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Health & Fitness

Jan Mtg, Webinar, Stanford Support Group, PanCan announcements

There are four elements to this LONG post (a bit more than 3 pages).  First is the monthly meeting, next a webinar summary, third a brief snapshot from the Stanford Pancreatic Cancer Support Group, and finally an email announcement from the Pancreatic Cancer Action Network.

 

1 We encourage you to attend the monthly meeting for the Silicon Valley Affiliate of the Pancreatic Cancer Action Network.  Dr. Monte Winslow, a PanCan grantee at Stanford University, will talk with us about his pancreatic cancer research.  This promises to be a very interesting discussion.  Additional details about Dr. Winslow and his research are found here http://winslowlab.stanford.edu/  and here

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Pancreatic Cancer Action Network GRANT SNAPSHOT

AACR Career Development Award

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Grantee: Monte Winslow, PhD

Institution: Stanford University

Research Project: Molecular Dissection of Hmga2 Function during Pancreatic Cancer Progression Award Period: July 1, 2013 – June 30, 2015

Amount: $200,000

Biographical Highlights

Dr. Winslow is an Assistant Professor in the Departments of Genetics and Pathology at Stanford University School of Medicine, as well as a member of the Stanford Cancer Institute. Monte performed his PhD work studying immunology and developmental biology with Dr. Jerry Crabtree at Stanford before doing his postdoctoral fellowship at Massachusetts Institute of Technology. There he worked with Dr. Tyler Jacks using mouse models of metastatic cancer to uncover the key determinants of cancer progression. Dr. Jacks received the Blum-Kovler Innovative Grant from our organization in 2012.

Dr. Winslow’s laboratory is focused on understanding the mechanisms that drive cancer progression and metastasis. The goal of his pancreatic cancer research is to use genomic methods and animal models to uncover the molecular and cellular changes that underlie cancer invasion and metastasis.

Project Overview

One of the features of pancreatic tumors that make them so difficult to treat is their propensity to spread to additional parts of the body, through a process called metastasis. For metastases to occur, pancreatic cancer cells need to leave the tumor, invade the surrounding tissue, survive in the bloodstream, and thrive in a different organ environment. The molecular steps necessary for metastasis to occur have not been fully elucidated.

Dr. Winslow proposes to analyze the role of a protein called high-mobility group AT-hook 2 (Hmga2) in pancreatic cancer progression and metastasis. Interestingly, Hmga2 is normally present and active in the developing embryo, but typically silenced in adult tissue. However, pancreatic and other cancer types have been found to re-express Hmga2. Preliminary data suggest that Hmga2 plays a role in the cancer cells’ ability to invade the surrounding tissue and colonize other organs. To test this hypothesis, Dr. Winslow and his colleagues will extend upon a previously established mouse model of pancreatic cancer where the disease is induced by alterations to K-Ras and p53. In addition, they will delete the Hmga2 gene. The research team expects that deletion of Hmga2 will lead to pancreatic tumors that are significantly less aggressive and have decreased likelihood to spread outside of the pancreas. Since the function of Hmga2 is to interact with DNA and affect the expression of specific genes, Dr. Winslow will also determine which genes’ expression is altered by the absence of Hmga2 in pancreatic tumors. The overall goal of Dr. Winslow’s work is to increase understanding of the key components that make pancreatic cancer so aggressive, to allow the development of therapies to inhibit invasion or uncover vulnerabilities that could be exploited to eradicate pancreatic cancer metastases and significantly improve patient outcome.

 

It will be great if when we can understand the Grant Summary in layman’s English!

I hope you can make it.

Meeting is Wednesday, January 22, 2012, 6:00 pm - 8:00 pm, at the Sports Basement in the Pruneyard, Campbell, CA

 

 

2 PanCan webinar 8 Jan 2014 Prof Guari Varadhachary, MD from MD Anderson … very articulate with concise answers

Treatment Approaches for Pancreatic Cancer

The webinar (presentation slides and audio) is not yet posted, but previous webinars are posted here http://www.pancan.org/section_facing_pancreatic_cancer/learn_about_pan_cancer/educational_events/index.php

Adenocarcinoma version diagnosed for 39K patients/yr in the US, but only 3%-4% survive to 5 years

Adjuvant therapy worked well 20 yr ago (doubled survival rate), but now pre-op and Whipple doing the whole job

SMAD4 is a good biomarker … if present, that’s good (many other biomarkers, see below)

Pancreatic cancer progress is slow vs other cancers as there are12 different processes and 63 mutations active

However KRAS mutation is present in >90% of cases

Trial with Gemstar and erlotinib show that rash due to the latter is good!

Folfirinox is nasty (frequent side effects) but effective and there is some evidence that smaller dose is still effective

Paclitaxel (aka Abraxane) bad for neuropathy, but my personal experience w/ sublingual B12 is an antidote to neuropathy

Questions after the presentation

How can one ensure sufficient spatial resolution during CT scan?   Ask if cuts are thin (at least 16 slices), ie multi detector

Why would post op chemo (adjuvant) be omitted?  If patient too weak, too much elapsed time … or too much metastasis

What is status for immuo-therapy?  Too early to say, but lots of work underway, even vaccines

Why is progress slow vs other cancers?  Blood marker is unreliable and difficult to get tissue, but progress on the latter

Why is pancreatic cancer progress slow vs other cancers? 

 Complex, but approach is to look for differences in retained tumors for fast deaths vs survivors to identify markers

Do adenocarcinoma chemo treatments differ from endoctrine?  YES, all different

Effect of diet?  Worthy of full presentation, but nothing definitive (at least not a useful snippet)

Why is value of blood markers different than scan? Muddled response (see own personal view below)

End seminar, Start personal soapbox

 

  CA19-9 is universally denigrated by MDs as it responds in only 75% of the cases or so, but stating it the other way, a false negative would occur a distressingly large 25% of the cases.  As such it cannot be used for screening, but when it DOES respond, it is a good index of treatment efficacy … and it can be measured more frequently than scan (no radiation exposure jeopardy and CT contrast agents are tough on compromised kidneys).  Due to large percentage of cases (tens of %) for which CA19-9 does not work, the MDs rely upon what they can see in a scan.  A few words about scans … CT scan is probably the most effective and cheapest, but I am ineligible as one or more of the chemo agents damaged my kidneys to such an extent that I cannot tolerate iodine-based contrast agents.  I am less familiar with MRI (no radiation or chemical hazard) but I am ineligible for MRI also.  I happen to have a pacemaker, whose gold-plated leads into the heart muscle would get very hot in the intense magnetic field (huge eddy currents).  It is possible to remove pacemaker leads in favor of MRI-compatible plating, BUT the process has a low success rate (about 70%), is invasive and expensive.  Thus, the only imaging open to me is PET (Positron Emission Tomography).  The procedure consists of injecting a sugar with a radioactive fluorine atom (very radioactive, half-life only two hours).  This sugar migrates to areas of the body with large metabolism rate, such as tumors.  However, the radioactive sugar can produce signals elsewhere in the body as well and spatial resolution is poor (maybe 5X worse than CT?).  When I WAS able to tolerate CT, the radiologist would compare CT patterns with those from PET to deduce what image was truly a tumor candidate.  Having said all of this, I would discourage use of PET for several reasons: it’s 10X more expensive than other scans; spatial resolution is poor; one is “hot” for a day; it exhibits a large percentage of false positives (PET suggests something is happening when all is quiescent ... happened twice for me).  I have an agreement with my oncologist that I will forgo PET scans UNTIL something happens.  For example, it might be that I start feeling poorly … or my daily data acquisition provides me a red flag.  Let me explain my data routine.  I log blood pressure, weight, morning temperature, and exercise stats (distance, calories and watts on a bicycle dynamometer).  When I look back at those data (I have more than 10 years of data), I can pinpoint when my pancreatic cancer started … within a single week, about 6 months before jaundice made it obvious.  Up to Feb 2009 my average output was 118 watts but from Feb to August it steadily declined (slowly enough I didn’t notice).  Then in Aug watts output declined precipitously (10% at first and much more at end), I felt terrible, became non-functional and finally jaundiced.  Fortunately, I embarked quickly on an effective Phase 2 clinical trial.  FYI, my power output (watts) is back to the same values before pancreatic cancer.

 

3 Dr. George Fisher joined the Stanford Pancreatic Cancer Support Group on 8 Jan. Dr. Fisher is a Professor of Medicine (Oncology) at Stanford University Medical Center and the Director of the Oncology Clinic at Stanford. He is a renowned oncologist and valued member of PanCan (recently appointed a member of the Medical Advisory Board). We’ll had a round table discussion regarding clinical trials, treatment options, and coping with cancer.  Betsy Harris, a Social Worker, at Stanford is the coordinator (ELHarris@StanfordMed.org ) of this group which meets the 2nd Wednesday each month.

Dr Fisher talked about biomarkers such as the traditional CA19-9 and new ones under evaluation.  I heard of a new biomarker in the webinar, but was shocked to learn how many are being evaluated, see this for a survey https://www.google.com/search?q=Paxlitaxol+Abraxane&oq=Paxlitaxol+Abraxane&aqs=chrome..69i57.6955j0j4&sourceid=chrome&espv=210&es_sm=93&ie=UTF-8#es_sm=93&espv=210&q=biomarker+pancreatic+cancer

It is hoped that effective biomarkers can lead to early detection and even screening.  An ideal biomarker would be specific to the target disease, not prone to errors of omission or commission, inexpensive and quick.  We are not there yet.  Using any of the prospective biomarkers would require PCR (see http://en.wikipedia.org/wiki/Polymerase_chain_reaction ) to get a sufficient volume or mass for analysis.  The beauty of PCR is that one can get a billion-fold quantity increase in just a day of heating and cooling (20-40 cycles).

An element that I heard that was new to me is that cancer cells shed these proteins into the blood (and lymph?) system, providing opportunities to find biomarkers.  A couple other things that surprised me: all cells in a tumor are NOT cancerous, as cancer cells need normal cells for blood supply and scaffolding.  Also it’s sometimes difficult to know if a treatment is working or not based on tumor size, as sometimes the tumor “plumps up” (my interpretation of sketchy notes).  A terminology I had not heard … an adenoma (cell) is pre-cancerous, while a pancreatic cancer cell is called adenocarcinoma.

There was lots more but my note-taking prowess was overwhelmed.

 


 

4 Recent news from the Pancreatic Cancer Action Network

Making More Treatment Options Possible / January 2014 Pancreas Matters

Personal/Pancreatic Research

x

Pancreatic Cancer Action Network communications@pancan.org via mail.pancan.netcommunity1.com 

Jan 7 (2 days ago)

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Our guest columnist this month is Vincent Picozzi, MD, chair of the Pancreatic Cancer Action Network's Medical Advisory Board and a practicing physician at Virginia Mason Medical Center in Seattle, Washington. 
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Find out why a pancreatic cancer clinical trial may be the best treatment option. Read more.

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How does a new pancreatic cancer drug get from an initial idea and laboratory testing to being used by patients? 
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