Ovarian Cancer

*Researchers who conducted the study who conducted the use of Selumetinib in low grade serous Ovarian cancer were still puzzled because its activity did not follow presence of KRAS or BRAF. They have been wondering if it used another pathway.  But remember MEK is the revolving door to de-differentiation and to the reversal of mesengialization and as such increase tor susceptibility not only to chemotherapy drugs, but also to the secondary angiogenic potentiation of MEK.  That is, with anti-MEK, there is a down regulation of MAPK (as suggested) and therefore  the C-JUN and TGF and cyclins, but also down regulation of the VEGF!

They say " Our results suggest that selumetinib is an active agent, but not necessarily because of BRAF or KRAS mutational activation per se,” the authors concluded.

In an interview, Gershenson said that one reason for the lack of correlation could be biomarker instability. Among the 52 patients, specimens were available for only 40, mutational analysis was done in 34, and in 28 of those the tissue was from the primary therapy and not from the recurrent tumor. “The question arises, are these biomarkers stable over time or do they change, so that what you find in the primary tumor may not be what you find in the recurrent tumor,” he said."   They suggesting here that the lack of correlation could be due to a changing nature of Biomarker.  But the existence of other factors and pathways could not be be excluded!

Gene-Expression Profiling May Help Select Best Drugs for Pancreatic Cancer

Caroline Helwick 

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In this study patient with pancreatic cancer had reportedly circulating cell and their genes could predict response to therapy but unfortunately they did not spell out which genes were reviewed.  We will investigate further this article...

INTERESTING DEBATES

1.NF1 Mutation is upstream from
BRAF
and MTOR
But NF-1 is Mutated in Melanoma
can infusion of protein resulting from NF-1 be used to strengthen effect of MTOR inhibitor and BRAF inhibitor by maintaining these pathways open!

2.  Discriminating Redundancy in cellular language
same gene base corresponding to same Amino Acid
same receptors at membrane being sensitive by different stimuli
but when it comes to the RAS, nature and intensity need to matter and this also a function of tissue involved!
some time however the nature of the stimulus is more important particularly inside the cell where ie HP90 seems to stimulate more the CoN to achieve PTEN suppression. And you know that CoM stimulation raise Bcl2 level...we will say more in our upcoming article of langaue of the cell as it pertains to pathways!

3. PTEN is repressed by low expression of gene or mislocalization (reported PNUTS 'role) at Nuclear level or both?

Attended Mark G Kris lecture on Lung Cancer  (KRIS IS FROM MSKCC)

Now genetic sequencing is important

Prescribe the following

1)  EGFR-------------ERLOTINIB, GEFITINIB
2)  ALK-----------------CRIZOTINIB
3) HER-2--------------HERCEPTIN, LAPATINIB
4) BRAF -------------------VEMURAFENIB
5) ROS-1-----------------CRIZOTINIB  (AGAIN)
6) RET--------------------------VANDETANIB  (CABOZANTINIB)
7)MET------------------------CRIZOTINIB (AGAIN)

NICE THE PRESCRIPTION SPELLING OUT ONLY THE GENE SEQUENCING, AND LET YOUR PHARMACIST DO THE REST.
QUESTION: COULD THESE DRIVER GENE ABNORMALITIES BE THE SAME IN TRIPLE NEGATIVE BREAST CANCER?

We believe in the cure for Cancer:

People talk about a cure and skeptics balk!
But the cure is possible and actually exists already in every survivor who had a remote history of cancer.
Remember this, a cancer cell is full of messages encrypted in chemical messages when to grow, when to start aging and when to die.  Yes cancer cells have an internal message when to start apoptosis (self destruction).
It means you could tell it to start apoptosis and kill itself.  Our challenge is to know how to speak to a cell.
Research are starting to learn that language in what is now known as Target Therapy.  Cancer treatment is now becoming a Piano tune.  if you hit the right keys in a song and the cancer cell get it, it will find its way to self destruction.  We are at the early stage of this music, still learning it.  Hitting this key here and seeing what happens.  We are finding out that even tough cancers such as Melanoma, if you hit the BRAF key, things start happening.  In some lung cancers, if you hit the EGFR key, you start getting somewhere.  It is just a matter of time before we start asking to a cell, now time for an increase in BAX or Caspases, and self destruct.  The cell has some redundancy and networking to complicate the road to self destruction, but we still believe that with the right tune, cancer cells will dance to self destruction, and yes cure is within our reach!