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Oncogenesis and Metastasis
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Cell are supported by surrounding connective tissue—stroma.Stroma has a structural and supportive role.Connects different cell populations.Source of nutrients—vascular network.Allows immune cells to weave through to their target.
Regulation and Targeting of MUCINS in Pancreatic Cancer
Published in Surinder K. Batra, Moorthy P. Ponnusamy, Gene Regulation and Therapeutics for Cancer, 2021
Shailendra K. Gautam, Abhijit Aithal, Grish C. Varshney, Parthasarathy Seshacharyulu
Pancreatic cancer (PC) is the 4th leading cause of cancer-related mortalities in the United States with an estimated 56,770 new cases and more than45,750 deaths in 2019 [1]. Despite the clinical advances and ongoing efforts in therapeutic management, PC is predicted to be the second leading cause of cancer-related deaths in the United States by 2030 [2]. Its asymptomatic nature attributed to the worst five-year survival rate in PC patients, late diagnosis, early metastasis, un-resectability, high recurrence rate, drug resistance, and immunosuppressive tumor microenvironment (TME) [3–6]. Only less than 20% PC patients who were eligible for resection, showed improved survival rates [7, 8]. In all other cases, survival did not improve significantly, emphasizing the need for novel therapeutic approaches in PC management. A better understanding of PC pathogenesis associated genetic and epigenetic regulations, molecular mechanisms and altered signaling pathways, metabolic alterations and mechanisms of drug resistance, tumor microenvironment, and immunosuppression, is essential to improve the ongoing diagnostic and therapeutic approaches [4, 5]. In addition, efforts are also needed to be directed towards the biomarker development for early detection and targeted therapies in a combination of immunotherapy and anti-stromal therapies for better therapeutic response in PC patients.
Comparative Anatomy and Physiology of the Mammalian Eye
Published in David W. Hobson, Dermal and Ocular Toxicology, 2020
The choroidal stroma varies from being darkly pigmented to a complete absence of pigmentation depending on the species, breed, and individual. In those animals lacking pigmentation, the fundic reflex appears red and on ophthalmoscopic examination the choroidal vessels are visible. The stroma itself is composed of collagen fibrils, melanocytes, fibroblasts, nerves, and larger blood vessels.3,33 The majority of the vessels are veins with arteries situated among them. The arteries have a capillary-free zone surrounding them. Associated with the arteries are nonmyelinated nerve fibers, most of which are motor fibers to the smooth muscle of the arteries.
COL28 promotes proliferation, migration, and EMT of renal tubular epithelial cells
Published in Renal Failure, 2023
Linlin Li, Hong Ye, Qiaoling Chen, Lixin Wei
COL28 was evaluated in obstructive nephropathy. COL28 staining in renal tubules increased with the aggravation of obstructive lesions (Figure 2(A–B)). In the UUO mouse models, H&E and Masson’s staining showed that renal tubules were dilated, flattened, and detached in the UUO1W group. A few inflammatory cells infiltrated the stroma. The expression of COL28 was significantly increased in the UUO1W group, and all tubules were stained, especially the dilated tubules (Figure 2(C–F)). In the UUO2W group, renal tubule atrophy and necrosis were obvious. Renal interstitial fibrosis was obvious. The staining of COL28 was most obvious in the renal tissues of the UUO2W group, especially in the atrophic tubules, showing block-like staining (Figure 2(C–F)). Compared with the CON and UUO1W groups, the total renal histopathological score and fibrotic area percentage of the UUO2W group were higher (both p < 0.05), while the expression of COL28 in the UUO2W group was increased compared with the UUO1W group (Figure 2(G–H)). We collected the pathological sections of eight mice in the control, UUO1W, and UUO2W groups, carried out COL28 immunohistochemistry and Masson staining, and analyzed the correlation between the optical density of COL28 staining and the collagen volume fraction of Masson staining. The results showed that the optical density of COL28 staining in mice was positively correlated with the volume fraction of collagen. It is suggested that with the aggravation of renal fibrosis in mice, COL28 staining is also gradually increased (Figure 2(I)).
Modulating multidrug resistance to drug-based antitumor therapies through NF-κB signaling pathway: mechanisms and perspectives
Published in Expert Opinion on Therapeutic Targets, 2023
Dapeng Wu, Sai Tian, Wenjing Zhu
Mesenchymal stem cells (MSCs) are known for being multi-potent, implicated in a wide range of physiological events including maintenance of tissue homeostasis and organogenesis as well as tissue repair and regeneration. Various studies have shown that the tumor stroma plays crucial roles in the survival, growth, metastatic progression, and chemotherapy resistance of cancer. MSCs derived from multiple myeloma (MM-MSCs) activate the NF-κB signaling pathway, and inhibition of NF-κB signaling by NF-κB inhibitor IκBα could reverse the protective effect of MM-MSCs on multiple myeloma cells from chemotherapy [68]. Moreover, inhibition of IL−1β sensitizes the acute myeloid leukemia cells co-cultured with MSCs to chemotherapy through a NF-κB/IL−1β signaling network [69]. Collectively, the roles of NF-κB signaling in TME give it a status in drug resistance, and the underlying mechanisms need further investigation.
Cancer-associated fibroblasts and the tumor microenvironment in non-small cell lung cancer
Published in Expert Review of Anticancer Therapy, 2022
Jun Suzuki, Masahiro Tsuboi, Genichiro Ishii
As with targeted therapies for cancer cells, the possibility of regulating the tumor stroma by targeting specific proteins expressed by stromal cells has long been explored. Studies in the late 1990s and the early 2000s using sibrotuzumab, a 131I-radiolabelled anti-FAP monoclonal antibody targeting activated CAFs, found no clinical benefit during the phase I trial in patients with advanced or metastatic FAP-positive cancers, including NSCLC, or the subsequent phase II trial in colorectal cancer. This may be because the antibodies might not mediate antibody-dependent cytotoxicity against FAP-expressing stromal cells [113,128,129]. In the 2000s, methods for binding drugs to anti-FAP antibodies and eliminating FAP-positive cells, including cancer cells and CAFs, were reported using the endogenous protease activity of FAP, but none of these methods passed the clinical phase [130–132].