Showing posts with label molecular biology. Show all posts
Showing posts with label molecular biology. Show all posts

Sunday, March 24, 2013

INTERESTING FACTS

Most Oncologists get more practice changing information from the JCO and the New England Journal of Medicine than from BLOOD which has turned "Molecular" on them!  Blood has become more of a research tool than of impact on day to day Oncology/Hematology practice.  A balance is needed guys over there!  Even the Lancet is now better perceived by "practitioners"!
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*Researchers keeps ahead of Oncology practice, and that is good.
While we are still coming or waking to the reality of the existence of Crizotinib.

Crizotinib

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Crizotinib
Systematic (IUPAC) name
3-[(1R)-1-(2,6-dichloro-3-fluorophenyl)ethoxy]-5-(1-piperidin-4-ylpyrazol-4-yl)pyridin-2-amine
Clinical data
Trade names Xalkori
MedlinePlus a612018
Licence data US FDA:link
Pregnancy cat. D (US)
Legal status -only (US)
Routes Oral
Pharmacokinetic data
Half-life 46 hours
Identifiers
CAS number 877399-52-5 
ATC code L01XE16
PubChem CID 11626560
DrugBank DB08700
ChemSpider 9801307 Yes
UNII 53AH36668S Yes
KEGG D09731 Yes
ChEMBL CHEMBL601719 Yes
Synonyms PF-02341066
1066
Chemical data
Formula C21H22Cl2FN5O 
Mol. mass 450.337 g/mol
  (what is this?)  (verify)
Crizotinib (trade name Xalkori,[1] Pfizer), is an anti-cancer drug acting as an ALK (anaplastic lymphoma kinase) and ROS1 (c-ros oncogene 1) inhibitor, approved for treatment of some non-small cell lung carcinoma (NSCLC) in the US and some other countries, and undergoing clinical trials testing its safety and efficacy in anaplastic large cell lymphoma, neuroblastoma, and other advanced solid tumors in both adults and children.[2]
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RESEARCHERS ARE MOVING FORWARD
LOOKING NOW IN COMBINATION OF
1.  FIG-ROS1
2.  SLC34a2-ROS1
3.  COEXISTENCE  OF EGFR AND ROS1

THIS IS A GOOD SIGN.
IT IS ONCE AGAIN A SIGN OF HOW A CELLULAR PROCESS GETS COMPLICATED QUICKLY JUST AS YOU START UNDERSTANDING.

LESS THAN 0.5% OF ONCOLOGIST HAVE USED CRIZOTINIB TO DATE!

Saturday, December 29, 2012

AS WE SEARCH FOR THE CURE, IT IS IMPORTANT TO REMEMBER THAT:
Molecular Biology offers tremendous opportunities to fight cancer.  In fact, it is surprising that we seem so early (or late, depending on how you understand this) in the game.  The cell can be affected in so many ways that we are late reacting. Using integrated methods and our computer abilities, we should by now be involved in developing patterns of attacks by cancer cell type.
We should define clearly the major drivers by type of cancer, and pick the counter attacks specifically per type of cancer.  We should be at the stage where each patient who presents to us has his genotype defined, changes in his membrane receptors described, driver mutations enunciated,  status of P53,  level of major Cyclins and various cell protections (P-gp, Bcl-2), status and quantitative expression of transcription factors, expression of Metastatic potential (E-Cadherin, Metallo-protease, TGF), histone conformation, level of Endonuclases, status of mitotic speed, types of protein Anchor at cell membranes, and Kinesins (Kif2a,b,c) and so on so forth, all spelled out on his file!

IT IS ONLY WITH THIS LEVEL OF DEFINITION, THAT WE CAN PICK AND CHOOSE AN APPROPRIATE TREATMENT, OR UNDERSTAND THE SHORTCOMINGS OF OUR CURRENT STANDARD TREATMENTS.  Computers should also be used to tell us if combination treatments should be used sequentially or concurrently, and at which sequences, order and time our therapeutics should be given.

Molecular Biology, so many "distractions" and stuff that some scientists are spending days on, and may lead to something some day, but as we work in a race against death situation, and people are dying every day, it is time to pause and regroup, look at how to create this panel per patient, and develop computer supported patterns of therapy.  And every 2-5 years make a stop, update our computer and reload for the Cure!