COCA-COLA LOTTERY ORGANIZATION
TICKET FREE/ONLINE E-MAIL ADDRESS WINNINGS DEPARTMENT.
Greetings Winner,
If you are the correct owner of this email address? If yes then be glad this day as the result of the Coca-Cola lotto online e-mail address free-ticket winning draws of July 2020 ,held in United States of America has just been released and we are glad to announce to you that your email address won you the sweepstakes in the first category and you are entitled to claim the sum of One Million Two Hundred And Fifty Thousand United States Dollars(US$1,250,000.00). Your email address was entered for the online draw on this ticket No: 546-373-66773 and won on this Lucky No: (14)-(8)-(5)-(19)-(28)-(12)-(30).
On how to receive your won prize of US$1.250,000.00M. (One Million Two Hundred And Fifty Thousand United States Dollars Only) to enable Mr.James Curtise ascertain you as the rightful winner and receiver of the US$1.250,000.00M.Make sure you include the below listed information in your contact email to him.
Your complete official names, country of origin and country of residence/work, contact telephone and mobile numbers, amount won,lucky numbers, date of draw. OPTIONAL: - [Sex, age, occupation and job title].
Just in case you are thinking of how you won without entering then know again that this very draw of the Coca-Cola Lottery Organization in which you have emerged as a winner was a free ticket online email address draws were thousands of email addresses was collected from almost all world wide websites and used for the online draws/sweepstakes and during winners selection your email address came out among the first ten which won you the lottery in the first winnings category and entitles you to claim the US$1,250,000.00 dollars.
Yours Faithfully,
Mr.James Curtise
COCA-COLA LOTTERY ORGANIZATION.
Online Winning Notification Department.
Tel: +1-403-607-1548
Wednesday, November 18, 2020
Thursday, November 5, 2020
Fwd: CSHL Virtual Meeting: Biological Data Science
Topics in Precision Oncology
My talk will focus on leveraging thousands of cancer genomes and
functional genomics datasets to discover disease-associated regulators
and variations. First, I will go over the ENCODE annotations related
to the cancer genome. I will show these can be recast into a
comprehensive regulatory network of transcription factors and
RNA-binding proteins (TFs and RBPs). I will showcase the value of this
joint regulatory network by highlighting how SUB1, a previously
uncharacterized RBP, drives aberrant tumor expression and amplifies
the effect of the well-known oncogenic TF MYC. Next, I will describe
how ENCODE non-coding annotations can be applied to the comprehensive
PCAWG mutation dataset. The goal is to determine the overall burdening
of various elements in cancer genomes. I will show how this correlates
with patient survival time and tumor clonality. Finally, I adapt an
additive-effects model from complex-trait studies to show that the
aggregated effect of putative passengers, including undetected weak
drivers, provides significant additional power (~12% additive
variance) for predicting cancerous phenotypes, beyond identified
driver mutations. Furthermore, this framework allows one to estimate
potential weak-driver mutations in samples lacking any
well-characterized driver alterations.
https://meetings.cshl.edu/meetings.aspx?meet=data&year=20
i0bds20
My talk will focus on leveraging thousands of cancer genomes and
functional genomics datasets to discover disease-associated regulators
and variations. First, I will go over the ENCODE annotations related
to the cancer genome. I will show these can be recast into a
comprehensive regulatory network of transcription factors and
RNA-binding proteins (TFs and RBPs). I will showcase the value of this
joint regulatory network by highlighting how SUB1, a previously
uncharacterized RBP, drives aberrant tumor expression and amplifies
the effect of the well-known oncogenic TF MYC. Next, I will describe
how ENCODE non-coding annotations can be applied to the comprehensive
PCAWG mutation dataset. The goal is to determine the overall burdening
of various elements in cancer genomes. I will show how this correlates
with patient survival time and tumor clonality. Finally, I adapt an
additive-effects model from complex-trait studies to show that the
aggregated effect of putative passengers, including undetected weak
drivers, provides significant additional power (~12% additive
variance) for predicting cancerous phenotypes, beyond identified
driver mutations. Furthermore, this framework allows one to estimate
potential weak-driver mutations in samples lacking any
well-characterized driver alterations.
https://meetings.cshl.edu/meetings.aspx?meet=data&year=20
i0bds20
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