The
switching between the more mature and the stem-like states has
been intensely studied in melanoma (Sharma et al, 2010; Hoek and
Goding, 2010), where the bidirectional switching, that is, the
reversibility of differentiation of CSC into multiple cell types, long
thought to be an one-way process, supports the emerging notion
that CSCs do not represent a static mutant clone but rather a
functional state that can be induced in some cells under some
conditions (Gupta et al, 2009a; Dirks, 2010; Gerlinger et al, 2012)
Hi,
One mechanism proposed is that the dysregulation of p53 during oncogenesis can support de-differentiation. Supporting this is the publication showing that reprogramming of somatic cells to iPS cells becomes more efficient in the absence of p53.
Hong, H. et al., Suppression of induced pluripotent stem cell generation by the p53-p21 pathway. Nature 460 (7259), 1132-1135 (2009).
Hello
i agree with Maurice Canham absence of p53 one of important reason for return cancer cell to CSC .
find link here will help you Good Luck
http://www.hope4cancer.com/stem-cells.html
http://www.nature.com/srep/2012/120607/srep00441/full/srep00441.html
http://www.stembook.org/node/613
http://link.springer.com/book/10.1007%2F978-1-4614-0809-3
http://www.intechopen.com/books/cancer-stem-cells-theories-and-practice
http://www.ncbi.nlm.nih.gov/pubmed/11689955
Trans-differentiation and de-differentiation of relatively differentiated cancer cells defined as progenitor cells are considered to be due to the plasticity with epigenetic regulation. Tumor tissue including several kinds of histology is likely to exhibit this phenomenon after the anti-cancer treatment which provokes redox stress, hypoxic stress, UPR with unfolded protein accumulation, and chronic inflammation.
That is the million dollar question!
If a common pathway were found that could be activate (or inactivated), cancer could be cured.
- Badges
- Science topic
- Similar topics
- Medicine
- Oncology
- Cancer Research
- Cancer Biology
- Cancer Cells
- Cancer Stem Cells