True enough, nor what causes cancer to begin with -- all the chemical
pollution we're submerged in ....
Still, I like the idea of a physical mechanism -- the density of a tumor
-- a physically quantitative and measurable condition that sets in motion
a qualitative change (an "emerging property" in current
See, for example, cell biologist Stuart Newman's brilliant research on
how the proximity and location of cells -- all with the same genetic
complement -- cause those cells to differentiate and form, for example,
the human hand or eye. It's wonderful dialectical "stuff", and
it seems to me could easily integrate with the new research on cancers
At 11:17 AM 6/17/2017, [log in to unmask] wrote:
As usual, no mention of the role
of nutrition and immune enhancing treatments- esp as an adjunct to
On Jun 17, 2017, at 10:55 AM, Mitchel Cohen
[log in to unmask] [sprayno]
<[log in to unmask]
JOHNS HOPKINS RESEARCHERS SAY THEY'VE UNLOCKED KEY TO
CANCER METASTASIS AND HOW TO SLOW IT
by Carrie Wells
<[log in to unmask]>
The Baltimore Sun
June 16, 2017
Hasini Jayatilaka was a sophomore at the Johns Hopkins University working
in a lab studying cancer cells when she noticed that when the cells
become too densely packed, some would break off and start
She wasn't sure what to make of it, until she attended an academic
conference and heard a speaker talking about bacterial cells behaving the
same way. Yet when she went through the academic literature to see if
anyone had written about similar behavior in cancer cells, she found
Seven years later, the theory Jayatilaka developed early in college is
now a bona fide discovery that offers significant promise for cancer
Jayatilaka and a team at Johns Hopkins discovered the biochemical
mechanism that tells cancer cells to break off from the primary tumor and
spread throughout the body, a process called metastasis. Some 90 percent
of cancer deaths are caused when cancer metastasizes. The team also found
that two existing, FDA-approved drugs can slow metastasis
"A female patient with
cancer doesn't succumb to the disease just because she has a mass on
her breast; she succumbs to the disease because [when] it spreads either
to the lungs, the liver, the brain, it becomes untreatable," said
Jayatilaka, who earned her doctorate in chemical and biomolecular
engineering this spring in addition to her earlier undergraduate degree
"There are really no therapeutics out there right now that directly
target the spread of cancer. So what we came up with through our studies
was this drug cocktail that could potentially inhibit the spread of
The study was published online May 26 in the journal Nature
Communications. The next step for the team is to test the effectiveness
of the drugs in human subjects.
Typically, cancer research and treatment has focused on shrinking the
primary tumor through chemotherapy or other methods. But, the team said,
by attacking the deadly process of metastasis, more patients could
"It's not this primary tumor that's going to kill you
typically," said Denis Wirtz, Johns Hopkins' vice provost for
research and director of its Physical Sciences-Oncology Center, who was a
senior author on the paper.
Jayatilaka began by studying how cancer cells behave and communicate with
each other, using a three-dimensional model that mimics human tissue
rather than looking at them in a petri dish. Many researchers believe
metastasis happens after the primary tumor reaches a certain size, but
Jayatilaka found it was the tumor's density that determined when it would
"If you look at the human population, once we become too dense in an
area, we move out to the suburbs or wherever, and we decide to set up
shop there," Jayatilaka said. "I think the cancer cells are
doing the same
When the tumor reaches a certain density, the study found, it releases
two proteins called Interleukin 6 and Interleukin 8, signaling to cancer
cells that things had grown too crowded and it was time to break off and
head into other parts of the body.
Previously, Wirtz said, the act of a tumor growing and the act of cancer
cells spreading were thought to be very separate activities, because
that's how it appeared by studying cancer cells in a petri dish, rather
than the 3-D model the Hopkins team used. Many researchers study only
cancer cell growth or its spread, and don't communicate with each other
often, he said.
Once the cancer cells start to sense the presence of too many other
cancer cells around them, they start secreting the Interleukin proteins,
Wirtz said. If those proteins are added to a tumor that hasn't yet
metastasized, that process would begin, he said.
The team then tested two drugs known to work on the Interleukin receptors
to see if they would block or slow metastasis in mice. They found that
using the two drugs together would block the signals from the Interleukin
proteins that told the cancer cells to break off and spread, slowing Â
though not completely stopping Â metastasis.
The drugs the team used were Tocilizumab, a rheumatoid arthritis
treatment, and Reparixin, which is being evaluated for cancer
The drugs bind to the Interleukin receptors and block their signals,
Though metastasis was not completely stopped, Jayatilaka said, the mice
given the drug cocktail fared well and survived through the experiment.
She said adding another, yet-to-be-determined drug or tweaking the dose
might stop metastasis entirely.
Contrary to the hair loss, nausea and other negative side effects
patients undergoing chemotherapy suffer, Wirtz said the side effects from
the drugs used in the study would be minimal.
Anirban Maitra, co-director of a pancreatic cancer research center at the
MD Anderson Cancer Center at the University of Texas, cautioned that
clinical trials in humans are needed to prove the theory.
"There's a risk that something that looks so great in an animal
model won't pan out in a human," he said.
But Maitra said the study looked promising, in particular because the
researchers had used drugs already on the market. It can take a decade to
identify a drug that would perform similarly and get it approved, and
many similar observations don't advance because of the time and expense
it can take to get drug approval, he said.
Muhammad Zaman, a professor and cancer expert at Boston University,
called the Hopkins discovery "exciting."
"This paper gives you a very specific target to design drugs
against," he said. "That's really quite spectacular from the
point of view of drug design and creating therapies."
Zaman said it was important for cancer researchers to use engineering to
better understand cancer, as the Hopkins team did.
"This really brings cancer and engineering together in a very unique
way, and it really takes an approach that is quantitative and
rigorous," he said. "We have to think of cancer as a complex
system, not just a disease."
Wirtz predicted a future where cancer would be fought with a mix of
chemotherapy to shrink the primary tumor and drug cocktails like the one
the Hopkins team developed to ensure it would not metastasize. He
compared such a treatment to how HIV/AIDS is treated today.
"We're not going to cure cancer with one therapy or even two
therapies; it's going to be drug cocktails," Wirtz said.
"That's what saved the day with HIV/AIDS."
Immunotherapy, which uses the body's immune system to fight cancer, also
could play a role in a combined method, Wirtz added.
"We're, in research, sometimes incentivized to look at one pathway
at a time, one type of cancer at a time," Wirtz said. "I think
oncology has started realizing we're going to need more than one
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