and not feeling starved.

When you give yourself the HCG injections, you will also incorporate a specific very low-calorie diet (VLCD) with detailed phases and rules. The actual diet and allowed foods will really reshape your body and provide tremendous health benefits. Your body does need good fats such as reserve and structural to survive but can function without the abnormal adipose fat. Therefore, HCG shots or injections coupled with our 4 phase VLCD will trigger rapid weight loss that is primarily comprised of bad fat.

Absolutely! In fact, men perform better on the HCG Diet than women, sorry ladies. HCG injections have been used in men for years to help treat low testosterone. Physicians have prescribed HCG to men while taking testosterone therapy because HCG helps men to not shut down their own natural testosterone production. If a man took HCG injections alone without testosterone, they would likely increase their own testosterone naturally and gradually with the HCG injection alone. So aside from the benefits of weight loss, HCG injections in men would also help increase natural testosterone levels safely. HCG has also been used in treatments for men who are no longer fertile due to long term drug or steroid abuse. The HCG helps these men produce sperm again after long periods of being shut down.

Dr. Simeons stated years ago, When a male patient hears that he is about to be put into a condition which in some respects resembles pregnancy, he is usually shocked and horrified. The physician must therefore carefully explain that this does not mean that he will be feminized and that HCG in no way interferes with his sex. He must be made to understand that in the interest of the propagation of the species, nature provides for perfect functioning of the regulatory headquarters in the diencephalon during pregnancy and that we are merely using this natural safeguard as a means of correcting the diencephalic disorder which is responsible for his being overweight.

If you undergo a very low-calorie diet long term you will definitely lose weight. The problem is that you will undoubtedly lose high amounts of muscle mass in the process and this spells bad news for your metabolism. If just reducing calories were the simple solution, then why has it not worked in the past? If you landed on our website and are researching the HCG Diet, wed say youve tried other diets with poor or no success at all. The two most obvious reasons one should avoid just reducing calories to lose weight are:

These two simple and straightforward reasons are why so many people fail at weight loss attempts. A combination of HCG injections and the modern VLCD can mobilize and reduce your abnormal fat without hurting your metabolic rate.

The HCG Diet is the hottest medical weight loss program in existence today. If this is your first time learning about it, congratulations, your life is about to change. The original HCG Diet by Dr. Simeons dates back to the 1950s. The original rules called for 500 calories per day for everyone on the diet! This simply does not work for todays society. Everyone has a different engine and motor.

At HCG Near Me, we will customize your daily caloric need and you will be on a Very Low-Calorie Diet thats right for you. Another thing to keep in mind is the evolution of the human body, we are bigger, faster, and stronger than we were almost 70 years ago. We simply all need more calories! We also process foods much different today than foods were processed 70 years ago. Foods were way more organic back then. For these reasons, we have modernized and perfected the HCG Diet for todays patient.

For anyone researching the best way to lose weight with HCG injections, two fantastic sources of updated information as of 2020, are HCG Near Me and HCG Diet Miami. Both these licensed health care clinics are owned and operated by the same weight loss consulting group. They employ only licensed health professionals to bring you the very best weight loss information and medications necessary for a successful HCG Diet program.

Located in Miami, FL, these two clinics can serve both the local Miami population and anyone located in the United States. With the use of telemedicine, our clinics can ship your HCG kit with all supplies to you after a simple and legal 10 to 15-minute Telemed or Telehealth consultation. If you searched HCG Diet Near Me and landed on our page, you should be glad you did. HCG Near Me is Near You!

Many clinics in the United States offering the HCG Diet are completely overpriced. For this reason, we get many patients from all around the United States. The HCG Diet is our niche. We have very low costs compared to other spas or clinics that offer other treatments with expensive machinery and other high-cost items. These other spas or clinics must factor in these high expenses when deciding what to charge for their services.

Our clinic has the very best medications from some of the top compounding pharmacies in the country. We provide all of our patients with information on the pharmacies we use. If you are considering working with us, ask us about our FDA approved compounding pharmacies.

We encourage you to navigate our site further to learn about doing the HCG Diet, starting the program, and learning how to effectively keep the weight off after the diet. A detailed diet plan is provided with information about every phase of the program and our customer service is the best youll find around.

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HCG Near Me. #1 Online or Local U.S. HCG Diet Clinic. We ship HCG fast.

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Hepatic stellate cells in liver development, regeneration, and cancer

Posted: July 11, 2022 at 1:54 am

J Clin Invest. 2013 May 1; 123(5): 19021910.

1Department of Biochemistry and Biophysics, Programs in Developmental and Stem Cell Biology, Genetics and Human Genetics, Liver Center and Diabetes Center, Institute for Regeneration Medicine, and 2Department of Pathology, UCSF, San Francisco, California, USA. 3Southern California Research Center for ALPD and Cirrhosis and Department of Pathology, Keck School of Medicine of the University of Southern California, Los Angeles, California, USA.

1Department of Biochemistry and Biophysics, Programs in Developmental and Stem Cell Biology, Genetics and Human Genetics, Liver Center and Diabetes Center, Institute for Regeneration Medicine, and 2Department of Pathology, UCSF, San Francisco, California, USA. 3Southern California Research Center for ALPD and Cirrhosis and Department of Pathology, Keck School of Medicine of the University of Southern California, Los Angeles, California, USA.

1Department of Biochemistry and Biophysics, Programs in Developmental and Stem Cell Biology, Genetics and Human Genetics, Liver Center and Diabetes Center, Institute for Regeneration Medicine, and 2Department of Pathology, UCSF, San Francisco, California, USA. 3Southern California Research Center for ALPD and Cirrhosis and Department of Pathology, Keck School of Medicine of the University of Southern California, Los Angeles, California, USA.

1Department of Biochemistry and Biophysics, Programs in Developmental and Stem Cell Biology, Genetics and Human Genetics, Liver Center and Diabetes Center, Institute for Regeneration Medicine, and 2Department of Pathology, UCSF, San Francisco, California, USA. 3Southern California Research Center for ALPD and Cirrhosis and Department of Pathology, Keck School of Medicine of the University of Southern California, Los Angeles, California, USA.

1Department of Biochemistry and Biophysics, Programs in Developmental and Stem Cell Biology, Genetics and Human Genetics, Liver Center and Diabetes Center, Institute for Regeneration Medicine, and 2Department of Pathology, UCSF, San Francisco, California, USA. 3Southern California Research Center for ALPD and Cirrhosis and Department of Pathology, Keck School of Medicine of the University of Southern California, Los Angeles, California, USA.

Authorship note: Chunyue Yin and Kimberley J. Evason contributed equally to this work.

Hepatic stellate cells are liver-specific mesenchymal cells that play vital roles in liver physiology and fibrogenesis. They are located in the space of Disse and maintain close interactions with sinusoidal endothelial cells and hepatic epithelial cells. It is becoming increasingly clear that hepatic stellate cells have a profound impact on the differentiation, proliferation, and morphogenesis of other hepatic cell types during liver development and regeneration. In this Review, we summarize and evaluate the recent advances in our understanding of the formation and characteristics of hepatic stellate cells, as well as their function in liver development, regeneration, and cancer. We also discuss how improved knowledge of these processes offers new perspectives for the treatment of patients with liver diseases.

Hepatic stellate cells are located in the space of Disse between the sinusoidal endothelial cells and hepatic epithelial cells, and account for 5%8% of the cells in the liver. In a healthy liver, stellate cells are quiescent and contain numerous vitamin A lipid droplets, constituting the largest reservoir of vitamin A in the body (reviewed in ref. 1). When the liver is injured due to viral infection or hepatic toxins, hepatic stellate cells receive signals secreted by damaged hepatocytes and immune cells, causing them to transdifferentiate into activated myofibroblast-like cells (reviewed in ref. 2). As the primary extracellular matrixproducing (ECM-producing) cells in liver, activated stellate cells generate a temporary scar at the site of injury to protect the liver from further damage. In addition, hepatic stellate cells secrete cytokines and growth factors that promote the regeneration of hepatic epithelial cells. In chronic liver disease, prolonged and repeated activation of stellate cells causes liver fibrosis, as characterized by widespread scar formation and perturbation of liver architecture and function (reviewed in ref. 3). Recent clinical and experimental evidence indicates that hepatic fibrosis is reversible upon removal of the underlying etiological agent (46). During the regression of liver fibrosis, the number of activated hepatic stellate cells is greatly reduced by the induction of cellular senescence and apoptosis, or by the return to the quiescent state (2, 57). Because of their pivotal roles in liver repair and disease pathogenesis, hepatic stellate cells have been a major focus of liver research. However, our knowledge of their cell biology is far from complete, mainly due to the challenges of studying these cells in vivo.

This Review focuses on the recent insights and emerging investigations into the formation of hepatic stellate cells and their function in liver development, regeneration, and hepatocellular carcinoma (HCC). The regulation of stellate cells in liver fibrosis as well as the design of antifibrotic therapies is reviewed separately in this issue (8).

Over the past two decades, the development of cell culture system and genetic animal models (summarized in Figure ) has greatly advanced our understanding of the cellular properties of hepatic stellate cells and their function in healthy as well as injured livers. When cultured on plastic, freshly isolated hepatic stellate cells undergo spontaneous activation (911). This cell culture system, along with other hepatic stellate cell lines (1214), recapitulates many aspects of hepatic stellate cell activation in vivo. But hepatic stellate cells activated in culture do not fully reproduce the changes in gene expression observed in vivo, making it difficult in some cases to correlate in vitro results with hepatic stellate cell behaviors in vivo (15).

(A) Phase contrast image of mouse hepatic stellate cells cultured for 2 days. These hepatic stellate cells are still quiescent, as evidenced by their vitamin A lipid deposition, a stellate morphology, and presence of dendritic processes. (B) Phase contrast image of mouse hepatic stellate cells cultured for 14 days. By this time, hepatic stellate cells are fully activated and exhibit dramatic changes in their morphology and reduction in lipid deposition. (C) Fluorescence image of hepatic stellate cells in healthy adult mouse liver stained for desmin. (D) Fluorescence image shows -SMA immunostaining in CCl4-induced fibrosis in the adult mouse liver. (E) Confocal single-plane image of Tg(hand2:EGFP) expression in zebrafish hepatic stellate cells at 5 days after fertilization. The hepatic stellate cells exhibit a stellate morphology and send out complex protrusions (23). (F) Confocal single-plane image of hepatic stellate cells labeled by Tg(hand2:EGFP) expression in zebrafish larvae treated with 2% ethanol from 4 to 5 days after fertilization. Hepatic stellate cells become activated upon the acute ethanol assault, as evidenced by the loss of complex cellular processes and elongated cell body, suggestive of changes in contractility (24).

In the animal, hepatic stellate cells can be identified based on expression of desmin (16) and glial fibrillary acidic protein (GFAP) (17) in the quiescent state and -SMA in the activated state (18). The identification of promoters that selectively drive transgene expression in hepatic stellate cells might facilitate both in vivo observations and genetic manipulation of these cells. Components of collagen 1(I), collagen 2(I), and SMA promoters were used to direct reporter gene expression in activated hepatic stellate cells in transgenic mice (19). Promoter elements of the Gfap (20, 21) and vimentin (6) genes drive gene expression in quiescent hepatic stellate cells. However, neither promoter is specific for hepatic stellate cells: Gfap promoter activity is detected in neuronal tissues and cholangiocytes (21), whereas the vimentin gene is also expressed in vascular smooth muscle cells and portal fibroblasts (6).

The zebrafish has emerged as a valuable vertebrate model system to study liver development and disease. The rapid external development and translucence of zebrafish embryos and larvae make them well suited for in vivo imaging (22, 23). The availability of transgenic lines that express fluorescent proteins in different hepatic cell types allows easy visualization of cell behaviors in the animal and greatly facilitates genetic and chemical screens to identify regulators of liver development and disease pathogenesis. Our group recently reported a transgenic zebrafish line, Tg(hand2:EGFP), that expresses EGFP under the promoter of the hand2 gene (24). The transgene expression marks both quiescent and activated hepatic stellate cells. Zebrafish hepatic stellate cells exhibit all the hallmarks of mammalian hepatic stellate cells, including morphology, localization, vitamin A storage, and gene expression profile. Significantly, zebrafish hepatic stellate cells become activated in response to an acute alcohol insult, as evidenced by increased proliferation and ECM production (Figure and ref. 24). This zebrafish hepatic stellate cell reporter line thus represents a novel animal model that complements the cell culture and mammalian model systems.

Knowledge about the characteristics, lineage, and function of stellate cells during liver development is critical to obtaining a fundamental understanding of hepatic stellate cell activation and their role in liver diseases. Recent studies in animal models and cell culture systems have provided key insights regarding hepatic stellate cells during development, but important gaps remain in our knowledge of this process.

The embryonic origin of hepatic stellate cells is unresolved because they express marker genes of all three germ layers (reviewed in ref. 2). Lineage tracing of the Wilms tumor suppressor geneexpressing (Wt1-expressing) cells and mesoderm posterior 1expressing cells in mice showed that hepatic stellate cells develop from the septum transversumderived mesothelium lining the liver (25, 26), suggestive of a mesodermal origin. On the other hand, stellate cells in the human fetal liver express CD34 and cytokeratin-7/8, connecting them to an endodermal origin (27, 28). Along this theme, hepatic epithelial cells are thought to transdifferentiate into hepatic stellate cells in the injured liver through epithelial-mesenchymal transition (EMT) (29). However, the contribution of EMT to the hepatic stellate cell lineage is highly controversial (30). Lastly, bone marrowderived mesenchymal cells are also thought to contribute to both quiescent and activated hepatic stellate cells (31, 32), although several reports indicate that this contribution is negligible (33, 34).

It is noteworthy that in mice, the septum transversum-derived mesothelial cells give rise not only to hepatic stellate cells, but also to perivascular mesenchymal cells, including portal fibroblasts, smooth muscle cells around the portal vein, and fibroblasts around the central vein (26). Following liver injury, activated stellate cells are the major source of myofibroblasts. However, portal fibroblasts and vascular myofibroblasts can also become myofibroblasts, but their contribution to fibrogenesis might be different from the hepatic stellate cellderived myofibroblasts (35, 36). Therefore, an understanding of how the cell fate decision is made between hepatic stellate cells and perivascular mesenchymal cells might aid in the design of therapies to specifically target hepatic stellate cells.

In both fetal and adult livers, stellate cells are closely associated with sinusoidal endothelial cells, which also derive from mesoderm. Because of their physical proximity and shared expression of angiogenic factors (37), hepatic stellate cells and sinusoidal endothelial cells have been proposed to share a common precursor. This hypothesis is supported by observations in chick embryos that the mesothelium contributes to both cell populations (38). In zebrafish, however, stellate cells are still present in the liver of cloche mutants that lack sinusoidal endothelial cells and their precursors (24). This result indicates that neither endothelial cells nor their precursors are required for hepatic stellate cell differentiation or their entry into the liver.

To date, only a few studies have addressed early hepatic stellate cell behaviors in vivo. Tracking of the Wt1-expressing septum transversum cells in mice showed that these cells migrate inward from the liver surface while differentiating into hepatic stellate cells (ref. 25 and see Figure A). A similar migration behavior of hepatic stellate cells was observed in zebrafish (24). Furthermore, the migration of septum transversum cells from the liver surface likely constitutes the main source of new stellate cells during zebrafish development, as they rarely proliferate after entering the liver.

(A) Hepatic stellate cell development. Lineage-tracing analyses in mice indicate that during development, the mesodermal cells within the septum transversum invade the liver while differentiating into hepatic stellate cells and perivascular mesenchymal cells. VEGF and retinoic acid signaling are both required for hepatic stellate cell formation, potentially affecting the migration of septum transversum cells, the differentiation of hepatic stellate cells, or both. Wt1, Wnt/-catenin signaling, and Lhx2 inhibit aberrant activation of hepatic stellate cells in the developing liver. (B) Contribution of hepatic stellate cells to hepatic organogenesis. The biological processes influenced by hepatic stellate cells are indicated in blue. For endothelial cells, hepatic stellate cells secrete the chemokine SDF1, whereas endothelial cells express its receptor CXCR4. Concurrently, endothelial cells produce PDGF, whereas hepatic stellate cells express its receptor. SDF1 and PDGF signaling maintain the close association between hepatic stellate cells and endothelial cells, which is critical for vascular tube formation and integrity. For hematopoietic stem cells (HSCs), hepatic stellate cells mediate their recruitment to the liver via SDF1/CXCR4 signaling. For hepatic epithelial cells, hepatic stellate cells regulate the proliferation of hepatoblast progenitor cells and hepatocytes by producing growth factors such as Wnt, FGF, HGF, and retinoic acid. They may also modulate the differentiation of hepatocytes and biliary cells from hepatoblasts by controlling the ECM composition within the liver. Lastly, hepatic stellate cells may contribute to the development of biliary cells by expressing the Notch ligand jagged 1 (Jag1).

Studies in mutant mice have revealed the roles of several mesenchymal-specific genes in hepatic stellate cell development (summarized in Figure A). Wt1 and the LIM homeobox gene Lhx2 are both expressed in the septum transversum and hepatic stellate cells during development (26, 39). Wt1-null fetal livers show an abnormal increase of -SMA expression (40), suggestive of ectopic stellate cell activation. Similarly, Lhx2 knockout embryos contain numerous activated hepatic stellate cells and display a progressively increased deposition of ECM proteins associated with fibrosis (41). Therefore, despite being dispensable for hepatic stellate cell formation, both Wt1 and Lhx2 appear to keep these cells quiescent during development. The signal downstream of Wt1 and Lhx2 that prevents hepatic stellate cell activation is unclear. One candidate is the Wnt/-catenin pathway, as conditional deletion of -catenin in the mesenchyme results in increased -SMA expression and ECM deposition in the liver (42, 43). On the other hand, freshly isolated hepatic stellate cells from adult mice exhibit hedgehog (Hh) pathway activity, and inhibition of Hh signaling via pharmacologic inhibitor or neutralizing antibodies to Hh impairs hepatic stellate cell activation and decreases their survival (44). It will be interesting to investigate the role of the Hh pathway during the development of hepatic stellate cells.

Studies of the zebrafish hepatic stellate cell reporter line have shed light on the regulation of their differentiation and migration into the liver. Inhibition of VEGF signaling by global knockdown of VEGFR2 or by treatment with a VEGFR2 pharmacologic inhibitor during the course of hepatic stellate cell differentiation and migration drastically reduces their numbers (24). VEGF signaling does not appear to be essential for hepatic stellate cell survival, as blocking VEGFR2 during later stages only caused a moderate decrease in hepatic stellate cell numbers. Rather, VEGF may be required for hepatic stellate cell differentiation and/or their entry into the liver. Studies of liver injury and cancer have documented VEGF ligand expression by hepatocytes and biliary cells (4547). Likewise, hepatic epithelial cells could be the source of VEGF for hepatic stellate cell development. Using an unbiased chemical screen approach, our group discovered two retinoid receptor agonists that have an opposing effect on hepatic stellate cell development (24). Compounds that modulate stellate cell differentiation, proliferation, or the switch between their quiescent and activated states during development could potentially affect hepatic stellate cell behavior during injury, and thus have direct clinical implications.

Throughout development, hepatic stellate cells are in close proximity to endothelial, hematopoietic, and hepatic epithelial cells, which suggests that hepatic stellate cells may modulate the growth, differentiation, or morphogenesis of these cells (summarized in Figure B). The interactions between stellate cells and other hepatic cells during development could be reactivated when the liver responds to injury.

Hepatic stellate cells contact sinusoidal endothelial cells by means of complex cytoplasmic processes, which ideally positions them for paracrine signaling with endothelial cells (48). During angiogenesis, interactions between pericytes and endothelial cells are essential for vascular tube maturation and integrity (49). Hepatic stellate cells are thought to be the pericyte equivalent in the liver and therefore may have the same impact on the development of the hepatic vasculature (50). In support of this notion, in mice that lack -catenin in the liver mesenchyme, hepatic stellate cells become aberrantly activated and the liver is filled with dilated sinusoids (42).

During mammalian embryogenesis, the liver is the main site of hematopoiesis (51). In mice lacking the hepatic stellate cellexpressing homeobox gene Hlx, fetal liver hematopoiesis is severely impaired (52), implicating hepatic stellate cells in this process. Fetal hepatic stellate cells express stromal cellderived factor 1 (SDF1; also known as CXCL12) (51), a potent chemoattractant for hematopoietic stem cells, which themselves express the SDF1 receptor CXCR4 (53). Therefore, it is plausible that hepatic stellate cells are involved in recruiting hematopoietic stem/progenitor cells into the fetal liver.

Stellate cells first appear in mouse livers at around E10E11, when differentiation of hepatocytes and biliary cells from hepatoblasts is still underway (54). Mouse fetal liver mesenchymal cells promote the maturation of hepatoblasts through cell-cell contact in cell culture (55). In Wt1 and Hlx mutant mice, the hepatoblast population fails to proliferate, resulting in smaller livers (40, 52). Fetal hepatic stellate cells express growth factors and mitogens such as Wnt9a (56), HGF (57), pleiotrophin (58), and FGF10 (59, 60), all of which have profound effects on the proliferation of hepatic epithelial cells during organ development and regeneration. In addition, hepatic stellate cells in the Wt1-null fetal livers show decreased expression of retinaldehyde dehydrogenase 2, an enzyme that catalyzes retinoic acid synthesis (40). The impairment of retinoic acid production could in turn affect hepatoblast proliferation. The role of hepatic stellate cells in hepatoblast differentiation is less clear. Nagai et al. reported that cell-cell contacts between hepatic stellate cells and hepatic epithelial cells induce the differentiation of the hepatocyte fate (61). On the other hand, the emergence and distribution of hepatic stellate cells also seem to correlate with the development of intrahepatic biliary cells (62). Hepatic stellate cells in rats express Notch receptors and target genes of Notch signaling (63), and Notch signaling plays key roles in the differentiation and morphogenesis of intrahepatic biliary cells (64). A recent study showed that inactivation of the Notch ligand jagged 1, which is expressed in the portal vein mesenchyme, leads to a paucity of intrahepatic bile ducts (65). Given that hepatic stellate cells also express jagged 1 (66), it will be interesting to investigate whether they modulate biliary cell development via Notch signaling. Alternatively, hepatic stellate cells could influence hepatoblast differentiation through production of ECM proteins, as different ECM components have different effects on the determination of the hepatocyte and biliary cell fate (67, 68).

The directed differentiation of human pluripotent stem cells into hepatocytes in culture could lead to new cell transplantation therapies for a wide range of acute and chronic liver diseases. Although important progress toward this goal has been made in recent years, liver cells differentiated in vitro do not share all the key characteristics of mature hepatocytes (reviewed in refs. 69, 70). Co-culturing primary human liver progenitor cells or hepatocytes with mesenchymal cells promotes or stabilizes hepatocyte differentiation (7173). Therefore, understanding the interactions between hepatic stellate cells and hepatic epithelial cells during development is essential to create more efficient cell culture protocols for programmed differentiation of stem cells into hepatocytes.

Much as studies of liver development are highly relevant to creating new stem cell therapies, an understanding of liver regeneration has important implications for improving current methods of differentiating and propagating hepatocytes in vitro, as well as for stimulating hepatic recovery and improving survival after acute liver failure, liver transplantation, or resection. One of the oldest and most commonly used rodent models of liver regeneration is partial hepatectomy (PH), in which two-thirds of the animals liver is surgically removed (74, 75). Liver regeneration following PH is mainly driven by replication of existing hepatocytes and occurs in the absence of substantial necrosis and inflammation (74). To model how the liver regenerates when the ability of hepatocytes to divide is compromised, hepatocyte proliferation inhibitors such as 2-acetylaminofluorene can be administered before PH (2AAF/PH), which results in liver repopulation mediated by activation of liver progenitor cells or oval cells rather than proliferation of hepatocytes (74). Other rodent models of liver injury and regeneration involve chemical treatments with carbon tetrachloride (CCl4) or acetaminophen (reviewed in ref. 76) or bile duct ligation (BDL) (77). While the PH model of liver regeneration may be particularly relevant to clinical scenarios in which the quantity of liver tissue is a limiting factor, such as small-for-size syndrome following liver transplantation, chemical injury and BDL models may more faithfully recapitulate the necrosis, inflammation, and/or fibrosis that accompany regeneration in chronic viral hepatitis, biliary tract disease, and/or drug-induced liver injury.

Activated hepatic stellate cells have been implicated in assisting liver regeneration by producing angiogenic factors as well as factors that modulate endothelial cell and hepatocyte proliferation and by remodeling the ECM (78). Recent evidence also suggests that in progenitor cell-mediated liver regeneration, hepatic stellate cells may, through a process of mesenchymal to epithelial transition, give rise to hepatocytes (21). Supporting the involvement of stellate cells in liver regeneration, inhibiting activated hepatic stellate cells using gliotoxin (79) and l-cysteine (80) prevents normal regenerative responses of both hepatocytes and oval cells in acetaminophen and 2AAF/PH-induced liver injuries, respectively. In addition, Foxf1+/ mice subjected to CCl4 injury show decreased hepatic stellate cell activation and more severe hepatocyte necrosis during the regenerative period (81). Notably, the mechanisms by which activated hepatic stellate cells help mediate liver regeneration in human patients and experimental animals remain to be determined and the relative importance of different subtypes of hepatic stellate cells/myofibroblasts is likely to depend on the nature of the initial insult.

Activated hepatic stellate cells produce a wide array of cytokines and chemokines (2). These factors may directly enhance the proliferation of liver progenitor cells and hepatocytes, or they may act indirectly through sinusoidal endothelial cells and immune cells to promote regeneration (ref. 2 and summarized in Figure ). Conditioned media collected from hepatic stellate cells harvested from rats during early liver regeneration following 2AAF/PH injury contain high levels of HGF and promote oval cell proliferation (82). One potential mediator of HGF production by hepatic stellate cells is the neurotrophin receptor P75NTR, which is expressed in human hepatic stellate cells following fibrotic liver injury. Murine hepatic stellate cells deficient for P75NTR do not differentiate properly into myofibroblasts in vitro or following liver injury induced by fibrin deposition in plasminogen-deficient (Plg/) mice (83). Consequently, HGF production and hepatocyte proliferation are impaired in P75NTR;Plg double-mutant mice (83). Hepatic stellate cell differentiation can be restored by constitutively active Rho in P75NTR-deficient hepatic stellate cells in vitro (83). These findings support a model in which P75NTR promotes hepatic stellate cell activation via Rho, and activated stellate cells secrete HGF to stimulate hepatocyte proliferation during regeneration (83). Hh signaling is another important mediator of hepatic stellate cellhepatocyte interactions during regeneration. Culture-activated hepatic stellate cells synthesize sonic hedgehog (Shh), which serves as an autocrine growth factor for these cells (84). In vivo, Hh ligands induce hepatocyte proliferation after PH (85).

The biological processes that are influenced by hepatic stellate cells are indicated in blue. At early phases of liver regeneration, hepatic stellate cells promote the proliferation of liver progenitor cells and hepatocytes. They also stimulate angiogenesis in the wounded area and assist in the recruitment of hematopoietic stem cells and immune cells to the liver (reviewed in ref. 48). Recent studies suggest that activated hepatic stellate cells may undergo a mesenchymal-to-epithelial transition to transdifferentiate into liver progenitor cells. At late phases, hepatic stellate cells participate in the termination of regeneration, likely via high expression of TGF-. Hepatic stellate cells have also been proposed to contribute to HCC development, potentially through dysregulation of some aspects of liver regeneration described above. On the other hand, liver fibrosis, which results from ectopic hepatic stellate cell activation, has controversial roles in HCC. Most evidence suggests that fibrosis promotes HCC, but it is possible that in some clinical settings fibrosis and HCC might occur due to the same underlying factor(s) rather than one promoting the other.

Notably, activated hepatic stellate cells are the main source of matrix metalloproteinases and their inhibitors that participate in ECM remodeling. The production of cytokines and remodeling of the ECM are likely to be coupled, as the ECM is capable of sequestering biologically active molecules (86, 87). Thus in addition to directly secreting cytokines, activated hepatic stellate cells may modulate their function by cleaving or releasing cytokines from the ECM.

Liver regeneration is a multistep process involving both initiation and termination of liver growth. The liver stops regenerating when it attains the mass required for the needs of the organism (88). The most well-known hepatocyte antiproliferative factor is TGF-, and one of the primary TGF-producing cell types in the liver are hepatic stellate cells (89). How do hepatic stellate cells mediate both the initiation and cessation of liver regeneration? As mentioned earlier, conditioned medium collected from hepatic stellate cells at early phases of liver regeneration in a 2AAF/PH injury model contains high levels of HGF. This strong mitogen may override the antiproliferative effect of TGF-1 (82). In contrast, at terminal phases of liver regeneration, hepatic stellate cells produce high levels of TGF-1, which inhibits hepatocyte proliferation and even induces apoptosis. Serotonin has been shown to increase expression of TGF-1 in cultured primary mouse hepatic stellate cells via the 5-hydroxytryptamine 2B (5-HT2B) receptor, and 5-HT2B inhibition promotes hepatocyte proliferation following PH, BDL, and CCl4-induced liver injury (90). Thus, hepatic stellate cells may change their cytokine expression profile during the process of liver regeneration, regulating both its initiation and termination.

To fully characterize the role of hepatic stellate cells in liver regeneration, their specific ablation would be highly useful, ideally at different time points in the regenerative process. While some chemical tools, including gliotoxin (79) or l-cysteine (80), exist for selective inhibition of hepatic stellate cells in rodent models, the possibility that these drugs also affect other hepatic cell types is difficult to exclude. A recent study indicates that hepatic stellate cells can be depleted in mice by using the GFAP promoter to drive the herpes simplex virusthymidine kinase gene expression, rendering proliferating hepatic stellate cells susceptible to gancyclovir-induced death (20). An advantage of this new model is the ability to target proliferating hepatic stellate cells in vivo without affecting quiescent hepatic stellate cells or other myofibroblasts. However, hepatic stellate cells cannot be completely ablated using this model, as GFAP is not universally expressed in these cells.

Any single animal model is unlikely to completely mimic all relevant aspects of human liver regeneration, particularly given that the cellular and molecular pathways mediating regeneration are likely to vary somewhat depending on the nature of the initial injury. Therefore, future studies of hepatic stellate cells in liver regeneration will be facilitated by the availability of multiple animal models, which are likely to yield complementary insights. Advantages of rodent models include the ability to isolate, culture, and activate hepatic stellate cells in vitro, facilitating follow-up cell culture studies focused on molecular mechanisms involved in regeneration. On the other hand, the excellent live-imaging technologies available in zebrafish are well suited for studying the cellular interactions at play during the regenerative process. As with rodents, PH or toxic chemicals can be used to induce liver regeneration in zebrafish (reviewed in ref. 74). Genetic tools have enabled the development of additional regeneration models including the nitroreductase/metronidazole cell ablation system (91) and morpholino-based knockdown of a mitochondrial import gene to induce hepatocyte death (92). One promising approach is to perform high-throughput chemical screens in various zebrafish models of liver injury, seeking drugs that affect stellate cells during liver regeneration (24).

While promotion of hepatocyte proliferation and liver regeneration may be desirable in some clinical settings, aberrant activation of such processes can also be associated with human diseases, most notably HCC (summarized in Figure ). The majority of human HCCs occur in the setting of clinically significant fibrosis or cirrhosis (93), implicating hepatic stellate cells in their pathogenesis as the major ECM-producing cell type of the liver. The associations between HCC and fibrosis are incompletely understood, but likely involve inflammatory cells, integrin signaling, growth factor interactions with the ECM, and communication between activated hepatic stellate cells and tumor cells (reviewed in ref. 94). Activated hepatic stellate cells are present between endothelial cells and cancer cell trabeculae in patients with HCC (95), and conditioned media from activated hepatic stellate cells increases proliferation and migration of human HCC cells (96). Thus, most evidence suggests that fibrosis promotes HCC, but it is possible that in some clinical settings fibrosis and HCC might occur due to the same underlying factor(s) rather than one promoting the other.

Chemical compounds such as N-nitrosodiethylamine, CCl4, and aflatoxin B1 cause HCC in rodents that is preceded by chronic liver injury, mimicking the injury-fibrosis-malignancy sequence that characterizes most human HCCs (97). However, tumor phenotypes in these models are dependent on animal age, strain, and the route of drug administration, and tumor latency can be quite long (97). On the other hand, liver tumors induced genetically in mice via expression of growth factors such as TGF-, oncogenes such as Myc, and viral proteins such as HBX are more tractable but are not usually preceded by substantial fibrosis (98, 99). Thus, the opportunity for studying hepatic stellate cellHCC interactions in transgenic mouse models of HCC has been somewhat limited, with the notable exception of the PDGF-C transgenic mouse (100). These mice, whose hepatocytes express human PDGF-C, show hepatic stellate cell activation and collagen deposition followed by hepatomegaly and HCC. These in vivo findings correlate with in vitro studies demonstrating that PDGF-C promotes the proliferation, survival, and migration of fibroblasts and pericytes (101).

Interactions between hepatic stellate cells and HCC cells in vivo have also been studied by co-transplanting hepatic stellate cells and malignant hepatocytes into immunocompromised mice. These studies have implicated TGF- signaling (102, 103) and regulatory T cells (104) as mechanisms by which hepatic stellate cells may promote HCC growth. On the other hand, experiments performed in lecithin retinol acyltransferasedeficient mice have revealed ways by which HCC growth might be inhibited via targeting of hepatic stellate cells (105, 106). These mice lack retinoid-containing lipid droplets in hepatic stellate cells, exhibit increased retinoic acid signaling, and show decreased tumor formation in response to diethylnitrosamine, suggesting that altering retinoic acid signaling in stellate cells may inhibit HCC growth.

Zebrafish develop liver tumors that are morphologically and genetically similar to human HCC (107110). Similar to many rodent models, zebrafish HCC models are not typically preceded by cirrhosis, although co-expression of hepatitis B virus X and hepatitis C virus core proteins in zebrafish liver leads to fibrosis and cholangiocarcinoma (111). This model may thus be useful to study hepatic stellate cell interactions with primary liver tumor cells in vivo.

While many pathways that mediate hepatic stellate cellHCC interactions have been implicated (reviewed in ref. 94), the effects of specifically inhibiting or activating these pathways in vivo have not been fully explored. Driving expression of candidate positive or negative regulators specifically in hepatic stellate cells or creating stellate cellspecific gene knockouts could be useful in this regard. A major challenge for these experiments, as in studies of hepatic stellate cell development, is the identification of promoters with improved specificity. Similarly, improved techniques for ablating or inhibiting hepatic stellate cells could help tease out the role of these cells at different time points in HCC formation. Such studies could help define when and how hepatic stellate cells could be targeted to prevent or treat HCC.

A more efficient way to detect HCC could profoundly improve prognosis by enabling earlier diagnosis and more effective treatments. New HCC biomarkers that have been proposed include molecules produced by hepatic stellate cells, such as HGF and IGF (112). Patients with HCC also show elevated plasma levels of TGF-1 (113) and osteopontin (114), compared with patients with chronic hepatitis and/or cirrhosis. As many of the same factors are produced by hepatic stellate cells during cirrhosis and during carcinogenesis, it is likely that a combination of biomarkers will be required to optimize early HCC detection.

Studies of hepatic stellate cell behavior during development, regeneration, and tumor formation using cell culture and animal models have provided substantial insights regarding the cellular and molecular mechanisms involved in these processes. It will be crucial to identify promoters with improved cell type specificity, as they will facilitate hepatic stellate cellspecific manipulations, including gene knockouts and cell ablation. Given the critical roles that hepatic stellate cells play in diverse aspects of liver pathophysiology, this intriguing cell type represents a major, and mostly untapped, potential reservoir for the development of therapies targeting a wide variety of human liver diseases, ranging from acute liver failure to drug-induced liver injury to HCC.

The authors thank Jacquelyn Maher for her critical comments and support. C. Yin is supported by grant K99AA020514 from the NIH and the University of California San Francisco Liver Center Pilot/Feasibility Award (NIH grant P30DK026743). K.J. Evason is a Robert Black Fellow supported by the Damon Runyon Cancer Research Foundation (grant DRG-109-10). K. Asahina is supported by a grant from the NIH (R01AA020753). Our work on hepatic stellate cells and liver development was further supported by grants from the NIH (R01DK060322) and the Packard Foundation (to D.Y.R. Stainer).

Conflict of interest: The authors have declared that no conflict of interest exists.

Citation for this article:J Clin Invest. 2013;123(5):19021910. doi:10.1172/JCI66369.

Chunyue Yins present address is: Division of Gastroenterology, Hepatology and Nutrition, Cincinnati Childrens Hospital Medical Center, Cincinnati, Ohio, USA.

Didier Y.R. Stainiers present address is: Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.

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Hepatic stellate cells in liver development, regeneration, and cancer

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Samer A. Srour, MB, ChB, MS, Reviewed Findings of CB-NK Cells and Elotuzumab Regimen in High-Risk Multiple Myeloma – Cancer Network

Posted: July 3, 2022 at 2:43 am

Samer A. Srour, MB, ChB, MS, assistant professor in the Department of Stem Cell Transplantation and Division of Cancer Medicine at the University of Texas MD Anderson Cancer Center, spoke with CancerNetwork at the 2022 American Society of Clinical Oncology (ASCO) Annual Meeting about results observed in a phase 2 (NCT01729091) which assessed the use of umbilical cord bloodderived natural killer cells with elotuzumab (Empliciti), lenalidomide (Revlimid), and high-dose melphalan (Evomela) followed by autologous stem cell transplantation for patients with high-risk multiple myeloma.

Srour noted a progression-free survival (PFS) rate of 83% and an overall survival (OS) rate of 97% among patients who were treated with the regimen.

This expansion phase 2 cohort was included in the final platform of elotuzumab, lenalidomide, and the cord bloodderived expanded [natural killer] cells. We started this in early 2018, and we accrued the last patient in early 2021, so over 2 years. Despite COVID, we were able to accrue very well on this study. Now we have mature data after an immediate follow-up of 26 months for these 30 patients who all have high-risk multiple myeloma. Historically, we know the median survival is short, [about] less than 3 to 5 years, and with all the new treatments in myeloma, we were not able to overcome much of the resistance in [many] of the high-risk patients.

Thirty patients were included in this study over a 2 plus year period. The primary end point was best response rate on day 100 after transplant, [including] VGPR, very good partial response or better, and MRD [minimal residual disease] negativity at day 100 after transplant. We gave this regimen in the context of the transplant. Patients took elotuzumab, lenalidomide, and high-dose melphalan [followed by] the [natural killer] cells. After that, we gave them back their autologous stem cells, and then they were engrafted as with any other [patients with] myeloma. They engrafted on time within 10 to 11 days from the transplant. We looked at the best response at 3 months after transplant before getting any other treatments. We found out that the VGPR or better was 97%. We dont see that in the high-risk [patients with] myeloma. The MRD negativity rate was 75%. [This is also rarely] seen in high-risk [patients with] myeloma even after transplant.

The primary endpoint was very impressive for us. We waited over 2 years to show [whether] this MRD-negativity rate and the VGPR translate to better progression-free survival [PFS] and overall survival [OS]. We found out that the 2-year PFS was 83%which historically [has been] around 60% or lessand then the OS was 97%. Only 1 patient died from COVID-19 infection.

This is a new regimen, and its being used in a new era where theres many other treatments; maybe the outcomes are better because of other confounders. We looked around the same time period of 2018 to 2021, and we chose a control of high-risk [patients with] myeloma who were treated with us at MD Anderson. We looked at the data to compare our study patients to these control patients who were treated homogeneously in the same way, but without the [natural killer] cells without the elotuzumab without the lenalidomide. We found a statistically significant improvement in our study patients compared [with] the control. In the control arm, the 2-year, PFS was only 60%, and the 2-year OS was only 83%. Thats compared [with] 83% PFS in our study and 97%; it is statistically significant.

Srour SA, Mehta RS, Shah N, et al. Phase II study of umbilical cord bloodderived natural killer (CB-NK) cells with elotuzumab, lenalidomide, and high-dose melphalan followed by autologous stem cell transplantation (ASCT) for patients with high-risk multiple myeloma (HRMM). J Clin Oncol. 2022;40(suppl 16):8009-8009. doi:10.1200/JCO.2022.40.16_suppl.8009

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Samer A. Srour, MB, ChB, MS, Reviewed Findings of CB-NK Cells and Elotuzumab Regimen in High-Risk Multiple Myeloma - Cancer Network

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WATCH: How to donate your stem cells to help people in need as Easter Ross family issue fresh appeal for daughter – RossShire Journal

Posted: July 3, 2022 at 2:43 am

AT Piping Inverness, reporters Imogen James and Rachel Smart added themselves to the stem cell donor database in a bid to become the perfect match for an Easter Ross three-year-old.

Josie Davidson, of Alness, suffers from a rare genetic mutation and her parents are desperately seeking a match so she can undergo a bone marrow transplant.

Blood cancer charity DKMS had a stall at Piping Inverness in Bught Park yesterday and it only takes a few simple steps to potentially save a life.

First, you have to fill out a simple form with your contact information.

Next, you take two swabs and rub them against your the inside of your cheek for a minute.

Then you take the final swap and rub it in the same place again.

You have to let all three air dry for about 30 seconds, then they are packaged up by the helpful volunteers and sent away to be added to the list.

You will be contacted about a month later with your details.

The process could not be simpler.

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WATCH: How to donate your stem cells to help people in need as Easter Ross family issue fresh appeal for daughter - RossShire Journal

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Global Circulating Tumor Cells (CTCs) and Cancer Stem Cells (CSCs) Market Application, Trends, Growth, Opportunities and Worldwide Forecast 2022 To…

Posted: July 3, 2022 at 2:43 am

Insights of Global Circulating Tumor Cells (CTCs) and Cancer Stem Cells (CSCs) Market from 2022 to 2028, according to MarketsandResearch.biz, is a specialist and in-depth analysis of the sector with a specific focus on the Key Trends. The study aims to give readers a high-level overview and thorough segmentation by kind, end-use, application, and area. Over the projection period of 2022-2028, global growth is expected to be strong. The report looks into competing variables critical for moving your company to the next level of development.

The market rise in trends for this industry is then estimated in this study. This section also looks at upstream raw materials, downstream demand, and actual market movements. In addition, the market study examines the global Circulating Tumor Cells (CTCs) and Cancer Stem Cells (CSCs) industry in terms of market segmentation, regional coverage, growth factors, and market difficulties.

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Emerging market players in the worldwide market:

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CellSearch, Others,

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Breast Cancer Diagnosis and Treatment, Prostate Cancer Diagnosis and Treatment, Colorectal Cancer Diagnosis and Treatment, Lung Cancer Diagnosis and Treatment, Other Cancers Diagnosis and Treatment,

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North America (United States, Canada and Mexico), Europe (Germany, France, United Kingdom, Russia, Italy, and Rest of Europe), Asia-Pacific (China, Japan, Korea, India, Southeast Asia, and Australia), South America (Brazil, Argentina, Colombia, and Rest of South America), Middle East & Africa (Saudi Arabia, UAE, Egypt, South Africa, and Rest of Middle East & Africa)

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Global Circulating Tumor Cells (CTCs) and Cancer Stem Cells (CSCs) Market Application, Trends, Growth, Opportunities and Worldwide Forecast 2022 To...

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Stem Cells Cryopreservation Equipments Market Insights 2022 And Analysis By Top Keyplayers Chart, Worthington Industries, Cesca Therapeutics,…

Posted: July 3, 2022 at 2:43 am

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Stem Cells Cryopreservation Equipments Market Insights 2022 And Analysis By Top Keyplayers Chart, Worthington Industries, Cesca Therapeutics,...

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Cellectis Publishes Article in Nature Communications Unveiling Novel Immune-Evasive Universal Allogeneic CAR T-cells with Potential for Improved…

Posted: July 3, 2022 at 2:43 am

NEW YORK, June 30, 2022 (GLOBE NEWSWIRE) -- Cellectis (the Company) (Euronext Growth: ALCLS NASDAQ: CLLS), a clinical-stage biotechnology company using its pioneering gene-editing platform to develop life-saving cell and gene therapies, today publishes research data on its novel immune-evasive universal CAR T-cells in Nature Communications, following an oral presentation at the American Society of Cell and Gene Therapy (ASGCT) on May 16.

Cellectis next generation of universal CAR T-cells have the potential to improve the persistence and to allow large-scale deployment of T-cell product candidates in allogeneic settings against multiple malignancies.

Universal CAR T-cell therapies are poised to revolutionize the treatment of selected hematologic malignancies. However, realizing the full potential of CAR T in an allogeneic setting requires universal CAR T-cells that can kill target tumor cells, avoid depletion by the host immune system via the host versus graft reaction (HvG), and proliferate without attacking host tissues via the graft versus host reaction (GvH).

While the prevention of GvH can be readily addressed by the inactivation of T cell receptor T (TCR) expression in a CAR T-cell, prevention of HvG remains a major challenge.

To address this challenge, the Cellectis investigators engineered CAR T-cells to be deficient in Class 1 major histocompatibility complex (MHC-1) and to express the Natural Killer (NK) inhibitor HLA-E, in order to endow them with immune-evasive properties toward alloreactive Tc ells and NK cells.

This engineering approach is very promising and could enable the universal CAR T-cells to become transiently invisible to NK and alloreactive T-cells, allowing them to eradicate tumor cells before being rejected by the patients immune system. This could enable the broad use of universal CAR T-cells in allogeneic settings, for the benefit of a wider population of patients, said Julien Valton, Ph.D., Vice President Gene Therapy at Cellectis.

One potential advantage of this approach is to spare endogenous immune effectors and allow them to work in concert with CAR T-cells in the fight against hard-to-treat cancers, including solid tumors, said Laurent Poirot, Ph.D. Senior Vice President Immuno-Oncology at Cellectis.

The research data show that:

This article is available on Nature Communications website by clicking on this link:https://www.nature.com/articles/s41467-022-30896-2

About Cellectis

Cellectis is a clinical-stage biotechnology company using its pioneering gene-editing platform to develop life-saving cell and gene therapies. Cellectis utilizes an allogeneic approach for CAR-T immunotherapies in oncology, pioneering the concept of off-the-shelf and ready-to-use gene-edited CAR T-cells to treat cancer patients, and a platform to make therapeutic gene editing in hemopoietic stem cells for various diseases. As a clinical-stage biopharmaceutical company with over 22 years of expertise in gene editing, Cellectis is developing life-changing product candidates utilizing TALEN, its gene editing technology, and PulseAgile, its pioneering electroporation system to harness the power of the immune system in order to treat diseases with unmet medical needs. As part of its commitment to a cure, Cellectis remains dedicated to its goal of providing lifesaving UCART product candidates for multiple cancers including acute myeloid leukemia (AML), B-cell acute lymphoblastic leukemia (B-ALL) and multiple myeloma (MM). HEAL is a new platform focusing on hemopoietic stem cells to treat blood disorders, immunodeficiencies and lysosomal storage diseases.

Cellectis headquarters are in Paris, France, with locations in New York, New York and Raleigh, North Carolina.

Cellectis is listed on the Nasdaq Global Market (ticker: CLLS) and on Euronext Growth (ticker: ALCLS).

For more information, visit http://www.cellectis.com

Follow Cellectis on social media: @cellectis, LinkedIn and YouTube

For further information, please contact:

Media contacts:

Pascalyne Wilson, Director, Communications, +33776991433, media@cellectis.com Margaret Gandolfo, Senior Manager, Communications, +1 (646) 628 0300

Investor Relation contact:

Arthur Stril, Chief Business Officer, +1 (347) 809 5980, investors@cellectis.com Ashley R. Robinson, LifeSci Advisors, +1 (617) 430 7577

Forward-looking StatementsThis press release contains forward-looking statements within the meaning of applicable securities laws, including the Private Securities Litigation Reform Act of 1995. Forward-looking statements may be identified by words such as anticipate, believe, intend, expect, plan, scheduled, could, would and will, or the negative of these and similar expressions. These forward-looking statements, which are based on our managements current expectations and assumptions and on information currently available to management. Forward-looking statements include statements about the potential of our research or preclinical programs. These forward-looking statements are made in light of information currently available to us and are subject to numerous risks and uncertainties, including with respect to the numerous risks associated with biopharmaceutical product candidate development. With respect to our cash runway, our operating plans, including product development plans, may change as a result of various factors, including factors currently unknown to us. Furthermore, many other important factors, including those described in our Annual Report on Form 20-F and the financial report (including the management report) for the year ended December 31, 2021 and subsequent filings Cellectis makes with the Securities Exchange Commission from time to time, as well as other known and unknown risks and uncertainties may adversely affect such forward-looking statements and cause our actual results, performance or achievements to be materially different from those expressed or implied by the forward-looking statements. Except as required by law, we assume no obligation to update these forward-looking statements publicly, or to update the reasons why actual results could differ materially from those anticipated in the forward-looking statements, even if new information becomes available in the future.

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Cellectis Publishes Article in Nature Communications Unveiling Novel Immune-Evasive Universal Allogeneic CAR T-cells with Potential for Improved...

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Market Share, Supply, Analysis and Forecast of Human Insulin Drugs and Delivery Devices to 2026 Designer Women – Designer Women

Posted: July 3, 2022 at 2:41 am

The GlobalHuman Insulin Delivery Drugs and DevicesMarket will grow from its initial estimated value of USD 33.78 billion in 2018 to an estimated value of USD 61.38 billion by 2026, registering a CAGR of 7.75 % over the forecast period 2019-2026.This increase in market value can be attributed to the increasing incidence of diabetes and diabetic patients around the world.The increased incidence of diabetes may be linked to the unhealthy lifestyle and diet of the larger percentage of the population.

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Segmentation: Global Human Insulin Drugs and Delivery Devices Market

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Competitive Analysis: Global Human Insulin Drugs and Delivery Devices Market

The global human insulin delivery devices and drugs market is highly fragmented and the major players have used various strategies such as new product launches, expansions, agreements, joint ventures, partnerships, acquisitions, and others to increase their presence in this market.The report includes Human Insulin Delivery Devices and Drugs market shares for Global, Europe, North America, Asia-Pacific, South America, Middle- East and Africa.

Key Market Competitors: Global Human Insulin Drugs and Devices Market

Some of the major competitors currently operating in the human insulin drugs and delivery devices market include Novo Nordisk A/S, Eli Lilly and Company, Sanofi, B. Braun Melsungen AG, BD, Biocon, Albireo Pharma Inc., Julphar, WOCKHARDT, CeQur SA, Ypsomed, AstraZeneca, Boehringer Ingelheim International GmbH, Johnson & Johnson Services Inc., Novartis AG, Takeda Pharmaceutical Company Limited, Bayer AG and Merck & Co. Inc.

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Babys Cells Can Manipulate Moms Body for Decades

Posted: July 3, 2022 at 2:40 am

Sure, it looks cute now, but a new study explores why babies influence their moms' DNA for years. PeopleImages/iStock

Mothers around the world say they feel like their children are still a part of them long after they've given birth. As it turns out, that is literally true. During pregnancy, cells from the fetus cross the placenta and enter the mother's body, where they can become part of her tissues.

This cellular invasion means that mothers carry unique genetic material from their childrens bodies, creating what biologists call a microchimera, named after the legendary beasts made of different animals. The phenomenon is widespread among mammals, and scientists have proposed a number of theories for how it affects the mother, from better wound healing to higher risk of cancer.

Now a team of biologists argues that to really understand what microchimerism does to moms, we need to figure out why it evolved in the first place.

What we are hoping to do is not only provide an evolutionary framework for understanding how and why microchimerism came to be, but also to assess how this affects health, says lead author Amy Boddy, a geneticist at Arizona State University.

Maternal-fetal conflict has its origins with the very first placental mammals millions of years ago. Over evolutionary time, the fetus has evolved to manipulate the mother's physiology and increase the transfer of resources like nutrition and heat to the developing child. The mother's body in turn has evolved countermeasures to prevent excessive resource flow.

Things get even more intriguing when fetal cells cross the placenta and enter the mother's bloodstream. Like stem cells, fetal cells are pluripotent, which means they can grow into many kinds of tissue. Once in the mother's blood, these cells circulate in the body and lodge themselves in tissue. They then use chemical cues from neighboring cells to grow into the same stuff as the surrounding tissue, Boddy says.

Although the mother's immune system typically removes unchanged fetal cells from the blood after pregnancy, the ones that have already integrated with maternal tissues escape detection and can remain in mom's body.

Microchimerism can get especially complex when a mother has multiple pregnancies. The mother's body accumulates cells from each babyand potentially functions as a reservoir, transferring cells from the older sibling into the younger one and forming more elaborate microchimeras. The presence of fetal cells in the mothers body could even regulate how soon she can get pregnant again.

I think one promising area for further research concerns unexplained pregnancy losses, and whether older siblings, as genetic individuals, can play a role in delaying the birth of younger siblings, says David Haig, an evolutionary biologist at Harvard University.

Given all this complexity, microchimeras have been difficult to study until recently, the authors note in their paper, which will be published in an upcoming issue of BioEssays. The phenomenon was discovered several decades ago, when male DNA was detected in the bloodstream of a woman. But the technologies of the time couldn't get a detailed enough picture of the genetics to tease apart the minute cellular situation.

Now, deep-sequencing technologies allow researchers to identify the origin of DNA in a mother tissues more comprehensively by sampling many areas in the genome, including genes implicated in immunity. These genes are unique to an individual and thus can help differentiate a mothers DNA from that of her children with greater precision.

If the cell populations can be isolated, then modern techniques should allow the genetic individual of origin to be unambiguously identified, says Haig.

Still, understanding how the fetal cells are interacting with maternal cells is going to be difficult, says Boddy. Little is understood about the cellular signaling that causes fetal cells to regulate maternal physiology.

Its likely a negotiation between the maternal body and the fetal cells, where there is an expectation in the maternal body of a certain level of microchimerism that it needs to function properly, said Boddy. For example, previous experiments showed that when mouse fetal cells are exposed to lactation hormones in the lab, they take on similar attributes to those of mammary cells, hinting that breast tissue may be one hot spot for microchimerism.

Normal, healthy lactation may be the consequence of the fetal cells signaling to the mothers body to make milk, says co-author Melissa Wilson Sayres, also at Arizona State. But previous work has also suggested that the same features that allow fetal cells to integrate into the mothers tissueslike evading her immune systemalso makes them similar to cancer cells, which could lead to greater cancer vulnerability in the mother.

Based on evolutionary reasoning, the authors predict that fetal cells should be found primarily in the tissues that play a role in transferring resources to the fetus. That includes the breast, where they may impact milk production; the thyroid, where they can affect metabolism and heat transfer to the baby; and the brain, where they may influence neural circuitry and maternal attachment to the child.

The next steps will be to use modern sequencing tools to go looking for fetal cells in these spots, and then begin studying how the cells are communicating in each region of mom's body.

What is really interesting and novel about this work is putting the issue of microchimerism and maternal health into an evolutionary framework, says Julienne Rutherford, a biological anthropologist at the University of Illinois at Chicago.

If these fetal cells are interacting with maternal physiology, where in the maternal body would we expect the greatest effect on function? Thats been a big question mark. Putting this into an evolutionary context was incredibly clever and novel and very exciting. Its a beautiful example of theory driving testable predictions."

EDITOR'S NOTE: This story has been updated to clarify the results of the study on mouse fetal cells and mammary tissue.

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Cell Expansion Market Projection By Top Key Players, Regional Analysis Revenue Forecast Till 2030 Designer Women – Designer Women

Posted: July 3, 2022 at 2:40 am

New York(United States):- According to Report Ocean research report Global Cell Expansion Market: Analysis By Product Type (Instruments, Consumables, Disposables), By Cell Type (Human Cell and Animal Cell), By Application (Regenerative Medicine & Stem Cell Research and Cancer & Cell Based Research), By Region (North America, Europe, Asia Pacific, South America, and Middle East & Africa), (U.S, Canada, Germany, France, U.K., Japan, China, India): Opportunities and Forecast (2019 Edition): Forecast to 2024-, the cell expansion market is projected to display a robust growth represented by a CAGR of 17.33% during 2019 2024.

A comprehensive research report created through extensive primary research (inputs from industry experts, companies, stakeholders) and secondary research, the report aims to present the analysis of cell expansion market. The report analyses the Global Cell Expansion Market: Analysis By Product Type (Instruments, Consumables, Disposables), By Cell Type (Human Cell and Animal Cell), By Application (Regenerative Medicine & Stem Cell Research and Cancer & Cell Based Research), By Region (North America, Europe, Asia Pacific, South America, and Middle East & Africa), (U.S, Canada, Germany, France, U.K., Japan, China, India): Opportunities and Forecast (2019 Edition): Forecast to 2024, for the historical period of 2018-2019 and the forecast period of 2019-2024.

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Over the recent years, cell expansion market has been witnessing considerable growth directly on the back of increasing prevalence of chronic diseases such as cancer, diabetes, osteoarthritis, etc. Moreover, factors such as increasing investment in healthcare research, growing government initiatives, increasing adoption rate of new and technically instruments, rapidly evolving applicable segment market has been providing momentum to the overall market growth of cell expansion.

In addition, increasing demand for technically advanced products such as automated cell expansion systems and increasing number of cell GMP-certified cell expansion facilities are anticipated to fuel the market growth in forecasted period. However, recalls due to product failures have been hindering the market growth.

The report titled Global Cell Expansion Market: Analysis By Product Type (Instruments, Consumables, Disposables), By Cell Type (Human Cell and Animal Cell), By Application (Regenerative Medicine & Stem Cell Research and Cancer & Cell Based Research), By Region (North America, Europe, Asia Pacific, South America, and Middle East & Africa), (U.S, Canada, Germany, France, U.K., Japan, China, India): Opportunities and Forecast (2019 Edition): Forecast to 2024:-has covered and analysed the potential of cell expansion market and provides statistics and information on market size, shares and growth factors. The report intends to provide cutting-edge market intelligence and help decision makers take sound investment evaluation. Besides, the report also identifies and analyses the emerging trends along with major drivers, challenges and opportunities. Additionally, the report also highlights market entry strategies for various companies.

Scope of the Report

Global Cell Expansion Market (Actual Period: 2014-2018, Forecast Period: 2019-2024)

Cell Expansion Market Size, Growth, ForecastAnalysis By Product Type:Instruments, Consumables, Disposables.Analysis By Cell Type:Human Cells and Animal Cells.Analysis By Application Type:Regenerative Medicine & Stem Cell Research and Cancer & Cell Based Research.Regional Cell Expansion Market North America, Europe, Asia Pacific, South America, and Middle East & Africa (Actual Period: 2014-2018, Forecast Period: 2019-2024)

Cell Expansion Market Size, Growth, ForecastAnalysis By Product Type: Instruments, Consumables, Disposables.Analysis By Cell Type:Human Cells and Animal Cells.Analysis By Application Type:Regenerative Medicine & Stem Cell Research and Cancer & Cell Based Research.Country Cell Expansion Market U.S., Canada, Germany, U.K, France, China, Japan, India (Actual Period: 2014-2018, Forecast Period: 2019-2024)

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Cell Expansion Market Size, Growth, ForecastAnalysis By Product Type: Instruments, Consumables, Disposables.Analysis By Cell Type:Human Cells and Animal Cells.Analysis By Application Type:Regenerative Medicine & Stem Cell Research and Cancer & Cell Based Research.

Other Report HighlightsMarket Dynamics Drivers and Restraints.Market Trends.Porter Five Forces Analysis.SWOT Analysis.

Company Analysis Merck Millipore, Eppendorf, ThermoFisher Scientific, Becton Dickinson, Danaher Corporation, Corning Inc., Terumo Medical Corporation, CellGenix Technologie Transfer GmbH, Synthecon Inc., Stem Cell Technologies Inc.

Table of Content:

Key Questions Answered in the Market Report

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