Cancer is the common name for the set of illnesses interrelated in which it’s seen an uncontrolled process of cellular division. It could begin located and spread to another surrounding tissues. The biggest problem to control the disease is how they cells divide, because they can multiply their number without receive the signal of “now”. While normal cells stop dividing if there is genetic damage, cancer cells continue to divide. The results of this process is daughter cells which contain abnormal DNA or even abnormal number of chromosomes. These mutant cells are even more abnormal than their mother cells. So, cancer cells can evolve to become progressively more abnormal. This is not the only thing that cancer cells do abnormal, so how do cancer cells behave differently from healthy ones? And, how does cancer appear?
In Journal Cell Biology two articles have been published on May the 11th and say that an international consortium has identified new targets for cancer treatment which could be effective for the complete cure for some cancers, the articles are about a common issue and Professor Fry has said:
“Together, these two papers provide exciting new insights on how cells ensure that they faithfully pass on the right amount of genetic material to their offspring when they divide. They also highlight potential new targets for the development of novel cancer treatments”.
These papers identify a series of key steps that orchestrate the mechanics of cell division and highlight novel targets that could be inhibited to block cancer cell division, this is the main idea of the articles. Chaperones (proteins which are in every cell whose main functions are to promote the folding of proteins recently synthesized, assist in the proper folding of proteins after denaturing process and collaborate properly fold proteins that have been translocated into a cellular compartment), In the context of cancer, chaperones aren’t useful and work to protect cancer cells against the stressful environment of a tumour, and actually keep them alive. In this research chaperones have a really important paper, so companies are interesting in make chaperone inhibitors.
In the first paper they explain how As I explained before, when cancer cells divide they normally have more than the normal number of chromosomes and it is related with the need of a bigger number of proteins used for they division, proteins as Nek6, which is an enzyme so is protein-based, and Hsp72, which is a chaperone.
It was found that the kinase (enzyme that catalyzes the transfer of phosphate groups from high-energy, phosphate donating molecules) bound to Hsp72 and, during mitosis, phosphorylated a conserved specific aminoacid residue. This promoted Hsp72 recruitment to the mitotic spindle. Knocking down the chaperone caused mitotic HeLa cells (immortal cells used in experiments) to form fewer K-fibers, stable microtubule bundles that connect chromosomes to the spindle poles. As a result, chromosomes often failed to congress at the spindle equator during metaphase or failed to stay there once they had arrived, thus delaying anaphase onset. Hsp72 promoted the interaction between proteins ch-TOG and TACC3, essential for spindle pole organization. Both proteins were lost from mitotic spindles in the absence of either Hsp72 or Nek6. So Hsp72 and/or Nek6 could be used as therapeutic targets to inhibit cancer cell division.
The second document shows that there is another enzyme in the family of the Nek6 which could be useful, Nek5. Its functions is make sure that the centrosomes separate at right time. If Nek5 doesn’t work correctly centrosomes could separate late so it would generate mistakes in cell division that might cause cancer. The article suggest that targeting this proteins could help to find cure for the disease, or may be, in addition to other treatments it could be cured. Doctor Fry says again:
“If these proof-of-principle studies prove promising, then we would expect to launch the first clinical trials for drugs against these targets in cancer patients.”
How useful would be find a cure.
Obviously the original article have more technical terms, because it happens in every original source. I think that in the disclosure article there isn’t any process information, we can only read that chaperone, Nek6 and Hsp72 are involved in the experiment but it is impossible to understand what happens, so I had to look for the information in the original article, which is really difficult. I could only find the abstract but I think that in the complete article would explain how they discovered this, thing that does not appear in the disclosure article.
I chose this article because I am really interested in health, but I am conscious of the illness, because it affects million people in the world and, despite it works lots of times, it is still a big problem as people is yet dying and the secondary effects of the medication are really hard. I thought that despite being a difficult issue, people would be interesting in read it because there is no person who does not know anybody with this disease. I also chose this article because I normally read the page where I found the disclosure article and I had looked for this information before doing my post, because I am interested so I thouhgt that it was a good opportunity.