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Old 09-21-2012, 06:43 AM   #1
KDR
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Red face MD Anderson Set To Moon Shot Cancer

http://www.mdanderson.org/newsroom/n...s-program.html

The first announcement I heard on this indicated there would be eight cancers targeted.

Karen
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World Trade Center Survivor (56th Floor/North Tower): 14 years and still just like yesterday.
Graves Disease, became Euthyroid via Radioactive Iodine, June 2001.
Thyroid Eye Disease. 2003. Decompression surgery in 2009; eyelid lowering surgery in 2010.
Diagnosed: June 2010, liver mets. ER-/PR+10%; HER2+++.
July 2010: Begin Taxol/Herceptin. Eliminate sugar from diet. No surgery or radiation.
January 2011: NED
April 2011: Progression in liver only. Other previous affected areas eradicated. Stop Taxol/Herceptin after 32 infusions.
May 2011: Brain MRI: clear.
May 2011: Begin Tykerb daily, Xeloda twice per day for one week on, one week off, and Herceptin.
November 2011: Progression in liver. All other tumors remain eradicated.
December 2011: BEGIN TRIAL #09-093 Taxol, MCC-DM1 (T-DM1), Perjeta.
Trial requires scans every six weeks, bloodwork and infusions weekly.
Brain MRI: clear.
January 2012: NED. Liver mets, good riddance!
March 2012: NED. Developed SMA (rare blood clot) in intestinal artery and loss of sight in right eye due to optical nerve neuropathy. Resolved when Taxol removed this month.
Continue Protocol of T-DM1 weekly and Perjeta every 3 weeks.
May 2012: NED.
June 2012: Brain MRI: clear.
June-December 2012: NED.
December 2012: TRIAL CONCLUDED; ENTER TRIAL EXTENSION #09-037. CT, Brain MRI, bone scan: clear. NED.
January-March 2013: NED.
June 2013: Brain MRI: clear. CEA upticking; CT shows new met on liver.
July 3, 2013: DISASTER STRIKES during liver ablation: sloppy surgeon cuts intercostal artery and I bleed out, lose 3.5 liters of blood, have major hemothorax, and collapsed lung requiring emergency resuscitative thoracotomy, lung surgery, rib rearrangement and cutting deep connective tissue, transfusion. Ablation incomplete. This life-saving procedure would end up causing me unforgiving pain with every movement I make, permanently, otherwise known as forever.
July 26, 2013: Try Navelbine/Herceptin. Body too weak after surgery and transfusion. Fever. CEA: Normal.
August 16, 2016: second dose Navelbine/Herceptin; CEA: Normal. Will skip doses. Watching and waiting.
September 2013: NED, Herceptin only. CEA: Normal. Started Arimidex.
October-November 2013: NED. Herceptin and Arimidex. CEA, CA125, 15-3: Normal.
December 2013: Something brewing. PET lights up on little spot on liver; CEA upward trend, just outside normal. PET and triphasic liver scan confirm Little Met. Restart Perjeta with Herceptin, stay on Arimidex. Genomic sequencing completed for future treatments, if necessary.
January 2014: Ablate Little Met on the 6th. Happy New Year.
March 2014: Brain MRI: clear. PET/CT reveal liver mets return; new lung mets. This is not funny.
March 2014: BEGIN TRIAL #10-005 A(11)-Temsirolimus plus Neratinib.
April 2014: Genomic testing indicated they could work, they did not. Very strange drug combo for me, felt weird.
April 2014: Started Navelbine and Herceptin. Needed something tried and true, but had significant progression.
June 2014: Doxil and Herceptin.
July 2014: Progression. Got nothing out of it. Brain: NED.
July 2014: Add integrative medical hematologist-oncologist to my team. Begin supplements. These are tumor-busting, immune system boosters. Add glutathione, lysine and taurine IV infusions every three weeks.
July 2014: Begin Gemzar, Herceptin & Perjeta. Happy.
August 2014: ECHO perfect.
January 2015: Begin weekly Vitamin D Analog infusions. 25 mcg. via port.
February 2015: CT: stable.
April 2015: Gem working, but not 100%. Looking into immunotherapy. Finally, treatments for the 21st century!
April 2015: Penn Medicine. Dendritic cell immunotherapy.
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Old 09-21-2012, 08:47 AM   #2
michka
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Re: MD Anderson Set To Moon Shot Cancer

It's about time to bring all researchers together..
Only triple negative breast cancers? There are not enough women dying of breast cancer to be on the list (and more and more of young women)?
One of the criteria is "the potential for near-term measurable success in terms of cancer mortality". What does this mean? They think they have weapons, they think it is desperate or the list was made up by only men? I am wondering.
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08.2006 3 cm IDC Stage 2-3, HER2 3+ ER+90% PR 20%
FEC, Taxol+ Herceptin, Mastectomy, Radiation, Herceptin 1 year followed by Tykerb 1 year,Aromasin /Faslodex

12.2010 Mets to liver,Herceptin+Tykerb
03.2011 Liver resection ER+70% PR-
04.2011 Herceptin+Navelbine+750mg Tykerb
06.2011 Liver ned, Met to sternum. Added Zometa 09.2011 Cyberknife for sternum
11.2011 Pet clear. Stop Navelbine, continuing on Hercpetin+Tykerb+Aromasin
02.2012 Mets to lungs, nodes, liver
04.2012 TDM1, Ned in 07.2012
04.2015 Stop TDM1/Kadcyla, still Ned, liver problems
04.2016 Liver mets. Back on Kadcyla
08.2016 Kadcyla stopped working. mets to liver lungs bones
09.2016 Biopsy to liver. no more HER2, still ER+
09.2016 CMF Afinitor/Aromasin/ Xgeva.Met to eye muscle Cyberknife
01.2017 Gemzar/Carboplatin/ Ibrance/Faslodex then Taxotere
02.2017 30 micro mets to brain breathing getting worse and worse
04.2017 Liquid biopsy/CTC indicates HER2 again. Start Herceptin with Halaven
06.2017 all tumors shrunk 60% . more micro mets to brain (1mm mets) no symptoms
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Old 09-21-2012, 10:12 AM   #3
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Re: MD Anderson Set To Moon Shot Cancer

Go MD Anderson!
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dx 11/12/09 IDCI
Stage 3a
ER 98% PR 80%
Her2 +3
4/12 nodes
6 rounds TCH
Herceptin 12 months 3weeks
Rad. 30 tx
Tamoxifin 6 months stopped
Arimedex stopped 9/12 (side effects)
Aromasin 10/12
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Old 09-22-2012, 12:47 PM   #4
gdpawel
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Re: MD Anderson Set To Moon Shot Cancer

Great technology, but information of extremely limited value. People will think because they are being completely genotyped, this will give all the answers needed. But it won't. Genotyping will only be of value for drugs for which a gene mutation is informative -- basically KRAS and EGFR mutations -- and we already have tests for those and they are of very limited value. Otherwise, it's a ton of information for which the drug selection value is pretty useless.

What's more important than what genes are in the DNA is what genes are actively making RNA, which RNA is actively making protein, which protein is being turned off or turned on, and how all of the proteins in the cell are interacting with each other. The only way to get the latter information, which is ultimately what you want, is to treat the patient with phenotype analysis. In drug selection, phenotype analysis doesn't dismiss DNA testing, it uses all the information, measuring the interaction of the entire genome, to design the best treatment for each individual.

I believe this and other recent announcements have been overreached and giving us overexpectations. The research is exciting, but the path remains long and arduous.

Dr. Len Lichtenfeld of the American Cancer Society wrote:

“It is important to recall that despite the fact this is incredibly sophisticated and difficult work, it is still reasonably early in our ability to perform the analyses, interpret the data, and determine the best way to apply it to the clinic. We still have a long way to go, and we must always remember that cancer has a way of being more complicated at every turn that we might otherwise anticipate as our research and our knowledge advances. But research such as this also puts more of the pieces of the puzzle of breast cancer together in a way that a solution to the dilemma of understanding breast cancer and how we can apply the best treatment does appear to be more readily at hand.

What is the most important message from this research?

Unfortunately, it is not going to change lives immediately. Your doctor isn’t going to give you a different treatment for your breast cancer today, tomorrow, or next week because of this research. There is no question that doctors involved in breast cancer treatment are going to take a very careful look at this research and determine the best way to apply this information to new approaches to breast cancer as quickly as they can, but that will still take time.

To me, the most important message from this research is to confirm what many of us have been thinking for some time now: we are seeing the fruits of decades—yes, decades—of hard work in the laboratory taking us to a point we are going to have a significant impact on patient care and the outcomes of treatment for cancer. At the same time, the very support for that research is in jeopardy due to decreases in government funding, business investment, and private philanthropy.”

http://acspressroom.wordpress.com/20...ncertypes2012/
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Old 09-25-2012, 12:05 PM   #5
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CNN proclaims “BREAKING news: cure for cancer close”???

http://www.healthnewsreview.org/2012...-cancer-close/
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Old 09-25-2012, 09:54 PM   #6
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Re: MD Anderson Set To Moon Shot Cancer

This does not sound like the goal is to cure - sounds very TREATMENT based, even if the treatment is improved!
http://cancermoonshots.org/moon-shots/breast-ovarian/
  • Increase the five-year survival rate of women with triple-negative breast cancer or high-grade serous ovarian cancer
  • Identify women and families at risk for these cancers and implement programs to decrease the chance they will develop cancer
  • Change the upfront treatment to improve the outcomes of women with these cancers
  • Within the first year, implement clinical trials of promising new therapies
  • Develop new imaging technologies that can detect aggressive lethal breast tumors at an early stage
  • Convert temporary responses to durable therapy by identifying and targeting drug resistance mechanisms
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1996 cancer WTF?! 1.3 cm lumpectomy Er/Pr neg. Her2+ (20nodes NEGATIVE) did CMF + rads. NED.
2002 recurrence. Bilateral mastectomy w/TFL autologous recon. Then ACx2. Skin lymphatic rash. Taxotere w/Herceptin x4. Herceptin/Xeloda. Finally stops spreading.
2003 - Back to surgery, remove skin mets, and will have surgery one week later when pathology can confirm margins.
‘03 latisimus dorsi flap to remove skin mets. CLEAN MARGINS. Continue single agent Herceptin thru 4/04. NED.
‘04 '05 & 06 tiny recurrences - scar line. surgery to cut out. NED each time.
1/2006 Rads again, to scar line. NED.

3/07 Heartbreaking news - mets! lungs.sternum. Try Tykerb/Xeloda. Tykerb/Carbo/Gemzar. Switch Oncs.
12/07 Herceptin.Tykerb. Markers go stable.
2/8/08 gamma knife 13mm stupid brain met.
3/08 Herceptin/tykerb/avastin/zometa.
3/09 brain NED. Lungs STABLE.
4/09 attack sternum (10 daysPHOTONS.5 days ELECTRONS)
9/09 MARKERS normal!
3/10 PET/CT=manubrium intensely metabolically active but stable. NEDhead.
Wash out 5/10 for tdm1 but 6/10 CT STABLE, PET improving. Markers normal. Brain NED. Resume just Herceptin plus ZOMETA
Dec 2010 Brain NED, lungs/sternum stable. markers normal.
MAR 2011 stop Herceptin/allergy! Go back on Tykerb and switch to Xgeva.
May-Aug 2011 Tykerb Herceptin Xgeva.
Sept 2011 Tykerb, Herceptin, Zometa, Avastin.
April 2012 sketchy drug trial in NYC. 6 weeks later I’m NED!
OCT 2012 PET/CT shows a bunch of freakin’ progression. Back to LA and Herceptin.avastin.zometa.
12/20/12 add in PERJETA!
March 2013 – 5 YEARS POST continue HAPZ
APRIL 2013 - 6 yrs stage 4. "FAILED" PETscan on 4/2/13
May 2013: rePetted - improvement in lungs, left adrenal stable, right 6th rib inactive, (must be PERJETA avastin) sternum and L1 fruckin'worsen. Drop zometa. ADD Xgeva. Doc says get rads consultant for L1 and possible biopsy of L1. I say, no thanks, doc. Lets see what xgeva brings to the table first. It's summer.
June-August 2013HAPX Herceptin Avastin Perjeta xgeva.
Sept - now - on chemo hold for calming tummy we hope. Markers stable for 2 months.
Nov 2013 - Herceptin-Perjeta-Avastin-Xgeva (collageneous colitis, which explains tummy probs, added Entocort)
December '13 BRAIN MRI ned in da head.
Jan 2014: CONTINUING on HAPX…
FEB 2014 PetCT clinical “impression”: 1. newbie nodule - SUV 1.5 right apical nodule, mildly hypermetabolic “suggestive” of worsening neoplastic lesion. 2. moderate worsening of the sternum – SUV 5.6 from 3.8
3. increasing sclerosis & decreasing activity of L1 met “suggests” mild healing. (SUV 9.4 v 12.1 in May ‘13)
4. scattered lung nodules, up to 5mm in size = stable, no increased activity
5. other small scattered sclerotic lesions, one in right iliac and one in thoracic vertebral body similar in appearance to L1 without PET activity and not clearly pathologic
APRIL 2014 - 6 YRS POST GAMMA ZAP, 7 YRS MBC & 18 YEARS FROM ORIGINAL DX!
October 2014: hold avastin, continue HPX
Feb 2015 Cancer you lost. NEDHEAD 7 years post gamma zap miracle, 8 years ST4, +19 yrs original diagnosis.
Continue HPX. Adding back Avastin
Nov 2015 pet/ct is mixed result. L1 SUV is worse. Continue Herceptin/avastin/xgeva. Might revisit Perjeta for L1. Meantime going for rads consult for L1
December 2015 - brain stable. Continue Herceptin, Perjeta, Avastin and xgeva.
Jan 2016: 5 days, 20 grays, Rads to L1 and continue on HAPX. I’m trying to "save" TDM1 for next line. Hope the rads work to quiet L1. Sciatic pain extraordinaire :((
Markers drop post rads.
2/24/16 HAP plus X - markers are down
SCIATIC PAIN DEAL BREAKER.
3/23/16 Laminectomy w/coflex implant L4/5. NO MORE SCIATIC PAIN!!! Healing.
APRIL 2016 - 9 YRS MBC
July 2016 - continue HAP plus Xgeva.
DEC 2016 - PETCT: mets to sternum, lungs, L1 still about the same in size and PET activity. Markers not bad. Not making changes if I don't need to. Herceptin/Perjeta/Avastin/Xgeva
APRIL 2017 10 YEARS MBC
December 2017 - Progression - gonna switch it up
FEB 2018 - Kadcyla 3 cycles ---->progression :(
MAY30th - bronchoscopy, w/foundation1 - her2 enriched
Aug 27, 2018 - start clinical trial ZW25
JAN 2019 - ZW25 seems to be keeping me stable
APRIL 2019 - ONE DOZEN YEARS LIVING METASTATIC
MAY 2019 - progression back on herceptin add xeloda
JUNE 2019 - "6 mos average survival" LMD & CNS new single brain met - one zap during 5 days true beam SBRT to cord met
10/30/19 - stable brain and cord. progression lungs and bones. washing out. applying for ds8201a w nivolumab. hope they take me.
12/27/19 - begin ds8401a w nivolumab. after 2nd cycle nodes melt away. after 3rd cycle chest scan shows Improvement, brain MRI shows improvement, resolved areas & nothing new. switch to plain ENHERTU. after 4th cycle, PETscan shows mostly resolved or improved results. Markers near normal. I'm stunned but grateful.
10/26/20 - June 2021 Tucatinib/xeloda/herceptin - stable ish.
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Old 09-25-2012, 10:14 PM   #7
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The "Moon Shots Program" will focus on genomics to understand the genetic and molecular basis of cancers and to identify patient-specific treatments by making genomics routine in cancer care. Tumor analysis coupled with clinical trial literature search to try and match therapies to patient-specific biomarker information to generate a treatment approach. The problem is that genomics cannot predict for disease or patient-specific drug effects (drug selection).

No technology is more well suited to the investigation and simultaneous analysis of the relationships between patient-specific target molecules, cell functions and cell sub-populations than cytometry and Cytometric analysis of cell phenotype and function provides a very comprehensive overview of this ever-broadening field. It doesn't dismiss DNA testing, it uses all the information, measuring the interaction of the entire genome, to design the best treatment for each individual.

Replacing the one-size-fits-all paradigm with another one-size-fits-all paradigm isn't making personalized cancer therapy any more cost effective. Targeted therapy is still a one-size-fits-all model. Finding what targeted therapies would work for what cancers is very difficult. A lot of trial-and-error goes along trying to find out.

Molecular profiling measures the expression of protein only in the "resting" state, prior to drug exposure. There is no single gene whose expression accurately predicts clinical outcome. Efforts to administer targeted therapies in randomly selected candidates often result in low response rates at significant toxicity and cost.

Molecular profiling is based on the same clinical literature search (population study), which tries to match therapies to patient-specific biomarker information to generate a treatment approach. This is not really personalized medicine, but just a refinement of statistical data. In other words, information that may help when considering "potential" treatment options (theoretical analysis). It's never even measured against your actual cancer cells.

All the molecular profiling studies tell us is whether or not the cancer cells are potentially susceptible to a mechanism of attack. They don't tell you if one drug is better or worse than another drug which may target a certain mechanism. The cell is a system, an integrated, interacting network of genes, proteins and other cellular constituents that produce functions. You need to analyze the systems' response to drug treatment, not just one mechanism of attack.

None of the targeted drugs are cures, they are life savers by being a life lengthener. Targeted therapy is what is used to stabilize the disease rather than cure it. Will patients have to take the drugs indefinitely? How is that cost effective?

Most targeted drugs do not directly kill cancer cells, they just stop the growth of tumors. Therefore, patients must receive treatment for prolonged periods, and over time, they often develop secondary resistance. They eventually succumb to treatment resistance or disease recurrence.

To beat down individual cancer mortality, an oncologist needs to target all the many cancers that make up individual cancer, the dozens of different mechanisms that cells use to proliferate and spread. That is the leading edge of personalized research and treatment, determining how an individual's tumor cells work and hitting those pathways with multiple drugs, simultaneously or sequentially, each chosen because it targets one of those growth, replication and angiogenesis mechanisms.

Trying to mate a notoriously heterogeneous disease into one-size-fits-all treatments is disingenuous to all who are inflicted with it. And the criticism remains: All of the clinical trial resources have gone toward driving a square peg (one-size-fits-all chemotherapy) into a round hole (notoriously heterogeneous disease).
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Old 10-22-2012, 10:21 AM   #8
gdpawel
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Texas Turmoil: 'Vultures' In, Nobel Laureates Out

http://www.medscape.com/viewarticle/772706

In an apparent effort to play King Solomon, the University of Texas System vice chancellor for health affairs has granted a limited waiver from the institution’s conflict-of-interest policy to the president of the University of Texas MD Anderson Cancer Center, The Houston Chronicle reports.

And the move is prompting criticism because because the cancer center president Ronald DePinho will be allowed to maintain financial ties with his three drugmakers. His holdings in Aveo Pharmaceuticals, Karyopharm and Metamark Genetics will be placed in a blind trust as part of the waiver, the paper writes.

This is clearly an interesting and unusual situation. The vice chancellor appears to be suggesting that real-world experience is useful to the school and apparently does not want to make a move that might prompte DePinho to exit. On the other hand, the critics make a point that a partial waiver suggests a slippery slope.

Source: Pharmalot

http://www.chron.com/news/houston-te...ep-3976008.php
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