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Old 01-12-2018, 02:36 PM   #1
Lani
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Join Date: Mar 2006
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has this Stanford researcher stolen my puppy dog analogy???

JANUARY 8, 2018
Stanford mechanical engineers give breast cancer research a boost
Stanford researchers say one way to solve the mystery of why some breast cancers are more likely to spread could come from studying the cell’s mechanical properties.


BY NATHAN COLLINS


Ovijit Chaudhuri and his lab are studying how mechanical properties of breast tissue influence tumor cells. (Image credit: Courtesy Department of Mechanical Engineering)
One of the most puzzling questions in breast cancer research is why some tumors stay put, while rogue cells from others break free and spread to surrounding tissues, the first step toward creating a more lethal disease. Although researchers have found some signs in mutated genes or telltale proteins on the cell’s surface, those discoveries don’t tell the whole story.

Curiously, one path to unraveling this mystery may lie in a field not usually associated with cancer research: mechanical engineering.

“Over the last 20 years or so there’s been increasing evidence that mechanical properties of breast tissue play a key role in promoting breast cancer progression,” said Ovijit Chaudhuri, an assistant professor of mechanical engineering, and a member of both Stanford ChEM-H and Stanford Bio-X.

Working with researchers across campus, Chaudhuri’s group is now studying the interplay between mechanical properties, such as the stiffness of breast tissue, and why some tumor cells spread to other tissues. By understanding that interplay better, he said, they may – one day – be able to develop better treatments for the women most at risk and ease the often-painful burden for the many others who currently undergo treatment but are less at risk.

Force on the smallest scale

Although it might sound strange for a mechanical engineer like Chaudhuri to study breast cancer – or anything to do with biology for that matter – there is certainly precedent: More than 10 years ago, researchers showed that stem cells respond dramatically differently based on what they were grown on. On a stiffer surface, for example, stem cells mature into bone; on a soft one, they often form neurons, the building blocks of the brain.

That experiment and others like it encouraged more interest in what is now called mechanobiology, the study of how mechanical properties and forces, often at the molecular level, affect everything from what genes a cell turns on and the shape and structure of an entire animal to the chemical processes underlying disease.

A stiff enemy

As with stem cells that behave differently on surfaces with different mechanical properties, stiffer breast tissue seems to encourage tumor growth, invasion and spreading, but the details of that process – as well as the processes of cancer invasion and tumor growth – remain unclear.

Chaudhuri and his lab are taking several different approaches to clarifying how the tissue’s stiffness influences the tumor cells. One group in his lab is culturing mammary cells – the kind most likely to become cancerous – inside of a type of material called a hydrogel. These hydrogels were designed to present biochemical signals similar to those that would be received by mammary cells in tissues. By tuning the hydrogel stiffness, the lab can then examine how enhanced stiffness promotes the formation and growth of tumors in mammary cells.

Another group is trying to understand how cancer cells escape past the basement membrane that surrounds breast tissue when they first begin to spread – something they suspect requires the cells to actually push and pull on the membrane. A typical cancer cell is hundreds of times larger than the membrane’s pores, if not larger, and although it’s clear that cells get through, it’s not clear how. Chaudhuri said that this “would be like a dog trying to get through the tiny hole in the mesh on a screen door.” One theory is that cancer cells use enzymes called proteases to cut their way through, yet drugs that target proteases often don’t stop cancer’s spread, suggesting there’s more going on than just enzymes.

“What we think is happening is that part of it is force, so cancer cells are physically pushing and pulling and prying open a hole to crawl through,” Chaudhuri said. “What we’re trying to study is, What does this process look like?”

Finally, the team is also looking at how tumors themselves grow, given that the surrounding tissue becomes increasingly stiff over time. How tumors make space to grow remains an open question, Chaudhuri said.

An end game for breast cancer?

Tackling those problems, Chaudhuri said, would not be possible without the knowledge and insights of researchers outside of mechanical engineering. Although at its core the lab focuses on mechanical systems and tools – creating gels with tunable stiffness is just one example – it counts among its members mechanical engineers, biologists, bioengineers and chemical engineers, and the group collaborates closely with faculty from biology and chemistry as well as the School of Medicine. The long-term goal, he said, is treating – and perhaps preventing – breast cancer.

“A lot of our focus is on understanding the fundamental interactions between cells and the extracellular matrix underlying processes such as breast cancer progression,” Chaudhuri said. In five or 10 years, he said, he hopes that turns into improved treatments for breast cancer, but in the long term, the real hope is to prevent breast cancer from happening in the first place, not just to treat it. “This is pretty far off, but I think that should be the ultimate goal.”

Media Contacts

Nathan Collins, Stanford News Service: (650) 725-9364, nac@stanford.edu
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Old 01-17-2018, 01:06 PM   #2
SoCalGal
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Re: has this Stanford researcher stolen my puppy dog analogy???

Ha! No doubt
__________________
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, to remove skin mets. Not able to get clear margins. So schedule another 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 – cut out, cut out, 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. New onc orders PET/ct & Brain MRI to re-stage me.
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 trial but then 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. (premeds for Herceptin now)
Sept 2011 Tykerb, Herceptin, Zometa, Avastin. (switched back to Zometa, pet/ct bone mets seemed worse on Xgeva)
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 GAMMA ZAPPA continue HAPZ
APRIL 2013 - cancerversary 17 years from original diagnosis. 6 yrs stage 4. [/COLOR][/B]
"FAILED" PETscan on 4/2/13 (WTF)
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 - NEWSFLASH:
6 YEARS POST GAMMA ZAPPA, 7 YEARS STAGE 4 and 18 YEARS FROM ORIGINAL DX! (CUCK FANCER)
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 Herceptin, PERJETA, xgeva. Adding back Avastin to see if lungs will go quiet
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 and due for MRI brain check (check please!).
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: CA15‐3=46.9 CEA=12.3 CA 27.2=79 SCIATIC PAIN DEAL BREAKER.
3/23/16 Laminectomy w/coflex implant L4/5. NO MORE SCIATIC PAIN!!! Healing.
APRIL 2016 - 9 YEARS STAGE FOUR!
(20 years from original diagnosis) July 2016 - continue HAP plus Xgeva. Not NED but not DEaD.
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
2017 I AM COMING FOR YOU!
APRIL 2017 10 YEARS MBC
December 2017 - Progression - gonna switch it up
FEB 2018 - Kadcyla 3 cycles ---->progression :(
MAY30th - bronchoscopy, w/foundation one=her2+ er/pr negative. AUGUST hoping to start clinical trial if they would just get it together and accept me.
CuckFancer!! 11 years MBC.
Aug 27, 2018 - start clinical trial ZW25 aka this better fu*king work
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