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pranalipawarshinde · 3 years ago

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Solitary Fibrous Tumor Treatment Market Trends, 2021-2031

Healthcare Providers Increase Availability of Preventive & Curative Services During Coronavirus Pandemic

Healthcare utilization has repeatedly been observed to decrease during the ongoing COVID-19 pandemic. Such trends are affecting the growth of the solitary fibrous tumor treatment market. Many individuals still fear contracting the novel coronavirus infection. Hence, healthcare providers should increase the availability of preventive and curative services, especially for the most vulnerable populations such as older people, children, and for people living with chronic conditions.

Stakeholders in the solitary fibrous tumor treatment market are ensuring continuity of the delivery of essential healthcare services during the pandemic. They are taking efforts to adhere to government guidelines to reorganize and maintain safe access to essential health services. Pharmaceutical companies are maintaining optimum inventory levels to ensure robust supply of life-saving therapeutics.

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Lack of Evidence Base for Treatment Affecting Market Growth

The solitary fibrous tumor treatment market is expected to reach US$ 59.3 Mn by 2031. However, it has been found that there is no consensus guideline on the management of solitary fibrous tumors of the pleura (SFTP) and the evidence base for treatment is limited, resulting in large variations in care. Nevertheless, stakeholders are fueling their R&D efforts to increase the availability of treatments for solitary fibrous tumor (SFT).

Pazopanib holds promising potentials for advanced solitary fibrous tumor treatment. This multikinase inhibitor helps to address translocation-associated soft tissue sarcoma. Pazopanib therapy is being associated with radiological evidence of tumor response in many patients.

Multi-disciplinary Approach Holds Promising Potentials in Increasing Patient Outcomes

In order to increase patient outcomes, companies in the solitary fibrous tumor treatment market are increasing their research in a multi-disciplinary approach. They are mainly focusing on the identification of the hallmark NAB2-STAT6 fusion that is emerging as a foundation for future translational work to identify subtype-specific therapy for the subset of SFTs that require systematic treatments.

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Surgery remains the gold standard for increasing medical outcomes in the solitary fibrous tumor treatment market. On the other hand, antiangiogenic treatment is found to be effective for unresectable disease. There is a need for translational work to understand the biology driving the differential behavior of SFT and identify more effective treatments for patients with metastatic disease.

Adoption of Adjuvant Radiation Therapy Helps Control Subtotally-resected Pleural SFTs

The solitary fibrous tumor treatment market is projected to expand at a modest CAGR of 4.5% during the forecast period. Gross tumor resection remains the preferred choice for treatment of SFT. However, risk of blood loss, location, and adhesion might not always allow for this. This has led to the adoption of the adjuvant radiation therapy to achieve local control in subtotally-resected pleural SFTs.

The varying doses of external beam radiotherapy are being delivered to patients in order to improve clinical outcomes. Healthcare providers in the solitary fibrous tumor treatment market are gaining awareness that monitoring and surveillance of patients is important for better outcomes. As such, there is a need for further work on dedifferentiated SFT, which remains poorly understood.

Solitary Fibrous Tumor Treatment Market: Overview

Solitary fibrous tumor (SFT) is a very rare malignant condition that exhibits different clinical behaviors ranging from low to high aggressive SFT, with dedifferentiated SFT (DD-SFT) being the fastest-growing subtype

Solitary fibrous tumors can be classified by the site of origin: pleura, mediastinal, or pulmonary. The most common site of origin within the thorax is the pleura.

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Solitary Fibrous Tumor Treatment: Market Drivers

Increase in patient awareness about personal health boosts the demand for early diagnosis of rare cancer. Patients are more aware and proactive about their health and are willing to seek physician’s advice at an early stage.

Increase in per capita disposable income is encouraging people to spend more on healthcare, which, in turn, propels the global solitary fibrous tumor treatment market

Awareness initiatives have increased public visibility of new treatments and diagnostic methods, thereby generating interest among solitary fibrous tumor patients

Market Segmentation: Solitary Fibrous Tumor Treatment Market

In terms of treatment, the global solitary fibrous tumor treatment market has been classified into surgery, radiation therapy, and adjuvant chemotherapy

Based on end-user, the global solitary fibrous tumor treatment market has been divided into hospitals, ambulatory surgical centers, and clinics

Each of the segments has been analyzed in detail for trends, recent trends & developments, drivers, restraints, opportunities, and useful insights. The solitary fibrous tumor treatment market report provides current and future revenue (US$ Mn) for each of these segments for the period from 2017 to 2031, considering 2020 as the base year. The compound annual growth rate (percentage CAGR) has been provided for each segment and market from 2021 to 2031 along with market size estimations.

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Regional Overview: Solitary Fibrous Tumor Treatment Market

The global solitary fibrous tumor treatment market has been segmented into North America, Europe, Asia Pacific, Latin America, and Middle East & Africa. The regions have been divided into major countries and sub-regions.

The U.S. held significant share of the solitary fibrous tumor treatment market in North America in 2020. The country is expected to retain market share during the forecast period. Robust healthcare infrastructure and early adoption of advanced treatment procedures can be attributed to the U.S.’s dominance of the solitary fibrous tumor treatment market in the region.

Asia Pacific is likely to gain market share during the forecast period. Product launches, acquisitions, distribution agreements, alliances, and geographical expansion by players, especially in China and India, are projected to drive the solitary fibrous tumor treatment market in the region.

Current and future market sizes in terms of value (US$ Mn) of these regional markets and major countries have been provided in the solitary fibrous tumor treatment market report for the period from 2017 to 2031, along with their CAGRs for the period from 2021 to 2031

The study also offers a list of recommendations, highlights, and useful insights of the market, which are likely to help new companies willing to enter the solitary fibrous tumor treatment market and existing companies to increase market share and in the decision-making process

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Major Players

Pfizer, Inc.

F. Hoffmann-La Roche Ltd.

Eli Lilly and Company

Bayer AG

Novartis AG

About Us

Transparency Market Research, a global market research company registered at Wilmington, Delaware, United States, provides custom research and consulting services. The firm scrutinizes factors shaping the dynamics of demand in various markets. The insights and perspectives on the markets evaluate opportunities in various segments. The opportunities in the segments based on source, application, demographics, sales channel, and end-use are analysed, which will determine growth in the markets over the next decade.

Our exclusive blend of quantitative forecasting and trends analysis provides forward-looking insights for thousands of decision-makers, made possible by experienced teams of Analysts, Researchers, and Consultants. The proprietary data sources and various tools & techniques we use always reflect the latest trends and information. With a broad research and analysis capability, Transparency Market Research employs rigorous primary and secondary research techniques in all of its business reports.

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tumsozluk · 3 years ago

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Codiak BioSciences Announces Program Reprioritization and Corporate Restructuring

Codiak BioSciences, Inc. – Recruitment Continues in Phase 1 Clinical Trial of exoASO™-STAT6 Administered Intravenously in Patients With Advanced Hepatocellular Carcinoma – – Prioritize CEPI-funded vaccination program and advancement of engEx-AAV™ for gene delivery – – Plans to launch phase 2 studies on exoSTING™ and exoIL-12™ suspended – – Codiak expanding strategic discussions; align workforce…

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moleculardepot · 8 months ago

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Phospho-Stat6 (Tyr641) Rabbit APC Conjugate

Phospho-Stat6 (Tyr641) Rabbit APC Conjugate Catalog number: B2018691 Lot number: Batch Dependent Expiration Date: Batch dependent Amount: 10 ug Molecular Weight or Concentration: N/A Supplied as: Solution Applications: a molecular tool for various biochemical applications Storage: 2-8°C Keywords: Signal transducer and activator of transcription 6, IL-4 Stat Grade: Biotechnology grade. All…

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bostorbio · 3 years ago

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Boster Bio Anti-STAT6 Antibody Picoband™ catalog # PB9405. Tested in WB applications. This antibody (STAT6 antibody) reacts with Human, Rat.

#STAT6 antibody

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bloghealthcom · 4 years ago

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Vai trò của rối loạn vi sinh vật trong cơ chế bệnh sinh của viêm thực quản tăng Esinophil Update 07/2021

Bài viết Vai trò của rối loạn vi sinh vật trong cơ chế bệnh sinh của viêm thực quản tăng Esinophil Update 07/2021 được chia sẻ bởi website Blog-Health #bloghealth #suckhoe #lamdep #sinhly

Bài viết bởi Thạc sĩ, Bác sĩ Mai Viễn Phương - Khoa Khám bệnh & Nội khoa - Bệnh viện Đa khoa Quốc tế Vinmec Central Park

Cơ chế bệnh sinh viêm thực quản tăng Esinophil là một bệnh mãn tính qua trung gian miễn dịch của thực quản, đặc trưng bởi sự thâm nhiễm bạch cầu ái toan rõ rệt để đáp ứng với tế bào T helper type 2 (Th2). Các yếu tố như di truyền, môi trường, chất gây dị ứng và rối loạn vi khuẩn đường ruột đã được xác định là tác nhân gây ra bệnh mãn tính.

Dysbiosis là một thuật ngữ bao gồm sự thay đổi trong thành phần của hệ vi sinh vật kết hợp so với thành phần được tìm thấy ở những người khỏe mạnh. Khi phân biệt quần xã sinh vật của một thực quản khỏe mạnh bình thường với các trạng thái bệnh rối loạn sinh học, như viêm thực quản trào ngược, viêm thực quản tăng esinophil, Barrett thực quản hoặc ung thư biểu mô tuyến thực quản, rõ ràng là chứng rối loạn sinh học có thể xảy ra trước tình trạng viêm. Các sản phẩm vi khuẩn Gram âm kích hoạt thụ thể Toll-like-receptor có trên tế bào nội mô thực quản gây ra một đợt viêm, dẫn đến giãn cơ vòng thực quản dưới ở hạ lưu. Prevotella được tìm thấy nhiều hơn ở thực quản xa bị rối loạn sinh học, đã được chứng minh là nơi sản xuất chính của lipopolysaccharide, góp phần kích hoạt thụ thể Toll-like-receptor.

1. Viêm thực quản tăng Esinophil (EoE) do rối loạn vi khuẩn đường ruột

Cơ chế bệnh sinh viêm EoE là một bệnh mãn tính qua trung gian miễn dịch của thực quản, đặc trưng bởi sự thâm nhiễm bạch cầu ái toan rõ rệt để đáp ứng với tế bào T helper type 2 (Th2). Các yếu tố như di truyền, môi trường, chất gây dị ứng và rối loạn vi khuẩn đường ruột đã được xác định là tác nhân gây ra bệnh mãn tính.

Một số gen đã được xác định là những yếu tố góp phần tạo nên EoE, bao gồm lymphopoietin mô đệm (TSLP), calpain 14 (CAPN14), vi sinh vật thực quản SY, LRRC32, STAT6 và ANKRD27. Trong số các gen đã xác định, TSLP dường như là yếu tố chính gây ra tình trạng này, vì nó được kích hoạt bởi các tế bào biểu mô và gây ra sự biệt hóa Th2.

Các chất dị ứng khác nhau cũng gây ra một loạt triệu chứng làm tăng các dấu hiệu viêm, như IL-5 và IL-13, tạo ra một con đường viêm tiềm ẩn của EoE. Ngoài yếu tố di truyền và tiếp xúc với môi trường, rối loạn vi khuẩn đường ruột của thực quản được xem là một chất trung gian tác động trong quá trình sinh bệnh EoE.

Rối loạn vi khuẩn đường ruột có thể tác động đến quá trình bị bệnh viêm thực quản tăng Esinophil

2. Vai trò của hệ vi sinh vật

Phân tích hệ vi sinh vật ở EoE đã báo cáo sự gia tăng của vi khuẩn proteobacteria, đặc biệt là Neisseria spp. và Corynebacterium spp., ở trẻ em có EoE hoạt động. Nghiên cứu này kết hợp với bằng chứng về sự thay đổi hệ vi sinh vật đường ruột do sử dụng kháng sinh ở trẻ sơ sinh và sinh mổ, hỗ trợ thêm rằng chứng loạn khuẩn trong hệ vi sinh vật ở người có vai trò trong EoE.

Phân tích bằng một bài kiểm tra chuỗi thực quản để đánh giá hệ vi sinh vật của trẻ em và người lớn có EoE hoạt động cho thấy, lượng vi khuẩn Haemophilus spp dồi dào hơn. Đáng chú ý, cũng có sự giảm các đơn vị phân loại cụ thể của Clostridia ở những bệnh nhân có EoE hoạt động. Ở những con chuột được điều trị bằng thuốc kháng sinh, việc bổ sung hệ vi sinh vật chứa Clostridia ngăn ngừa sự nhạy cảm với một chất gây dị ứng thực phẩm cụ thể. Sự cảm ứng IL-22 bởi các tế bào lymphoid bẩm sinh có liên quan đến thụ thể RAR và tế bào T trong lớp đệm ruột, được đề xuất như là cơ chế ngăn chặn nhạy cảm với chất gây dị ứng thực phẩm. Các bằng chứng gần đây cho thấy, vi sinh vật thực quản có thể tham gia vào cơ chế bệnh sinh của EoE và đại diện cho các phương pháp điều trị mới.

3. Kết luận

Vi sinh vật thực quản đóng một vai trò chính trong cơ chế bệnh sinh của bệnh thực quản. Rối loạn vi khuẩn đường ruột có thể góp phần vào trạng thái tiền viêm, qua trung gian cytokine, bắt đầu ở lớp dưới niêm mạc. Hậu quả gây bệnh, ảnh hưởng đến niêm mạc thực quản, trước đây được cho là vì tổn thương niêm mạc do axit, nhưng hiện nay có vẻ là do đa yếu tố, trong đó vi sinh vật thực quản đóng vai trò chính. Hệ thực vật cụ thể gần đây đã được xác định có thể đóng một vai trò gây bệnh trong quá trình này.

Để được tư vấn trực tiếp, Quý Khách vui lòng bấm số HOTLINE hoặc đăng ký lịch trực tuyến TẠI ĐÂY. Tải ứng dụng độc quyền MyVinmec để đặt lịch nhanh hơn, theo dõi lịch tiện lợi hơn!

Tài liệu tham khảo: D'Souza SM, Houston K, Keenan L, Yoo BS, Parekh PJ, Johnson DA. Role of microbial dysbiosis in the pathogenesis of esophageal mucosal disease: A paradigm shift from acid to bacteria? World J Gastroenterol 2021; 27(18): 2054-2072 [DOI: 10.3748/wjg.v27.i18.2054]

source https://blog-health.com/vai-tro-cua-roi-loan-vi-sinh-vat-trong-co-che-benh-sinh-cua-viem-thuc-quan-tang-esinophil/

#bloghealth #suckhoe #lamdep #sinhly

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radrook2 · 5 years ago

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#proboards

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juniperpublisherscellscienc-blog · 6 years ago

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Development of Enpp1 Inhibitors as a Strategy to Activate Stimulator of Interferon Genes (STING) in Cancers and Other Diseases- Juniper Publishers

Abstract

Ecto-nucleotide pyrophosphatase/phosphodiesterase-1 (ENPP1/NPP1) is a membrane-bound nucleotide metabolizing enzyme that is implicated in a variety of physiological and pathological conditions. Recently, ENPP1 was discovered as the dominant 2’3’-cGAMP hydrolyzing enzyme. 2’3’-cGAMP is the endogenous STING agonist, generated from breakdown of cytosolic DNA by cGAS. Hydrolysis resistant 2’3’-cGAMP’s have been demonstrated to be potent activators of STING-dependent innate immunity and these are currently undergoing clinical trials in cancer. Here we discuss ENPP1 as a potential therapeutic target for activation of STING-dependent innate immune response.

Keywords: Innate immunity; STING; ENPP1/NPP1; Cytokines; Immunotherapies; Interferon; T-cell priming

Introduction

Innate immunity is the first response in the human body against pathogenic, or disease-causing stimuli. These stimuli can vary, and include viruses, perturbed normal tissue, and dying cancer cells. It is an important response, as it prevents continued proliferation of these pathogens and maintains a state of homeostasis within the body. It can also accommodate the development of a specific induced immune response during the first, or primary infection and, can therefore, establish inflammatory conditions. This induced response is specific because of the many different expressions that the cell surface gives off in the form of pattern recognition receptors, which can identify many of the molecules of life, such as, polysaccharides, glycoproteins, glycolipids, and nucleic acids [1].

The definition of innate immunity has altered over time. In earlier years, it was believed that innate immune response was premeditated. However, recent studies have shown that innate immunity is actually a specific response that results from damage or pathogen-associated molecular patterns (DAMP/PAMPs) [2]. In the initial phase, the innate immune system is able to coordinate inflammatory responses through cells of the hematopoietic compartment (neutrophils, macrophages and monocytes) and create conditions suitable for microbial clearance. In the second phase, other cells like dendritic cells are able to process antigens and present them on the surface in concert with major histocompatibility complex (MHC) to prime T-cells. This also allows the body to more effectively fight against infections of the same or similar type in the future. This “memory” is dependent on two specific types of cells: natural killer (NK) cells and macrophages. These cells provide crucial protection against reinfection in the immune system [3]. This “memory” found in innate immune systems is present in both vertebrate and invertebrate organisms.

Cytokines in Innate Immune Response

Cytokines are possibly the most indispensable component of the innate immune response. Cytokines are secreted by cells of the immune system and facilitate interaction between different types of cells. There are many different types of cytokines, and they are classified mainly by their biological functions. The main types of cytokines are: interferons (INFs), interleukins (ILs), transforming growth factors (TGFs), and tumor necrosis factors (TNFs) [4]. Interferons are the most commonly found type of cytokine in vertebrates and mammals and are crucial to mediate antiviral defense. To date, there have been three types of interferons discovered in vertebrates, and specifically mammals: Types 1, 2 and 3. Type 1 IFNs typically facilitate the antiviral response against microbial infection-causing pathogens. Type 2 IFNs also facilitate antiviral response, but at the same time, vitalize the process of phagocytosis and inhibit cell growth. Type 3 IFNs have been demonstrated to be strikingly similar in function to Type 1 IFNs [5,6]. Interleukins are a type of cytokines that also facilitate inflammatory responses in the immune system and help to stimulate cell growth [7]. Transforming growth factors (TGFs) regulate cell growth, help stimulate the growth of oocyte cells (which are found in the ovum), repair wounds inflicted upon the body, participate in immunosuppression, or reduce the activity of the immune system when naturally required [8]. Finally, tumor necrosis factors (TNFs) help to stimulate macrophages as they participate in the biological process of phagocytosis [9].

STING (Stimulator of interferon genes) as a DNA sensor

STING has been identified as a major signaling molecule that plays a pivotal role in innate immune response by inducing the production of interferons. STING is a cytoplasmic pattern recognition receptor activated by nucleic acid ligands known as cyclic dinucleotides (CDNs). These CDNs are generated by the DNA sensor cyclic GMP-AMP synthase (cGAS) using cytosolic DNA from extrinsic pathogens or endogenous aberrant self-DNA [10-12]. In case of tumors, it is probable that dying tumor cells are sources of dsDNA in the cytoplasm. In addition to CDN’s, STING can directly sense DNA and this dual sensing has been uncoupled with specific mutations in STING [10]. Activation of STING induces its binding with a kinase TBK1 (TANK-binding kinase 1) and further phosphorylation and dimerization of IRF3 (Interferon regulatory factor 3). IRF3 and another transcription factor that is activated by STING (STAT6) translocate to nucleus and bind to interferon promoters leading to production of type I interferons.

It is suggested that STING pathway is the main innate immune sensing pathway within tumor microenvironment and the main cell types in the tumor microenvironment that produce type I interferons are the dendritic cells [13,14]. In addition to the activation of STING pathway in response to tumor-derived DNA, dendritic cells prime T-cells by presenting tumor- associated antigens. These effects then create a signaling pathway, which allows T-cells, a main feature of the active immune response, to neutralize tumor cells [15,16]. Some tumor cells are able to “disguise” themselves to the innate immune response by upregulating immune checkpoints, or by having a lack of innate immune response within the tumor. A recent study reported that STING is epigenetically silenced in some cancers [17]. Additionally, oncoproteins from viruses such as human papillomavirus can bind and block activation of STING [18]. Thus, a cytosolic DNA sensing pathway is important for activation of innate immune response. In recent years, there has been considerable interest in the field of immune-oncology as well as an increase in the number of immunotherapies available [19,20].

ENPP1(Ectonucleotide Pyrophosphatase/Phosphodiesterase- 1) And Its Role in Innate Immunity

ENPP1 is a membrane bound enzyme that is an important regulator of extracellular inorganic pyrophosphate in osteoblasts and chondrocytes [21]. It is essential for prevention of soft tissue mineralization and ENPP1 deficient mice can have abnormal gait and progressive calcification in ectopic sites [22]. ENPP1 is responsible for hydrolysis of extracellular nucleotide triphosphates to produce inorganic pyrophosphates (PPi) [23]. Recent investigations have shown that ENPP1 plays a much larger role in limiting the innate immune response of the human body. It has been discovered that STING pathway is regulated by ENPP1[24]. ENPP1 was identified as the major hydrolase for the most potent endogenous CDN ligand for STING: 2’3’-cGAMP [25]. Importantly, it was demonstrated that denaturation of 2’3’-cGAMP can control the activation of the STING pathway [26]. Phosphothioate analogs of 2’3’-cGAMP resistant to ENPP1- mediated hydrolysis potently activate STING [25] and mediate anti-tumor responses. These analogs have now entered clinical trials as intra-tumoral injections in various advance cancers (Figure 1).

In another study, it was shown that Mycobacterium tuberculosis evades host immune response through a bacterial phosphodiesterase (CdnP) which inactivates host 2’3’-cGAMP. Loss of ENPP1 attenuated Mycobacterium tuberculosis infection, as did the inhibition of CdnP, the phosphodiesterase of Mycobacterium tuberculosis [27] More recently, inactivation of porcine ENPP1 was shown to attenuate pseudorabies infection through an interferon-β dependent response [28]. Many viruses generate antagonist proteins that can inactivate cGAS-STING pathway [29]. ENPP1 is differentially expressed in immune cells with low levels in NK cells, DC and macrophages and high levels in neutrophils [30]. ENPP1 is also expressed in a small subset of B-cells and studies suggest that these cells may be involved in modulation of T-cell activity [31]. Interestingly, ENPP1 expression was reported to be elevated in the M2 subtype of macrophages that are known to play a role in tumor promotion [28,32,33]. Other studies have indicated that expression of ENPP1 is increased in astrocytic tumors, breast cancers, and head and neck cancers [34-36]. Thus, inhibition of ENPP1 in humans may provide opportunities for treatment of cancers and pathogenic infections.

Challenges in Development of Inhibitors of ENPP1 for Human Use

Given the various functions for ENPP1 in regulating host immune responses, there is interest in development of ENPP1 inhibitors for human use. These inhibitors may have promising activity in human cancers and infectious pathologies. There are various practical challenges in development of these inhibitors. ENPP1 is a type II transmembrane glycoprotein that belongs to a family of ectonucleotide pyrophosphatase/phosphodiesterase (Enpp) family and consist of seven distinct proteins with distinct functions [37]. Thus, any inhibitor strategy will have to consider development challenges for specificity. In the published crystal structure of mouse ENPP1, there are important structural differences between ENPP2 and ENPP1. The N-terminal somatomedin-like (SMB) domains of ENPP1 do not interact with catalytic domains unlike those in ENPP2 [38,39]. ENPP1 appears to lack a hydrophobic pocket in contrast to ENPP2 although interdomain interactions are preserved [37-40]. Despite these challenges, our group and others have described novel selective and orally bioavailable inhibitors of ENPP1 [41-45].

Fundamental effects of ENPP1 inhibition on host immune response are still being determined. It is not known, for instance, if ENPP1 deficiency in mouse models impairs anti-tumor growth. Thus, optimal duration and intensity of ENPP1 inhibition is still being developed. This is important since systemic administration of these inhibitors can cause unwanted side effects due to excessive release of interferons. Interestingly, ENPP1 knockout mice are viable, thus pointing to possible avenues for development of such inhibitors. Prolonged administration of ENPP1 inhibitors may lead to unwanted effects on bony tissues and ectopic calcifications although this has been disputed in various studies in literature [46]. This is because bone and cartilage effects may not be entirely mediated by ENPP1. In other studies, oral administration of pyrophosphate can attenuate the connective tissue calcifications mediated by ENPP1 mutations in mouse models [47].

Conclusion

As hyper-activation of STING pathway may lead to production of abnormally high levels of proinflammatory cytokines, it is necessary to develop therapeutics that target STING pathway indirectly. Inhibition of ENPP1 activity is one approach that may result in optimal activation of STING pathway, enough to have anti-tumor effects, and minimize unintended consequences. Given the role of ENPP1 in immune modulation and tumor promotion, there is an increased interest to develop novel therapies based on inhibition of the ENPP1 activity and this will emerge as an interesting area in the coming years.

Acknowledgments

We thank Dr. Hariprasad Vankayalapati for advice in developing this review.

https://juniperpublishers.com/ijcsmb/IJCSMB.MS.ID.555655.php

For more Open access journals please visit our site: Juniper Publishers

For more articles please click on Journal of Cell Science & Molecular Biology

#Cell Science #Molecular biology #Stem cells #Open access journals #Juniper Publishers

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pranalipawarshinde · 3 years ago

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Solitary Fibrous Tumor Treatment Market Trends, and Forecast, 2021-2031

Healthcare Providers Increase Availability of Preventive & Curative Services During Coronavirus Pandemic

Read Report Overview@ https://www.transparencymarketresearch.com/solitary-fibrous-tumor-treatment-market.html

Lack of Evidence Base for Treatment Affecting Market Growth

Multi-disciplinary Approach Holds Promising Potentials in Increasing Patient Outcomes

Get Sample Copy of the Report@ https://www.transparencymarketresearch.com/sample/sample.php?flag=S&rep_id=37022

Adoption of Adjuvant Radiation Therapy Helps Control Subtotally-resected Pleural SFTs

Solitary Fibrous Tumor Treatment Market: Overview

Solitary fibrous tumors can be classified by the site of origin: pleura, mediastinal, or pulmonary. The most common site of origin within the thorax is the pleura.

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Solitary Fibrous Tumor Treatment: Market Drivers

Increase in per capita disposable income is encouraging people to spend more on healthcare, which, in turn, propels the global solitary fibrous tumor treatment market

Awareness initiatives have increased public visibility of new treatments and diagnostic methods, thereby generating interest among solitary fibrous tumor patients

Market Segmentation: Solitary Fibrous Tumor Treatment Market

In terms of treatment, the global solitary fibrous tumor treatment market has been classified into surgery, radiation therapy, and adjuvant chemotherapy

Based on end-user, the global solitary fibrous tumor treatment market has been divided into hospitals, ambulatory surgical centers, and clinics

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Regional Overview: Solitary Fibrous Tumor Treatment Market

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Major Players

Pfizer, Inc.

F. Hoffmann-La Roche Ltd.

Eli Lilly and Company

Bayer AG

Novartis AG

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