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Showing posts with the label cancer stem cell

Hypothesis on cancer

As far as I have heard and read; 1.Cancer stem cell Cancer behaves like a stem cell. It can divide indefinitely and can differentiate into the other cell type. 2.Field cancerization Cancer occurs when the normal cell has been chronically exposed to the carcinogens. Then the molecular genetics have been changed along the way until the injured cell loses control in cell division. 3.Mutator phenotype It relies on the fact that the machinery of DNA replication has been less effective over time and causing the error in replication, which leads to DNA mutations. Besides, DNA repair also contributes to the mutator phenotype. Defective in DNA repair causes the accumulated DNA mutations. All of these factors, in turn, change the cellular division regulation and thereby leading to carcinogenesis. What else?

Quick note for RSPO3 antagonism inhibits growth and tumorigenicity in colorectal tumors harboring common Wnt pathway mutations

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Paper: RSPO3 antagonism inhibits growth and tumorigenicity in colorectal tumors harboring common Wnt pathway mutations doi: 10.1038/s41598-017-15704-y I would like to start with my rough drawing since it can help me recognize by heart now. The concept of this paper relies on Wnt signaling that contributes to the growth of colorectal tumors. Mutation of genes in Wnt pathway that related to CRC is beta-catenin, APC and RNF43 and these type of mutations are found 90% of CRC. My understanding, this paper points out the microenvironment supporting the tumor growth. Not only Wnt ligand but also R-spondin is the ligand that can activate the Wnt signaling pathway. Wnt binds to the Fz directly whereas R-spondin (RSPO) quantitatively control RNF43. RSPO binds to RNF43 which leads to proteasomal degradation, therefore, controlling the availability of Fz on the membrane. It was shown that RSPO3 antagonism worked effectively with RSPO gene fusion type (RSPO-PTPRK) in CRC...

Quick note; Cancer: Tumours build their niche

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I have read the news and view in the nature which summarizes two articles demonstrating the tumor cells, esp. lung adenocarcinomas (advanced and aggressive stage) divided and gave rise to two cell populations. ( doi :10.1038/nature22494) 1. tumour cells - actively dividing cells 2. supporting cell or so called "niche cell" - which provide the microenvironment to support the growth of the tumour cells Picture indicates the tumour cell divides and gives rise to two subpopulations (a). Within the tumour tissue, there are two cell subpopulations, one support the growth of tumour by which it secretes the growth factor that can stimulate the tumour cell growth (b). Question remains; supporting cell can secrete and promote the cancer growth in the other cancer type besides the its own neighbouring cells