Modulation of mammary tumor vascularization by mast cells: Ultrasonographic and histopathological approaches

Faustino-Rocha, Ana I.; Gama, Adelina; Oliveira, Paula A.; Vanderperren, Katrien; Saunders, Jimmy; Pires, Maria dos Anjos; Ferreira, Rita; Ginja, Mário

doi:10.1016/j.lfs.2017.03.013

Cited by 7 publications

(6 citation statements)

References 56 publications

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“…The relationship between MC density of tumors, the progression of angiogenesis, and tumor development may highlight the possible role of MCs in tumor biology. Therefore, the possibility of targeting MC activation [67,68], inhibiting the release of mediators using c-Kit receptor tyrosine kinase inhibitors (TKI) (including imatinib, masitinib [69]), or using tryptase inhibitors (mainly gabexate mesylate and nafamostat mesylate, both inhibitors of trypsin-like serine proteases [69,70]) may be valuable therapeutic approaches to control the tumor development [71]. Masitinib, a TKI that targets c-kit receptors (CD117), has been used in veterinary medicine for years, and lately, human clinical trials were initiated to test its clinical efficacy as single or add-on treatment human cancers such as mastocytosis, gastrointestinal stromal tumors (NCT00998751), colon cancer (NCT03556956), prostate cancer (NCT03761225), and pancreatic cancer (NCT03766295) [72].…”

Section: Mcs As Therapeutic Targetsmentioning

confidence: 99%

Role of Mast Cells in Shaping the Tumor Microenvironment

Komi

Redegeld

2019

Clinic Rev Allerg Immunol

254

181

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Early mast cell (MC) infiltration has been reported in a wide range of human and animal tumors particularly malignant melanoma and breast and colorectal cancer. The consequences of their presence in the tumor microenvironment (TME) or at their margins still remain unclear as it is associated with a good or poor prognosis based on the type and anatomical site of the tumor. Within the tumor, MC interactions occur with infiltrated immune cells, tumor cells, and extracellular matrix (ECM) through direct cell-tocell interactions or release of a broad range of mediators capable of remodeling the TME. MCs actively contribute to angiogenesis and induce neovascularization by releasing the classical proangiogenic factors including VEGF, FGF-2, PDGF, and IL-6, and nonclassical proangiogenic factors mainly proteases including tryptase and chymase. MCs support tumor invasiveness by releasing a broad range of matrix metalloproteinases (MMPs). MC presence within the tumor gained additional significance when it was assumed that controlling its activation by tyrosine kinase inhibitors (imatinib and masitinib) and tryptase inhibitors (gabexate and nafamostat mesylate) or controlling their interactions with other cell types may have therapeutic benefit.

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Section: Mcs As Therapeutic Targetsmentioning

confidence: 99%

Role of Mast Cells in Shaping the Tumor Microenvironment

Komi

Redegeld

2019

Clinic Rev Allerg Immunol

254

181

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“…The administration routes that require less manipulation techniques are recommended [68]. In animal experimentation, several routes for substance administration are currently available, namely enteral (through the digestive tract), either oral (into the mouth) or gavage (esophageal, gastric, nasogastric or orogastric), intravenous (into a blood vessel), epicutaneous (onto the skin), intradermal (into the skin), subcutaneous (under the skin), transdermal (across the skin), intramuscular (into a muscle), transcorneal (onto the eye), intraocular (into the eye), intracerebral (into the brain), epidural (into the dura mater surrounding space), intrathecal (into distal spinal cord surrounding space), intraperitoneal (into the peritoneal cavity), intraosseous (into the marrow cavity), intranasal (sprayed into the nose and then absorbed by the nasal mucous membranes or into the lungs), intratracheal (into the lungs by direct tracheal instillation), inhalation, and other less common techniques, such as those using other body natural orifices, surgical exposure, and others regarding species-specific anatomic features [68,69,70,71,72].…”

Section: Administration Routesmentioning

confidence: 99%

Sugar-Lowering Drugs for Type 2 Diabetes Mellitus and Metabolic Syndrome—Strategies for In Vivo Administration: Part-II

Vieira

Souto

Sánchez-López

et al. 2019

JCM

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Diabetes is a complex disease characterized by hyperglycemia, together with polyuria, polydipsia, and polyphagia. While Type 1 diabetes mellitus (T1DM) results from genetic, environmental, or immune dysfunction factors leading to pancreatic β-cell destruction depriving the organism from endogenous insulin, Type 2 diabetes mellitus (T2DM) is characterized by peripheral insulin resistance. Depending on the type of diabetes mellitus and drug mechanism to study, the animal model should be carefully selected among the wide variety of the currently available ones. This review discusses the most common animal models currently employed to study T1DM and T2DM. Moreover, an overview on the administration routes that could be used is also discussed.

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“…The relationship between the presence of MCs in tumors, the progression of angiogenesis, and tumor development may increase the possible role of MCs in cancer biology. Therefore, blocking the release of mediators with KIT receptor tyrosine kinase inhibitors (TKIs) (for example, imatinib, mastinib) may affect MC function [128][129][130], while blocking the release of mediators with tryptase inhibitors (gabexate mesylate and nafamostat mesylate, both of which are inhibitors of trypsin-like serine proteases) [128,131] can be an important therapeutic treatment for reducing tumor growth [132].…”

Section: Targeted Therapiesmentioning

confidence: 99%

Genetic Changes in Mastocytes and Their Significance in Mast Cell Tumor Prognosis and Treatment

Zmorzynski,

Kimicka-Szajwaj,

Szajwaj

et al. 2024

Genes

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Mast cell tumors are a large group of diseases occurring in dogs, cats, mice, as well as in humans. Systemic mastocytosis (SM) is a disease involving the accumulation of mast cells in organs. KIT gene mutations are very often seen in abnormal mast cells. In SM, high KIT/CD117 expression is observed; however, there are usually no KIT gene mutations present. Mastocytoma (MCT)—a form of cutaneous neoplasm—is common in animals but quite rare in humans. KIT/CD117 receptor mutations were studied as the typical changes for human mastocytosis. In 80% of human cases, the KIT gene substitution p.D816H was present. In about 25% of MCTs, metastasis was observed. Changes in the gene expression of certain genes, such as overexpression of the DNAJ3A3 gene, promote metastasis. In contrast, the SNORD93 gene blocks the expression of metastasis genes. The panel of miR-21-5p, miR-379, and miR-885 has a good efficiency in discriminating healthy and MCT-affected dogs, as well as MCT-affected dogs with and without nodal metastasis. Further studies on the pathobiology of mast cells can lead to clinical improvements, such as better MCT diagnosis and treatment. Our paper reviews studies on the topic of mast cells, which have been carried out over the past few years.

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Modulation of mammary tumor vascularization by mast cells: Ultrasonographic and histopathological approaches

Cited by 7 publications

References 56 publications

Role of Mast Cells in Shaping the Tumor Microenvironment

Role of Mast Cells in Shaping the Tumor Microenvironment

Sugar-Lowering Drugs for Type 2 Diabetes Mellitus and Metabolic Syndrome—Strategies for In Vivo Administration: Part-II

Genetic Changes in Mastocytes and Their Significance in Mast Cell Tumor Prognosis and Treatment

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