Thursday, January 31, 2013

Dear Komen friends,
We are less than three weeks away from Race for the Cure! I hope you will consider joining me at Cohen Stadium on Sunday, February 17 for the 21st Annual Komen El Paso Race for the Cure. Thousands of women in El Paso rely on Komen funds for screening mammograms, treatment assistance, and wigs/prosthesis during treatment. Breast cancer services provided through Komen funds help diagnose breast cancer early when it is most treatable and save lives right here in El Paso. We need YOUR support in order to continue Komen El Paso’s work in our community.
You can join Team Suzy NOW and receive $5 off your registration fee. Register online for before 11:00 pm MST tomorrow, January 31 using Discount Code 2013RETURNINGCAPTAIN (case sensitive), and receive $5 off your Non-Competitive, Competitive, or Sleep in for the Cure registration!
But you may say, Stephanie, I will be out of town OR I don’t even live in El Paso. It doesn’t matter! With Sleep in for the Cure, you can show your support and don’t even need to get out of bed.  I will not love you less if you choose this option : )
You can also join me in the fight by donating in support of my participation in the Race. My goal is to raise $1,000 this year.  Please help me reach that goal with your financial support.  Online donations are simple, and the site is secure.  If you would prefer, you can also send me your tax-deductible contribution written out to Komen Race for the Cure. 
Any amount that you can give will help! I truly appreciate your support and hope to see you Sunday, February 17 bright and early!
ACTIVITY AT CRBCM

WE HAVE NOW APPLIED FOR PROJECTS WITH THE DEPARTMENT OF DEFENSE
ON RESEARCH ON TRAUMATIC BRAIN INJURY; OF COURSE, CHANCES OF SUCCESS APPEAR SLIM TO NONE.  MOTHER OF ALL POLITICS THERE.  BUT IT IS AN EXERCISE PREPARING US FOR BETTER.

WE HAVE NOW INITIATED EFFECTIVE CONTACT WITH OUR LOCAL UNIVERSITY - UTEP. WILL MEET DR RENATO J. AGUILERA ON MONDAY FOR CONSULTATION AND HAVE SUBMITTED FOR EXERCISE PURPOSE 2 LETTERS OF INTENT TO PARTICIPATE IN THE RESEARCH ACTIVITIES OF THE "BORDER BIOMEDICAL RESEARCH CENTER (BBRC)"- EXPECTATION AGAIN LOW.  WE WILL LEARN FROM WHAT THEIR CRITICISM WILL BE.

PLAN 2 GRANTS APPLICATIONS AT NIH AND 2 FOR ASCO THIS YEAR.
IF YOU THINK CPRIT IS A POLITICAL FARCE AND GIMMICK, THINK AGAIN WHEN YOU REACH ASCO AND THE OTHER REAL DEALS.

THE POINT IS THAT WE CANNOT BE FAULTED FOR TRYING.   WE ARE NOT THE MD ANDERSON WITH 42% SUCCESS RATE AT CPRIT, BETTER THAN MOST TARGET THERAPY RESULTS!   THE JOKE IS ON US WHO INNOCENTLY APPLIED BELIEVING IN A POTENTIAL FAIR SYSTEM THAT WAS A JOKE UNDER THE OLD LEADERSHIP AT CPRIT.  WE ARE EAGER TO SEE WHAT COMES OUT OF THE REFORMED CPRIT, IF ANY!  EVERY SESSION WAS AN OPPORTUNITY TO FUNNEL MORE MONEY TO MD ANDERSON AND BAYLOR, NO WONDER THE ENTIRE CPRIT SHIP WENT DOWN LIKE THE TITANIC, HOUSTON IS NOT TEXAS PEOPLE, WAKE UP!

HERE HOWEVER, THE NEED OF US IN THE MARKET IS PROPULSING US TO STAY ALIVE.  EL PASO IS AN UNDERSERVED AREA.  WE ARE NEEDED, SO DOORS ARE OPENING DESPITE NORMAL RESISTANCE...SO CRBCM IS ADVANCING EVEN IN TROUBLED WATERS...WE WILL BE HERE UNTIL WE ARE HEARD.   THE IRS WAS A SURPRISE OPPONENT, YOU WOULD THINK THAT THE GOVERNMENT WOULD BE THERE TO HELP SMALL BUSINESSES AND NON PROFIT ORGANIZATIONS.  NO, THEY ARE SITTING ON OUR FILE.  WE JUST LOST 60,000 DOLLARS THAT COULD HAVE HELPED THE PEOPLE OF EL PASO THROUGH OUR PROGRAM BECAUSE OF FAILURE OF IRS TO GRANT US THE NON PROFIT STATUS.  A COALITION IS NON PROFIT PAR-EXCELLENCE PEOPLE! WAKE UP.  EVEN THE IRS COMMISSIONER IS OUT TO LUNCH.  WE WROTE TO HIM.  NO RESPONSE.  HE SEEMS MORE BUSY WORKING TO STAY IN POWER TO DO NOTHING!  SOUNDS FAMILIAR.  PEOPLE WHO INDULGE IN POLITICS SOMETIME WORK SO HARD POLITICKING THAT THEY FORGET THEIR PRIMARY JOB!

WELL, WE ARE NOT DEAD YET; THE CRBCM WILL KEEP UP THE FIGHT!
LET'S GET READY, RACE FOR THE CURE IS COMING UP ON FEBRUARY 17TH.
GET THOSE SNEAKERS AND RUNNERS OUT AND GET INTO YOUR BEST SHAPE EVER!
=====================================================================
Dear Komen friends,
We are less than three weeks away from Race for the Cure! I hope you will consider joining me at Cohen Stadium on Sunday, February 17 for the 21st Annual Komen El Paso Race for the Cure. Thousands of women in El Paso rely on Komen funds for screening mammograms, treatment assistance, and wigs/prosthesis during treatment. Breast cancer services provided through Komen funds help diagnose breast cancer early when it is most treatable and save lives right here in El Paso. We need YOUR support in order to continue Komen El Paso’s work in our community.
You can join Team Suzy NOW and receive $5 off your registration fee. Register online for before 11:00 pm MST tomorrow, January 31 using Discount Code 2013RETURNINGCAPTAIN (case sensitive), and receive $5 off your Non-Competitive, Competitive, or Sleep in for the Cure registration!
But you may say, Stephanie, I will be out of town OR I don’t even live in El Paso. It doesn’t matter! With Sleep in for the Cure, you can show your support and don’t even need to get out of bed.  I will not love you less if you choose this option : )
You can also join me in the fight by donating in support of my participation in the Race. My goal is to raise $1,000 this year.  Please help me reach that goal with your financial support.  Online donations are simple, and the site is secure.  If you would prefer, you can also send me your tax-deductible contribution written out to Komen Race for the Cure. 
Any amount that you can give will help! I truly appreciate your support and hope to see you Sunday, February 17 bright and early!

TEMPLATE FOR HEPATOCELLULAR CARCINOMA FOLLOW-UP:

DOES THE PATIENT HAVE
- JAUNDICE OR ELEVATED LFT(S) FOR USE OF DOXORUBICIN
- POOR APPETITE
- ASCITES (?THROMBUS AT HEPATIC VEIN)
- ABDOMINAL PAIN
- NAUSEA ALREADY
- WEIGHT LOSS

HX OF DM-ROLE OF INSULIN
HX OF HEPATITIS B OR C
HX OF CIRRHOSIS (LOCAL INTERVENTION)
HX OF HEMOCHROMATOSIS

LAB
- ALPHA FETOPROTEIN LEVEL
- ? DES-GAMMA-CARBOXYPROTHROMBIN
- U/S FOR DETECTION
- CT FOR MEASUREMT OF LESIONS,
- MRI FOR EXISTENCE OF CAPSULE AND PERIPHERAL INVASION, EXACT NUMBER OF LESIONS,
- PET FOR METASTATIC LESIONS AND RESPONSE TO THERAPY

TYPE OF HISTOLOGY
- FIBROLAMELLAR
- PSEUDOGLANDULAR
- PLEIOMORPHIC (GIANT CELL)
- CLEAR CELL
- ANAPLASTIC

CANDIDATE FOR
- SANDOSTATIN
- TAMOXIFEN
- ORAL SYNTHETIC RETINOIDS
- GALLIUM

P53 STATUS, MICROSATELLITE INSTABILITY, MDR,
TO PREDICT RESPONSE TO DAORUBICIN, PLATINUM, 5-FU, INTERFERON, EPIRUBICIN, TAXOL,

SORAFENIB (FATIGUE,RASH,DIARRHEA,HYPERTENSION.HAND FOOT SYNDROME)
- EGFR,VEGF

CANDIDATE
- TRANSPLANT
- PERCUTANEOUS ETHANOL
- TACE (WATCH FOR TUMOR >8CM, PORTAL VEIN THROMBUS,LFT-BILURIBIN LEVEL, SHUNT)
- RADIOFREQUENCY ABLATION (TUMOR <5CM)
- STEREOTACTIC RT
- SIRT

WHAT ABOUT IMMUNEPHERESIS AND PEXA-VEC?????

MUTATIONS IN HEPATOMA?  (CONTINUE REVIEWING LITERATURE OF COURSE I DID NOT INVENT THIS)
NOMENCLATURE OF GENES IN SARCOMA  (TO BE FURTHER DEVELOPED)

1.ALT REPAIR GENE:  British researcher have suggested that this gene of Mesenchymal origin
is one of the 2 mechanism of control of cell mortality at Telomere level.  At this level, life of the cell which is linked to length of the Telomere tail can by activation of Telomere which release the ALT network of genes which in turn stop immortality.  Mesenchymal Cancers to keep living will desactivate this process by Mutation here.  Opening up a target therapy option.
 This Alternative lengthening of Telomere function is related to and work in conjunction with repair mechanisms at Nuclear DNA (ERCC-1, which impart susceptibility to Cisplatin), at transcription gene level (CSA, CSB) and at the level of the double strand DNA (ATM, Ku80, PKC, BRCA, RAD 50).  We should stress the inter-relation between Telomerase activity with both the failure of DNA repair which lead to aging, and the proliferative inputs from NSUN5 and MYEOF (Myeloma)... DSC54 and WNT54 are related gene.
British investigator suggest these changes to be seen in MFH, Liposarcoma, GBM, Osteosarcoma, and Ewing sarcoma.   We should stress the inter-relation between Histone and Telomerase activation which is mostly repressive of negative,  Mutation of in the histone is needed to unveil Telomerate amplification.   

2. P53 
---------------
At least half of the Sarcoma will show activity at P53, the cellular Molecule of the year in 1993,
in up to 10% of cases, the P53 will actually be mutated. It is either overexpressed or suppressed in the rest of the cases of Sarcoma.  The P53 is suppressed if repression occur at P14 or at CDKN2A or if MDM2 is overexpressed.  P14 shield P53 from the effect of MDM2.  P53 is also over expressed if its degradation is stopped at the proteasome.

At nuclear level, Acetylated P53 combines to P300 and promote P21 and Puma leading to Apoptosis.  This effect can be blocked by Fusion protein  EWS-Fli1 in Ewing Sarcoma, and by upregulation of Histone DE-Acelase 1 which effectively block down transcription effect of P53.

if you count right, there are 6 potential target of interaction with P53, if you include upstream toward the membranes...calling for Multitarget therapy in those condition where wild type P53 is overexpressed!

GENE PROFILING IS A MUST STEP IN CANCER TREATMENT!

MDM2
KRAS
BRAF
ETV3
EAT2
TGFBR
CDKN2A
FLI 1
ERG
EWSR
MIC   (CD99)
EA1F
PI3K
(LY29004)
EWS-ATF
MAP KINASE
KIT
PDGFR
PAX3-FKHR
EWS
TLS-CHOP
TAF2N
FACTOR 1 PROMOTER
ERB-2
HSP
PPAR
CDK
EGFR
PTEN
P21
RB
TELOMERE--LACK OF TRF-2
================================================
BASAL CELL
CK 5
CK 15
================================================
NG2 BRAIN NEUROGLIA 2

CHECK 185 DEL aG-1
6174DEL IT-2
5382 InS C
=============================
REGULATOR OF CELL CYCLE
CDK, CCNB, CENPE, AURORA KB, PLK1

ALSO CHECK MAD2,POLE2,CDC2,TOPK,GMNN
GPS,
======================================
BREAST CANCER
KI-67
=======================================
 EGFR IN MESOTHELIOMA
===================================

WE ARE WORKING HARD AT CRBCM
CELLULAR LANGUAGE

The challenge brought to us by the need of a cure and failure of destructive conventional chemotherapy have proven to human being that there is the need to understand better cellular function.  Our learning has led to discover that the Cell has many properties and can do many things on its own including dying on its own or cell programmed death.  Yes, coordinated Changes within the cell based on its age, position and state of independence or loss of input from other cell can trigger cell death.  These coordinated changes are indeed a language that one   must talk to send a message to the cell that it is time to die.  And it is now apparent to scientists that brutalizing and violence to a cell through chemotherapy and Radiation will never be sufficient to accomplish a cure.  Cells are ready for a violent attack. You need to convince the cell to die.  You need to target functions of the cell and already tough to conquer cancer start listening.  By targeting therapy we learn that cutting a signal could lead to death of a cell.  like a battery, there is a positive and negative.  in the cell, there switches which are on or off.  In a computer there 1 and zero.  What a computer can do with these 1 basic things is anybodies guess. The Morse language had only 2 signal Tic and Tan.  (Tic Tan Tic, Tan TAN tic!)
Through an ON and OFF switch, through a positive and negative electrical charge, the cell transfer an input that will lead to extensive result.
While empirically we tend to believe that more is better,  it it the OFF signal that is the most full off consequences.

AT CELLULAR LEVEL, LACK OF INPUT IS THE MOST FULL OF CONSEQUENCE AND CAN LEAD TO DEATH IF SPOKEN AT THE RIGHT PLACE AND THE RIGHT TIME.

1. If a cell is left alone.  lack of environment talking to it (ie.  IN MYELOMA), lack of sister cell talking to it, lack of positive excitatory stimulation, will kill it . We have called this ANOIKIS.

2.Target Therapy works because it BLOCKS the excitatory stimulation.

3. A post synaptic neuron will die if the pre-synaptic neuron stops sending excitatory input.

4. Muscle death or Atrophy will occur if synaptic input cease or desist.
5. Necrosis will occur if Oxygen ceases
6. Acid from Lysosome will kill the cell if it seeps in the Cytosol that is relatively basic

BASICALLY, IT 'S AGAIN IT'S ON OR OFF, TIC OR TAN, NEGATIVE POSITIVE, ONE OR ZERO EVEN AT CELLULAR LEVEL.

IF YOU GET THIS, THE YOU WILL ALSO UNDERSTAND THAT
AT GENE LEVEL, IT IS THE DECREASE OF GENE THAT IS MORE IMPORTANT THEN AMPLIFICATION

1. Suppression of PTEN in sarcoma or lung cancer will act on PI3K/MTOR
2. decrease or suppression of STAT1 will be present in triple negative Breast cancer
3. P53 silencing mutation
4. MDM2 silencing Mutation
5. gene deletion or silencing
6.
Oncogene. 2005 Sep 15;24(41):6269-80.

The polycomb group protein enhancer of zeste homolog 2 (EZH 2) is an oncogene that influences myeloma cell growth and the mutant ras phenotype.

Source

The Graduate Program in Molecular, Cellular, Developmental Biology, and Genetics, University of Minnesota, Minneapolis, MN 55455, USA.

Abstract

Three distinct proliferative signals for multiple myeloma (MM) cell lines induce enhancer of zeste homolog 2 (ezh 2) transcript expression. EZH 2 is a polycomb group protein that mediates repression of gene transcription at the chromatin level through its methyltransferase activity. Normal bone marrow plasma cells do not express ezh2; however, gene expression is induced and correlates with tumor burden during progression of this disease. We therefore investigated how EZH 2 expression is deregulated in MM cell lines and determined the consequence of this activity on proliferation and transformation. We found that EZH 2 protein expression is induced by interleukin 6 (IL-6) in growth factor-dependent cell lines and is constitutive in IL-6-independent cell lines. Furthermore, EZH 2 expression correlates with proliferation and B-cell terminal differentiation. Significantly, EZH 2 protein inhibition by short interference RNA treatment results in MM cell growth arrest. Conversely, EZH 2 ectopic overexpression induces growth factor independence. We found that the growth factor-independent proliferative phenotype in MM cell lines harboring a mutant N- or K-ras gene requires EZH 2 activity. Finally, this is the first report to demonstrate that EZH 2 has oncogenic activity in vivo, and that cell transformation and tumor formation require histone methyltransferase activity.
Oncogene (2005) 24, 6269-6280.

7.NME1/NM23


NME1

From Wikipedia, the free encyclopedia
Jump to: navigation, search
NME/NM23 nucleoside diphosphate kinase 1

PDB rendering based on 1be4.
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols NME1; AWD; GAAD; NB; NBS; NDKA; NDPK-A; NDPKA; NM23; NM23-H1
External IDs OMIM156490 MGI97355 HomoloGene128514 ChEMBL: 2159 GeneCards: NME1 Gene
EC number 2.7.4.6
Orthologs
Species Human Mouse
Entrez 4830 18102
Ensembl ENSG00000239672 ENSMUSG00000037601
UniProt P15531 P15532
RefSeq (mRNA) NM_000269.2 NM_008704.2
RefSeq (protein) NP_000260.1 NP_032730.1
Location (UCSC) Chr 17:
49.23 – 49.24 Mb
Chr 11:
93.96 – 93.97 Mb

PubMed search [1] [2]
Nucleoside diphosphate kinase A is an enzyme that in humans is encoded by the NME1 gene.[1] It is thought to be a metastasis suppressor.
This gene (NME1) was identified because of its reduced mRNA transcript levels in highly metastatic cells. Nucleoside diphosphate kinase (NDK) exists as a hexamer composed of 'A' (encoded by this gene) and 'B' (encoded by NME2) isoforms. Mutations in this gene have been identified in aggressive neuroblastomas. Two transcript variants encoding different isoforms have been found for this gene. Co-transcription of this gene and the neighboring downstream gene (NME2) generates naturally-occurring transcripts (NME1-NME2), which encodes a fusion protein consisting of sequence sharing identity with each individual gene product.[2]


Interactions

NME1 has been shown to interact with Aurora A kinase,[3] NME3,[4][5] Protein SET,[6] RAR-related orphan receptor alpha,[7] TERF1,[8] CD29[9] and RAR-related orphan receptor beta.[7]


------------------------------------------------------------------------------------------------------
8 IN SARCOMA, DELETION OF CDKN2A 
--------------------------------------------------------------------------------------------------------
9. DECREASE IN E-CADHERIN IN  METASTATIC DISEASE
AND EARLY TRANSFORMATION
-------------------------------------------------------------------------------

AND THE LIST OF TUMOR SUPPRESSION GENE GOES ON.

SO IN GENERAL CANCER IS CAUSED BY NEGATIVE. LACK OR SUPPRESSION OF A GENE
SO ANYTIME THAT YOU ARE LOOKING FOR CAUSE OF CANCER, PAY MORE ATTENTION TO THE SUPPRESSION NOT THE HYPERACTIVITY!
LET SUPPRESS  FOXO3 TO TELL CANCER TO DIE!  LET'S CONTINUE TO SUPPRESS GROWTH FACTORSAND THE CURE WILL BE OUR TO REACH!

Wednesday, January 30, 2013

State audit calls for extensive reforms of Texas’ cancer-fighting agency
 7  37
 
comments (2)
State Auditor John Keel (File photo)
Update at 2:25 p.m. by Daniel Lathrop: Now you can read the audit for yourself.
AUSTIN – Legislators should consider several changes in state law to make Texas’ cancer-fighting agency more accountable and transparent to taxpayers, according to a state audit obtained Monday by The Dallas Morning News.
The audit lists problems in seven major areas, from how the Cancer Prevention and Research Institute of Texas makes grant decisions to how it monitors how public dollars are spent.
“Weaknesses in CPRIT’s processes reduce its ability to properly award and effectively monitor its grants,” state Auditor John Keel concludes in the report.
The audit calls on the state agency, which is under criminal and civil investigations, to ensure that all decisions are free from real or apparent conflict of interest.
The report says CPRIT’s management “generally agreed” with the audit’s dozens of recommendations.
Bill Gimson, who resigned last month as CPRIT’s executive director, discussed grant recommendations with some members of the agency’s Oversight Committee before presenting recommendations to the 11-member panel. The audit, as is typical with its practices, does not identify the Oversight Committee members involved.
Also, auditors identified two members of CPRIT’s commercialization review council who had financial and personal interests in certain grant recipients. The audit also does not identify them.
One review council member also was a member of the board of directors for a grantee that received a $25.2 million research award, a nonprofit called the Statewide Clinical Trials Network of Texas, or CTNeT, which has offices in Dallas and Houston.
Another member of the review council worked as a consultant for two applicants applying for “incubator” grants. Incubators are designed to link research and business opportunities.
The person, however, was not listed as taking part in the review of incubator grant applications and neither applicant ultimately submitted a formal request for funding, the audit says.
The state auditor says CPRIT reports it does not receive final information about donors to the CPRIT Foundation – a nonprofit group formed to supplement funding for the state agency — or the donation amounts. But CPRIT has no assurances that it is not awarding grants to donors, which would create a conflict of interest, the audit says.
“CPRIT’s lack of controls for ensuring there are not any business or professional relationships between its peer reviewers and grantees impairs CPRIT’s ability to ensure the public that its award decisions are not improperly influenced,” according to the audit.
The audit notes two controversies revealed last year: the $20 million grant to a Houston area incubator in 2012 without a science review, and the $11 million award in 2010 to a Dallas-based biotechnology firm, Peloton Therapeutics, without both scientific and business reviews.
Keel adds a third grant with problems.
CPRIT awarded $25.2 million, its largest grant, in 2010 even though the recipient, a nonprofit group, did not exist at the time.
The grant originally went to the University of Texas-M.D. Anderson Cancer Center. It is unclear what allowed CPRIT to transfer the award from M.D. Anderson to the newly-formed CTNeT nonprofit group, the audit says.
“CPRIT also did not have documentation to support that the scientific review council recommended the original application for a grant,’ the audit says.
The audit also says:
* CTNeT’s grant application did not receive a favorable peer review
score.  CPRIT evaluated grant applications on a scale of 1 to 9, with 1
being the highest.  The CTNeT grant application received a peer review
score of 4.64.  Auditors reviewed the peer review scores for 44 other
applications and identified 9 applications that were not awarded grants
that received peer review scores ranging from 3.93 to 4.40.
*  CPRIT has a role in CTNeT’s business operations.
Without using names, the audit says Jimmy Mansour, chairman of CPRIT’s oversight committee chair; vice chair Dr. Joseph Bailes, and Gimson interviewed and
hired CTNeT’s chief operating officer, Patricia Winger, before the contract was executed.
In addition, Gimson, former chief scientific officer Dr. Alfred Gilman, and a
member of CPRIT’s commercialization review council were members of
CTNeT’s board of directors.
* CPRIT made $6.8 million in advance payments to CTNeT even though its
grant agreement with CTNeT allowed only reimbursement payments.
* CTNeT did not comply with matching funds requirements and annual
progress reporting requirements.
* CPRIT’s relationship with CTNeT and its lack of enforcing contract
requirements impair CPRIT’s ability to ensure that CTNeT is properly
using grant funds and complying with grant requirements.
 7 37
 
Dallasnews.com is now using Facebook Comments. To post a comment, log into Facebook and then add your comment below. Comments are subject to Facebook's Privacy Policy and Terms of Service on data use. If you don't want your comment to appear on Facebook, uncheck the 'Post to Facebook' box. To find out more, read the FAQ.
More in Open government, The Business of Government
Parkland Memorial cuts a $500,000 deal to enlist lobbying powerhouse for regulatory issues as fate rests with regulators
At a time Parkland Memorial Hospital needs a critical blessing from federal regulators to avoid a shutdown, its officials have...
Close
OPINION ON GENETIC TESTING

As our knowledge keep expanding, it is fair to suggest that Knowledge of Driver Mutation makes a difference in our patients particularly in instances where we have an effective inhibitor.  The frequency of the Mutation has been a frustrating basis for intervention since the high rate of an eventual mutation could be linked to its early occurrence in the cancerous transformation.  Giving a value in early detection with no effect on the outcome.
Dividing genetic abnormality in those of proliferation, those involved in amplification, and those of differentiation, those pointing to metastasis and finally those for survival, could prove useful.
It is not enough to know that P53 is amplified if it is not mutated. The reason for the amplification needs to be clarified by a comprehensive view of the ensemble of genetic change panel.

In many instances, our view of the events in a cell is frustratingly narrow.  Reading on Uterine cancer today I found out that Uterine cancer is divided in endometrioid and non Endometrioid.  I learned that 83% of endometrioid cancer have a PTEN depression or mutation abnormality.  This is thought to be an early event.  Meaning it may not matter that much in the outcome of our patient and MTOR inhibition turned out to have a mild effect.       On the non endometrioid cancer very little is said.  We know it is most of the time coming from an Atrophic mucosa, what this means at molecular level, lack of stimulation by Estrogen, Receptor insensitivity, a panoramic gene testing is needed to find a useful answer.  So it seems to us that any genetic testing report should tell us the state of gene alteration in each group of cellular functions to be useful.

In some tissue such has sarcoma, brain, (Melanoma) knowing the EGFR or VGEF amplification only appears a partial issue.  What is the status of gene of differentiation, and other genes.  Until we have a comprehensive panel for each cell type, our effort will not progress for the cure.   The flurry of progress in lung cancer came from a consistent panel reporting of genes mutation and drivers at one Institution (Harvard).  This is the way to go! WE GOT TO RAISE THE BAR.

UTERINE OR ENDOMETRIAL CANCER

WITH INCREASE OF OBESITY RATE, THIS CANCER IS ONE OF THOSE ON THE RISE
AFFECTING 46000 WOMEN A YEAR
WITH 8000 DYING EVERY YEAR

4 TYPES

1-ENDOMETRIOID (80%)

2.1-SEROUS
2.2-CLEAR CELL
2.3-MUCINOUS
2.4-MIXED

The Endometrioid type is preceded by Hyperplasia and is genErally localized and of good prognosis.
The serous type is preceded by atrophy and is of worse prognosis. 

 Of those with uterine inner third involvement,
-----------------------------------------------
55% of Serous will have spread of disease
17% with Endometrioid will have spread of disease
Median survival is 12 months in metastatic disease

11 genetic alterations described:
==========================

1,loss of function of PTEN: An early event see in 83 % of Endometriod cancer.
opening the door to MTOR inhibitor use
metformin seems to potentiate effect of Taxol through modulation of MTOR.

INHIBITION OF PTEN MAY PREDICT SENSITIVITY TO PARP INHIBITORS, SO OLAPARIB HAS BEEN TRIED.  PARP INHIBITOR TRIED IN THOSE POSITIVE FOR BRCA 1,2

2.PIK3CA Mutation

3.AKT mutation
4.Microsattelite instability
5.KRas Mutation : 26% of endometrioid cancer  (MEK Inhibition by Selumetinib trial)
6.Overexpression of EGFR (Avastin and Decoy Aflibercept with minimum response from Sutent, NEXAVAR, AND THALIDOMID)   Tarceva, Iressa,Erbitux

In non-endometrioid cancer, existence of ERBB2 poto-ocnocgen has led to trial of Trastuzumab, Lapatinib with minimal response
7.P53 mutation
8.Nuclear B Catenin
9.Her-2/Neu amplification
10.FGFR PRESENCE HAS LED TO TRIAL WITH DOVITINIB
11.P16 inactivation

Tuesday, January 29, 2013

COMPLICATIONS ENCOUNTERED AT DEFINING GENE AMPLIFICATION.

As we dig deeper into the 4th law of nature, we quickly encountered difficulty in defining primary and secondary amplification.

Primary gene Amplification:
---------------------------
It is now evident that an amplified gene could be the result of the effect of a growth factor or cyclins acting on a receptor at membrane level  and into the Cytosol.  This is a secondary gene amplification.
Once a cell has chosen a specific orientation, that is it has chosen between proliferation or differentiation, that orientation will be the focus of gene Amplification.  This amplification is generally non specific and is our definition of Primary Amplification.  This general amplification is generally mild like in a buzz.  when found, it is low level amplification. the gene is found generally in less than 10 percent of cells... Most of the time around 4-5% of cells.  It is a tone.  Our research locate this Amplification in the MLL and MYC genes and in the Histone Acetyl transferase and related molecules (PCAF, P300).  Sometime, this basic amplification and a secondary amplification can double up in the same gene, leading to an exacerbated amplification such as it occurs in Burkitt lymphoma.  This will prompt us to look into difference of Expression of MYC in Ovarian cancer Vs Myc expression the Burkitt lymphoma.  There must be a big difference, may be in the level of Cyclins.  we will investigate.

Suffice is to say the real reason of the Amplification to be in the MYC and Histone Acetyl transferase, is that both have regulatory powers on the P53 which needs to be downregulated to allow proliferation to continue in cancer.  So aside from the Regular MDM2 which the principal regulator, Histone acetyl transferase which MYC promotes, is the second main P53 regulator.  In our previous blog, we had discussed the interactions of P53 with upstream structure toward the membrane.

Secondary gene Amplification.
-------------------------------
 Secondary gene Anplification is the result of the action of proliferation genes,  Amplification gene and oncogenic driver and non driver  Mutations.
This Amplification targets
1. Membrane receptors (EGFR, FGFR-1, Her-2,)
2. RAS and GTPases (ie. RAp1GTPase, Hras)
3. growth factors and CYCLINS  (CCND1,FGFR and its related HST-1,c-MET)
4. Signal trasduction pathways (AKT/MTOR)
5. Regulators of pathways (TSG with impact on the AKT)
6.Transcription Factors (MLL, a regulator of transcription factor with activity on the TSG in the AKT/MTOR pathway
7. Histones and epigenetic triggers
8. DNA proper  (Ki 67 seen only in dividing cells, CDKs,  it may acts also on genes of differentiation such Myo, RET, TRK, int-1, hst-1 )
 Secondary amplification double up on the primary to multiply itself.

Some other Amplifier are downregulated for action to be unveiled (PTEN and its increase of AKT)
SECONDARY GENE AMPLIFICATION WILL TEND TO BE WITH HIGHER PERCENTAGE THAN 10% 

A note to make before
Downstream from MTOR is located a key to Apoptosis by the name of FOXO, check it out!  THE FOX HIDE THE PUMA GENE!

Monday, January 28, 2013




Travis County DA: “The CPRIT investigation is ongoing and aggressive”

 0  28
comments (0)
AUSTIN – The Travis County district attorney said Wednesday afternoon that her office’s investigation into Texas’ cancer-fighting agency is “very serious and we are far from finished in our efforts.”
“The CPRIT investigation is ongoing and aggressive,” said Rosemary Lehmberg.
Lehmberg’s six-line statement came a day after Jimmy Mansour, chairman of the Oversight Committee of the Cancer Prevention and Research Institute of Texas, released his own through Bill Miller, a powerful Austin lobbyist and political consultant.
Miller’s statement said Mansour met with the district attorney’s office last week and was assured that he and all other current board members “are free from suspicion in the ongoing CPRIT investigation.”
“Mr. Mansour is pleased that the cloud has lifted,” Miller said in his statement.
Reached for comment, Gregg Cox, director of the district attorney’s Public Integrity Unit, replied in an email that Mr. Mansour is cooperating in the investigation.
He said the Jan. 18 interview of Mansour focused on two topics – the divestment of stock that Mansour owned when he was appointed by Lt. Gov. David Dewhurst to serve on CPRIT’s Oversight Committee, and the committee’s  awarding of a grant to Peloton Therapeutics.
“His statement is accurate with respect to those areas,” Cox wrote.
The Dallas Morning News reported in November that companies run by Dallas businessman David Shanahan got $12.8 million in CPRIT grants after Shanahan and his associates gave $90,000 to the campaigns of Gov.Rick Perry and  Dewhurst.
One of those companies was Gradalis Inc., a biotechnology firm based in Carrollton, and one of those associates was Mansour, who had contributed $40,500 to Dewhurst in the eight years leading to his appointment to CPRIT.
Mansour, through spokesman Miller, told the newspaper that he invested in Gradalis in 2006 and became a board member. Mansour said he was advised that as a member of the Oversight Committee, he could hold investments in companies that received awards, and in which his ownership was no more than 5 percent of the firm. He said that was the case with the stock he owned in Gradalis, which he decided to sell.
Mansour said the sale of the Gradalis stock that he owned personally and through a limited partnership ended in what he called a “substantial loss” in 2009.
The following year, the Oversight Committee members, including Mansour, ratified a $748,905 award to Gradalis, as part of a much larger grant.
Also last November, CPRIT confirmed that an $11 million award to Peloton Therapeutics, a company on the campus of the UT Southwestern Medical Center, did not receive required commercial or scientific review.
Shortly after that news broke, theTravis County district attorney’s office said it had opened a criminal investigation into how CPRIT awards grants.
In her statement Wednesday, Lehmberg wrote: “Let me emphasize the investigation is very serious and we are far from finished in our efforts.”
CPRIT head resigns as Travis County DA confirms investigation of agency
Pressing CPRIT for answers after it awarded $11 million to Dallas’ Peloton Therapeutics without the required review
==============================================================

At CRBCM we now believe that if criminal activity is not found.
the competency of people in charge of the investigation needs further reevaluation, or the same network involved with CPRIT management is at work and stole the verdict.  With the extent of misrepresentation and conflict of interest unveiled at CPRIT, It will be a Blasphemy and misconduct of justice if no soul is held accountable! Or at least indicted! This is a fair prediction.
When a non existing company is given a grant.  I do not need a law degree to see a wrong-doing!
When people call this the "CPRIT CON",   These prosecutors need to deliver.   After this audit, the chance of no prosecution in our view is zero!  The bet is on.

The malice at CPRIT has been deliberate, ostentatious and, at time pugnacious.  What a sad day it will be if our prosecutors came back empty handed.  What a sad day it will be.  We will know the network got to them!  I agree with the auditors, prosecutor should not be part of the Oversight committee.  They become witnesses for the true prosecutors!

What a mess this is.  It will go in history!  let's write it right!
CPRIT AUDIT REPORT IS ON THE LEVEL.
==================================
The CRBCM would like to commend the Audit team for a job that is at the level within the time constraint.  The report, although partial, reveals that auditors intended to do a good job and the mess at CPRIT was blatant.  There is no aspect you could look at CPRIT to not find fault.  From cavalier rejection of applications, to payment of cronies, everything was there for the auditors to see.  Abduction of the system by universities which created phony companies (one such company got a grant before its existence),  What reviews were completed and non compliance with their own standards.  More than a messy company, CPRIT did not have a soul.  Basically, CPRIT as described, was hijacked by bandits and conspirators, people were so full of their powers, they were day and night imagining ways to detour the money.
With just 10% of projects reviewed at least 4 projects did not meet the requirements created by CPRIT.
Should time be given to the auditors to complete their work, we project that 40 or more projects will not have met CPRIT's own standards.  And that is being kind and conservative!


Basically, CPRIT was a mess, the leadership a joke, and plenty of politics and conspiracy were the rule.
CPRIT needs a soul and a vision.  Cure needs to be imagined, and steps to reach it carefully planned.

With 42% of funds going to the MD Anderson, and 15% to Baylor, the statewide vision was non-existent at CPRIT. Zero percent went to El Paso.  Basically while all resident of Houston could feel the money.  I was in Houston, I could see  many new shiny Buildings own and being built by Bio-tech companies. Tax-payers in El Paso paid for nothing!  Basically, the rest of Texas is paying bonds for the good of Houston.  On top of this, Applicants companies are now paying friends of CPRIT.  Bio-alliance is getting $1000 per application.  Why.  Tax payers have already paid for this service, this is another tax on businesses trying to pull pieces of  meat from within the jaw of the MD Anderson.  Bio-alliance may be a MD Anderson derivative.  With the complexity of the corrupt network put in place.  It is hard to determine anymore.

With half of the Money going to Houston, we are being robbed to feed the beast that is Houston.  Can CPRIT come back to its mission?  If the changes suggested are allowed to be put in place by the same team members. I really doubt it.  The legislature need to place a visionary at the head with muscle to replace contaminated apples in the bag!  It takes one rotten element to spoil the entire mission.

What is described by auditors is so bad that an outsider is needed with a big broom for a complete clean up.  For the sanity of the mission this is what should come!

CPRIT need a vision, fairness, a soul, and backbone to stand against big Universities!  CPRIT needs someone who believes CPRIT is an autonomous organization with answer to the people of Texas, not just the MD Anderson!

I was reading a commentary by a regional journalist who was trying to explain why El Paso was not getting any research fund.  "There is no institution in El Paso with matching fund available" he claimed being the reason.  Now we know this to be a pretext!  The MD Anderson could just write it has the money and CPRIT would comply.  This is what is defined as cavalier... and I don't make this stuff up!  Read the report and we can talk! 

CPRIT HAS BEEN AUDITED


An Audit Report on Grant Management at the Cancer Prevention and Research Institute of Texas and Selected Grantees




January 2013
Report Number 13-018

Overall Conclusion

The Cancer Prevention and Research Institute of Texas (CPRIT) should significantly improve the transparency and accountability of its grant management processes. Weaknesses in CPRIT's processes reduce its ability to properly award and effectively monitor its grants. Specifically, CPRIT should address deficiencies in the following areas:
- Making award decisions.
- Evaluating grant applications.
- Verifying compliance with matching funds requirements.
- Processing payments to grantees.
- Monitoring grantees' expenditures.
- Assessing and measuring research progress.
- Managing contract agreements with grantees.
Making Award Decisions
CPRIT should ensure that all award decisions are free from real or apparent conflicts of interest. The executive director discussed award recommendations with certain members of the oversight committee prior to presenting the recommendations to the full oversight committee. Also, CPRIT’s chief scientific officer, chief commercialization officer, and director of scientific review had office locations on the campuses of higher education institutions that received CPRIT awards. The chief scientific officer, the chief commercialization officer, and the director of scientific review are responsible for managing the peer review process for grant applications in their respective areas. In addition, auditors identified two members of CPRIT's commercialization review council with financial and personal interests in certain grantees. Specifically:
- One member of the commercialization review council was also a member of the board of directors for a grantee that received a $25.2 million research award from CPRIT. According to CPRIT's records, that individual did not participate in the review of the grant application for that grantee.
- Another member of the commercialization review council provided consulting services to two applicants applying for Texas life sciences incubator commercialization grants. That individual was not listed as participating in the review of grant applications for incubator grants, and neither applicant ultimately submitted a formal application for an incubator grant.
CPRIT also reported that it does not receive financial information about donors to the CPRIT Foundation or the amounts of the donations. Without that information, CPRIT has no assurances that it is not awarding grants to the CPRIT Foundation donors, which could create a conflict of interest. The General Appropriations Acts (81st and 82nd Legislatures) state that an individual; an organization; or an employee, officer, or director of an organization that makes a contribution to the CPRIT Foundation, or a person who has second-degree consanguinity or affinity to an employee of CPRIT, is not eligible to receive grants from CPRIT.
CPRIT's lack of controls for ensuring there are not any business and professional relationships between its peer reviewers and grantees impairs CPRIT's ability to assure the public that its award decisions are not improperly influenced.
Evaluating Grant Applications
CPRIT should ensure that its policies and procedures for evaluating grant applications are up to date and consistently followed. In addition, CPRIT should maintain records of all reviews that are performed.
Auditors could not verify that CPRIT consistently followed its process for withdrawing grant applications from the peer review process. CPRIT did not have reliable data to support grant applications that were withdrawn (see Chapter 1-B for more information).
Auditors identified the following significant issues for three grant applications tested:
- The Statewide Clinical Trials Network of Texas (CTNeT) received a $25.2 million research grant from CPRIT even though CTNeT did not exist at the time the grant was awarded. The CTNeT grant was the largest single grant that CPRIT had awarded as of June 2012. CPRIT originally awarded the grant to the University of Texas M.D. Anderson Cancer Center in June 2010. Subsequent to the award, CTNeT was formed and registered to become a Texas-based non-profit company in August 2010 and CPRIT executed a grant agreement with CTNeT in September 2010. It is unclear what allowed CPRIT to transfer the award from the University of Texas M.D. Anderson Cancer Center to CTNeT. CPRIT also did not have documentation to support that the scientific review council recommended the original application for a grant.
- CPRIT awarded a $20.0 million commercialization grant to the Houston-Area Translational Research Consortium (HATRC) and the Institute for Applied Cancer Science (IACS). Neither the HATRC grant application nor the IACS research proposal received scientific, due diligence, or intellectual property reviews. CPRIT reported that it rescinded the award in May 2012 after IACS requested to resubmit its research proposal for commercialization and scientific reviews.
- CPRIT awarded an $11.0 million commercialization grant to Peloton Therapeutics Inc. (Peloton, formerly Damascus Pharmaceuticals), whose application did not receive scientific, commercialization, due diligence, or intellectual property reviews.
Auditors reviewed the peer review scores for 218 (5.9 percent) of the 3,698 grant applications CPRIT reported receiving from September 2009 through June 2012 through the CPRIT Application Receipt System. Auditors identified four applications for which the peer review scores were not consistent with receiving a grant recommendation. CPRIT also did not have documentation to support the factors that peer reviewers used in making grant recommendations to CPRIT's executive director.
In addition, CPRIT did not document its review of recruitment grant applications or maintain records of those reviews in its Peer Review Management Information System. Recruitment grants are for the recruitment of investigators with the ability to make outstanding contributions to the field of cancer research, promote inquiry into new areas, foster collaboration, and stimulate growth in the field. Select scientific review council members manually review the recruitment grant applications; however, the only documentation maintained was a one-page summary statement that recommends the award of a recruitment grant. As of August 2012, CPRIT had awarded 60 recruitment grants totaling $184.9 million.
By not ensuring that all grant applications are properly evaluated and documented, CPRIT weakens its ability to ensure that its award decisions best align with the agency's mission.
Verifying Compliance with Matching Funds Requirements
CPRIT should verify the accuracy and availability of the matching funds its grantees report. The Texas Constitution, Article III, Section 67 (a)(3)(i), requires that before CPRIT awards a grant, the grantee must have funds equal to one-half the amount of the grant dedicated to the research that is the subject of the grant. CPRIT requires grantees to certify the amount of matching funds available for research at (1) the time of contract execution and (2) on an annual basis thereafter. However, CPRIT did not verify the accuracy and availability of the matching funds reported. In addition, during site visits to five grantees, auditors identified two methodologies, permitted by CPRIT, that allow a grantee to report funds that were not used on a CPRIT-funded research project as matching funds. Specifically:
- During interviews with auditors, staff at the University of Texas M.D. Anderson Cancer Center, the University of Texas Southwestern Medical Center, and the Baylor College of Medicine reported that the matching funds those institutions reported to CPRIT were based on the total amount of funding available to them for cancer research, excluding CPRIT funding. However, those reported matching funds were not dedicated to CPRIT-funded research projects. As of August 2012, those three institutions had received a combined 331 awards totaling $402.4 million.
- CTNeT, which received a $25.2 million research grant, did not dedicate $12.6 million in matching funds as required. Instead, CPRIT accepted certifications that the University of Texas M.D. Anderson Cancer Center and the Baylor College of Medicine would fulfill CTNeT's matching funds requirements for the first and second year of the grant agreement term, respectively. However, CTNeT did not receive those reported matching funds. For the first year of the CTNeT grant, CTNeT reported that the CPRIT grant accounted for 98.0 percent of its total revenue.
Processing Payments to Grantees
CPRIT should establish requirements to help ensure the appropriateness of advance payments and reimbursements it makes to grantees. Specifically:
- Advance payments. CPRIT's policies and procedures specify that CPRIT will distribute funds on a reimbursement basis. However, it made advance payments that totaled $40.2 million to 10 grantees from September 2008 through August 2012.
- Reimbursements. CPRIT relies on quarterly financial status reports and supporting documentation that grantees submit for reimbursement payments. However, CPRIT did not always obtain sufficient documentation from grantees to support the appropriateness of the reported expenditures. For 85 (84.1 percent) of the 101 reimbursements tested, or $9.4 million in reimbursements, CPRIT did not obtain documentation such as time sheets, invoices, contracts, and bill records to support the reimbursed expenditures. For those 85 reimbursements, grantees typically provided CPRIT with spreadsheets that summarized the expenditures.
Monitoring Grantees' Expenditures
CPRIT should improve its processes for monitoring grantee expenditures. CPRIT requires grantees to submit quarterly financial reports on research expenditures associated with awarded grants. In addition, CPRIT established a desk review process to assess grantees’ financial controls and reported expenditures. However, CPRIT did not ensure that all grantees submitted financial reports in a timely manner, did not maintain a complete record of all the financial reports it received from grantees, and had not performed any desk reviews of 487 grants totaling approximately $683 million as of June 2012.
Assessing and Measuring Research Progress and Compliance with Grant Milestones
CPRIT should ensure that grantees submit all required annual progress reports by required due dates, and it should review those reports and document those reviews. While CPRIT developed monitoring tools for tracking the due dates and submissions of annual progress reports, CPRIT lacked documentation to support that it followed up with grantees for past due reports. For a sample of 20 grant agreements that auditors reviewed, CPRIT had not received 12 (60 percent) of 20 annual progress reports that were due from September 2011 through June 2012. CPRIT's records indicated that it had started following up with grantees about past due reports beginning in May 2012. In addition, CPRIT has not developed review criteria for evaluating and measuring a grantee's reported progress. Although CPRIT used its peer reviewers to evaluate the eight annual progress reports it received, the peer reviewers did not document whether a grantee's reported progress met grant milestones or whether any problems had been identified that could affect the grantee's ability to complete the research project. CPRIT reported that it received emails from the peer reviewers indicating that a review was complete and that no issues had been reported by reviewers.
CPRIT should improve its management of the CTNeT research grant and other administrative practices.
Auditors identified significant weaknesses in CPRIT's award decision and management of the $25.2 million research grant to CTNeT (see Chapter 3 for more information about this grant). Specifically:
- CTNeT's grant application did not receive a favorable peer review score. CPRIT evaluated grant applications on a scale of 1 to 9, with 1 being the highest. The CTNeT grant application received a peer review score of 4.64. Auditors reviewed the peer review scores for 44 other applications and identified 9 applications that were not awarded grants that received peer review scores ranging from 3.93 to 4.40.
- CPRIT has a role in CTNeT's business operations. CPRIT’s oversight committee chair, vice-chair, and executive director interviewed and hired CTNeT's chief operating officer before the contract was executed. In addition, CPRIT's executive director, chief scientific officer, and a member of CPRIT's commercialization review council are members of CTNeT's board of directors.
- CPRIT made $6.8 million in advance payments to CTNeT even though its grant agreement with CTNeT allowed only reimbursement payments.
- CTNeT did not comply with matching funds requirements and annual progress reporting requirements.
CPRIT’s relationship with CTNeT and its lack of enforcing contract requirements impair CPRIT's ability to ensure that CTNeT is properly using grant funds and complying with grant requirements.
CPRIT also should improve certain procurement and payment practices for vendors and other professional services.
CPRIT should strengthen its vendor procurement and payment practices to ensure that the services and costs for grant management services and virtual management company services are reasonable and necessary. Specifically:
- The costs for a five-year contract for grant management services increased from $15.7 million to $21.2 million (35.2 percent) within the first three years of the contract. The cost increases were based on amendments to the contract that increased the workload of the grant management services contractor and the development of a grant management system.
- The costs for the first two years of a four-year contract for virtual management company services increased from $1.5 million to $4 million, approximately 166.7 percent. The cost increases were based on amendments to include services management, an entrepreneur-in-residence program, salaries for additional executive positions that were added to the contractor's staff, and other direct costs.
CPRIT also did not consistently obtain sufficient documentation to support the appropriateness of honorarium payments it made to its peer reviewers. From September 2009 through June 2012, honorarium payments to peer reviewers were approximately $6.7 million. In addition, CPRIT lacked documentation to justify increases in honorarium payments to officers of its peer review committees. Also, auditors identified honorarium payment amounts for certain peer reviewers that may be significantly higher than the payment amounts that the National Cancer Institute pays its peer reviewers.
Auditors communicated other, less significant issues to CPRIT's management separately in writing. Those issues were related to administrative reporting discrepancies, the forms grantees use for reporting, reporting practices for certain grantees' payment practices, performance feedback to grantees, executing grant agreements, and management of peer reviewer rosters.
The Legislature should consider amending statutory requirements to improve the transparency and accountability of CPRIT.
The Legislature should consider statutory requirements to:
- Allow peer reviewers to provide their grant recommendations to the executive director and members of the CPRIT oversight committee at the same time.
- Clarify what funds can be used and the intended use of matching funds reported by grantees.
- Clarify whether contributions made by non-profit foundations affiliated with grantees are appropriate.
- Prohibit an interlocking directorate between CPRIT and the CPRIT Foundation.
- Prohibit CPRIT employees from serving on a grantee's board of directors and related foundations.
- Clarify the positions of the oversight committee's presiding officer and other officers, including the responsibilities and specific term of service for those positions.
- Allow members of the oversight committee to affirmatively vote to approve the executive director's recommendations.
- Remove the Attorney General and the Comptroller of Public Accounts from CPRIT's oversight committee so that their statutory duties and responsibilities would not be impaired.
- Allow the executive director to provide CPRIT's oversight committee, along with grant recommendations, documentation of the other factors that the executive director considered when making grant recommendations.
- Require the CPRIT Foundation to make its records, books, and reports available to the public.

Contact the SAO about this report.

Download the Acrobat version of this report. (.pdf)