Metastatic cancer to ovary

Product name Metastatic cancer to ovary
Cat. No. FA
Current version FA2
Data sheet FA2.pdf
No. of samples 59
No. of patients 59
Core diameter 2.0 mm
Section thickness 4 micrometer
Price 244 EUR
320 USD
210 GBP

Metastatic cancer to ovary metastatic adenocarcinoma     Metastatic cancer to ovary metastatic adenocarcinoma 02Metastatic cancer to ovary metastatic adenocarcinoma 03

Product Related Literature

Metastasis is a major cause of death in cancer patients. However, it does not have the capability to all the tumor is transferred. This potential depends on the factors that determine growth, angiogenesis, invasion, the basic process of other tumor cells. In epithelial tumors of many epithelial – it is assumed (EMT) is a major event in the metastatic process mesenchymal transition. Including the acquisition of migratory mesenchymal phenotype and destruction of epithelial cell homeostasis, migration EMT, the reverse is included in embryonic development epithelial phenotype (MET) from between the leaves. EMT is displayed as controlled by the canonical pathway as transforming growth factor β and WNT pathway such. An important feature of EMT is the loss of membrane E-cadherin in the tight junctions may play an important role in β-catenin. The transfer of β-catenin, loss of E-cadherine, can lead to EMT then to adhesive bonding from the nucleus. There is evidence that can be direct transfer E-cadherine gene repressor SLUG activates EMT-related genes and subject to nuclear β-catenin of.

Recent evidence supports the notion that cancer cells undergoing EMT is a precursor of metastatic cancer cells, it may transition CSCS further  was measured at the end of a subset of invasive pancreatic cancer cells (CXCL12 chemokine receptor, also known as SDF1 ligand) that CD133 + CXCR4 +. These cells showed migration activity significantly more than its corresponding CD133 + CXCR4 cells, both cell subsets showed tumor development similar capabilities. Furthermore, the inhibition of CXCR4 receptor results in a reduced metastatic potential without changing the tumorigenic capacity.

On the other hand, CD44 + CD24-/low cells in breast cancer has been detected in the metastatic pleural effusion. Meanwhile, it was identified by distant metastasis in breast cancer patients with an increase in the number of CD24 + cells. There is a data arbitration mechanism of metastasis in breast cancer, but few, cell it is a CD44 + CD24-/low possible, and spread to the first in a new location, they change the phenotype and differentiation is limited. Move cell cancer stem (SCS) and the fixed cancer stem cells (MCS) – These results are based on the presence of two forms of cancer stem cells, resulting in a new dynamic phase long-term expression. The SCS, are incorporated into the fabric, and held in separate areas throughout tumor progression. MCS term, describes the cell is a tumor host interface. There is evidence through the acquisition of transient EMT, these cells that is derived from the SCS.

It is a stage of breast cancer metastatic breast cancer disease has spread to distant metastasis. Typically, the number of years you happen to resection of primary breast cancer, which is a complication of primary breast cancer. In many cases, it is possible to develop resistance to several lines of prior treatment, metastasize to distant sites them, and get a special property, metastatic cells of breast cancer, that it is very dangerous they, It is different from the properties of primary breast cancer as a recipient of the previous conditions often. That have a poor prognosis in many cases, distant metastases, accounting for about 90% of deaths from breast cancer. Bone metastatic lymph node, and lung, liver, brain, mainly breast cancer is a bone in the most common site. On several nodes and surrounding sentinel lymph node, it is considered metastatic breast cancer and local events treatable, and to be later or when it occurs in the presentation of the original lymph node metastasis.

Physical (basement membrane), chemical (ROS or reactive oxygen species, hypoxia and low pH) and biological barriers typical environment in the event of metastatic extracellular matrix and regulations (immune surveillance inhibit cytokine (ECM ) peptide) component is included. Anatomical study of organ-specific effects on the transition also includes a blood flow pattern of the primary tumor, and targeting ability of cancer cells to specific tissues. Perhaps, the targeting of cancer cells to specific organs is regulated by adhesion molecules and chemoattractant factors derived from cell surface receptors and organ specific expression on tumor cells.

Heparanase, the line is disconnected to heparin sulfate HSPG you have a large network with several proteins in the ECM and cell surface. Is composed of core proteins, proteins containing fibronectin ECM various laminin, interstitial collagen, HSPG basic structure (HS) chains are covalently bound O-bound binding linear heparin sulfate some heparin-binding The lipoproteins.HSPGs, well-known components of the vessel and acts as an assembly growth factors, chemokines. Bind vascular endothelial growth factor in (VEGFs), HS stable FGF protects them from inactivation. It helps the GFS removal functions as a low-affinity co-receptor that promotes dimerization of FGF factor in circulating low concentration of growth factors, HS chains induces activation of the signal tyrosine kinase receptor further. It is expressed by cancer cells involved in angiogenesis and neovascularization deterioration of skeletal polysaccharide endothelial BM, therefore, heparanase release of angiogenic growth factors from the ECM.