State of Texas Letter to CPRIT Oversight Committee

http://governor.state.tx.us/files/press-office/3_Signature_Letter_to_CPRIT_Oversight_Committee_dated_12_18_12.pdf

El Paso non-existent on CPRIT Funding MAP

It is shocking to see, once again, that El Paso finds itself completely excluded from the Texas map of the Funding granted by CPRIT, the Cancer Prevention Research Institute of Texas.
                                              We intend to put El Paso on the Map again!

COMBINATION OF XELODA, AND ANTICALMODULIN AND AN ANTI-P35 ANTIBODY FOR TRIPLE NEGATIVE BREAST CANCER.,

OR TAXOTERE-XELODA-VELCADE-ANTI-P35

If the fighting cancer strategy is to disrupt the cell where it hurts the most, the above combinations make the most sense.  These combinations achieve the following:

1.  Disruption of Microfilaments/Microtubules which in turn disrupt Anaphases in dividing cancer cells.  This also disrupts membrane attachment of  Cytochromes in Mitochondria by disrupting the Cytoskeleton, and leads to Caspase release.
2. Xeloda leads to an increase of intracellular 5-FU and to DNA breakage which triggers activation of P53 induced stoppage of cell division.
3. The Anti-Calmodulin will add and increase an intracellular release of Calcium leading to stimulation of Endonucleases which will further damage the DNA.
4. The Anti-P35 decreases resistance to Caspases since P35 is an inhibitor of  Caspases.
5. To lead to growth advantage, most cancers get a mutation of the MDM2 which leads to increased ubiquitination proteins/cyclins  favorable to apoptosis, making Velcade a powerful drug as it disrupts the proteasomes!

With these combinations, we are trying to harvest the strongest destructive forces in a cell!

NON-CASPASE WAY TO CELL DEATH
ONE OF THE WAYS CELLS DIE WHICH IS NON-CASPASE DRIVEN MAY RESULT FROM DISRUPTION TO THE CONCENTRATION OF THE CYTOSOL OR SOLUTION WITHIN THE CELL.   HOMEOSTASIS REQUIRES THAT SOLUTION TO BE SET AT A CERTAIN CONCENTRATION IN TERMS OF ELECTROLYTES, OXYGEN AND PH.  THE CELL HAS ION PUMPS TO MAINTAIN ELECTROLYTE CONCENTRATION.  ELECTIVE DISRUPTION OF ION PUMPS WILL LEAD TO DISRUPTION OF CONCENTRATIONS THAT MAY SEND DEVASTATING BLOW TO THE CELL.   WATER GOES FROM LESS CONCENTRATED TO MORE CONCENTRATED ENVIRONMENTS.  THIS IS A POWERFUL KNOWN LAW OF NATURE.  IN CLINICAL PRACTICE, WE DON'T USE THIS LAW ENOUGH.  NOT BECAUSE IT IS NOT REAL
BECAUSE THIS IS HOW DIABETES KILLS ITS VICTIMS.  THIS IS HOW DEHYDRATION KILLS AND SO ON.   OUR CHALLENGE HAS BEEN HOW TO ELECTIVELY USE IT TO ATTACK ONLY CANCER CELLS.  FOR THIS WE NEED TO FIND OUT IF IONS PUMPS FROM CANCER CELLS ARE DIFFERENT FROM THOSE OF NORMAL CELLS.

(TO BE CONTINUED)

Staying in touch with London: All I want for Christmas... is to use genetic profiles in cancer drug resistance

As things begin to wind down for the Christmas holiday, the build up to the Targeting Cancer Drug Resistance meeting is still accelerating. I am pleased to announce that we have added an additional pre-conference workshop to the programme. Brian Van Ness of the University of Minnesota Cancer Center will be leading an interactive workshop demonstrating how you can use genetic profiles in pre-clinical modeling to identify response and resistance signatures, secondary therapies and combination therapies.  If you have a chance in this last week of work, download the new brochure to read more about Brian’s workshop and everything else available at the meeting. Have a browse of the event content if you get some free time over the holidays or as you let the Christmas dinner(s) digest. In the new year, courtesy of the Targeting Cancer Drug Resistance meeting, I will be sending you a series of unique material sharing insights on the developments towards creating therapies that successfully overcome drug resistance in cancer. So please keep an eye out for this. In the meantime I hope you have a wonderful Christmas holiday. Best regards, Suzi Suzanne Rankine Programme Director Hanson Wade

Leukemia inhibitory factor

From Wikipedia, the free encyclopedia

Leukemia inhibitory factor
PDB rendering based on 1LKI.
Available structures PDB Ortholog search: PDBe, RCSB [show]List of PDB id codes
Identifiers
Symbols	LIF; CDF; DIA; HILDA; MLPLI
External IDs	OMIM: 159540 MGI: 96787 HomoloGene: 1734 GeneCards: LIF Gene
[show]Gene Ontology
RNA expression pattern
More reference expression data
Orthologs
Species	Human	Mouse
Entrez	3976	16878
Ensembl	ENSG00000128342	ENSMUSG00000034394
UniProt	P15018	P09056
RefSeq (mRNA)	NM_001257135.1	NM_001039537.1
RefSeq (protein)	NP_001244064.1	NP_001034626.1
Location (UCSC)	Chr 22: 30.64 – 30.64 Mb	Chr 11: 4.26 – 4.27 Mb
PubMed search	[1]	[2]

Leukemia inhibitory factor, or LIF, is an interleukin 6 class cytokine that affects cell growth by inhibiting differentiation. When LIF levels drop, the cells differentiate.
Function LIF derives its name from its ability to induce the terminal differentiation of myeloid leukemic cells, thus preventing their continued growth. Other properties attributed to the cytokine include: the growth promotion and cell differentiation of different types of target cells, influence on bone metabolism, cachexia, neural development, embryogenesis and inflammation. p53 regulated LIF has been shown to facilitate implantation in the mouse model and possibly in humans.^[1] It has been suggested that recombinant human LIF might help to improve the implantation rate in women with unexplained infertility.^[2]

Binding/activation

LIF binds to the specific LIF receptor (LIFR-α) which forms a heterodimer with a specific subunit common to all members of that family of receptors, the GP130 signal transducing subunit. This leads to activation of the JAK/STAT (Janus kinase/signal transducer and activator of transcription) and MAPK (mitogen activated protein kinase) cascades.^{[citation needed]}

Expression

LIF is normally expressed in the trophectoderm of the developing embryo, with its receptor LIFR expressed throughout the inner cell mass. As embryonic stem cells are derived from the inner cell mass at the blastocyst stage, removing them from the inner cell mass also removes their source of LIF.

Use in stem cell culture

Removal of LIF pushes stem cells toward differentiation, but they retain their proliferative potential or pluripotency. Therefore LIF is used in mouse embryonic stem cell culture. It is necessary to maintain the stem cells in an undifferentiated state, however genetic manipulation of embryonic stem cells allows for LIF independent growth, notably overexpression of the gene Nanog.
LIF is not required for culture of human embryonic stem cells.^{[3][4]
==================================================================
These comments from Wikepedia introduce our discussion today,
first of all, patient with leukemia have their cells stopped at various stage of differentiation
meaning some are stopped at baby stage, some at teenager stage, some at adult stage. And at each stage, the leukemia takes a different Name, agressiveness and prognosis. In General, the younger the stage the bad/worse the prognosis. So there is a benefit to HELP ALONG THE CELL TO GROWTH, IT ACTUALLY IS HELPFUL FOR THE CELL TO MATURE SO THAT THE TUMOR GETS A GOOD OR BETTER PROGNOSIS.
AS A MATTER OF FACT, THE MORE MATURE THE CELL BECOMES, THE LESS LIKELY IT WILL DIVIDE REDUCING THE LOAD OF THE TUMOR.  THE MORE MATURE IT GETS, THE MORE LIKELY IT WILL GET OLD AND DIE OF A NATURAL DEATH. 
ON THE OTHER END HOWEVER, THE MORE LIKELY IT MATURES, THE MORE LIKELY IT MAY COMPLETE OR PERFORM ITS NATURAL FUNCTION. SO IF ITS FUNCTION WAS TO BE ABLE TO SPREAD, THE MATURE CELL CAN SPREAD FASTER.  THAT'S WHY SCIENTISTS ARE REPORTING THAT AN INHIBITOR TO THIS LIF  MAY STOP THE SPREAD OF CANCER.  THE MD ANDERSON HAS BEEN WORKING ON THIS AND HAVE REPORTED SOME SUCCESS! THE FIGHT IS ON!}

Head of Texas’ cancer agency has moved out; spokeswoman says CPRIT still up and running

 2  1

comments (0)

By Sue Goetinck Ambrose
sgoetinck@dallasnews.com
1:38 pm on December 17, 2012 | Permalink

Bill Gimson, executive director of CPRIT

The head of Texas’ cancer-fighting agency has cleared out his office, according to a spokeswoman for the Cancer Prevention and Research Institute of Texas.
Bill Gimson, CPRIT’s executive director since 2009, submitted his resignation last week to the agency’s board. He offered to stay on until January. But he emptied his office Friday and is not in today, said agency spokeswoman Ellen Read.
Since October, the agency has lost two other top executives. A new chief scientific officer has been hired, but doesn’t start work until January. Asked who is running the agency, Read said other senior staff members are still in place. Applications for funding are still being accepted and reviewed, she said.
Gimson has not responded to a request for an interview.
The agency came under fire last month after announcing it had awarded $11 million to a Dallas biotechnology company without properly reviewing the company’s request for money.  The agency says emails surrounding the 2010 decision to award the grant, to Peloton Therapeutics, are no longer available.
--------------------------------------------------------------------------------------------
FOR FULL STORY  GO TO BLOG BY DALLAS NEWS

.