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
UNII	53AH36668S
KEGG	D09731
ChEMBL	CHEMBL601719
Synonyms	PF-02341066 1066
Chemical data
Formula	C21H22Cl2FN5O
Mol. mass	450.337 g/mol
SMILES[show]
InChI[show]
(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!

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!