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Research Assessment #1

Date: ​September 6, 2018

Subject: ​Oncology

MLA citation:

Railton, David. “Cancer Research from August 2018.” ​Medical News Today​,
MediLexicon International, 31 Aug. 2018,
www.medicalnewstoday.com/articles/322923.php.

Analysis:

Because of my interest in the clinical side to oncology as well as the direct physician
side, I decided to research this week of new research and discoveries in the medical field for
treatment of cancer. Due to the volatile nature of oncology, where new medicine and research is
discovered everyday, there is always hope for improvement and safer cures of cancer. I tried to
find new research, however I was having hard time finding a article that explained research
through a students viewpoint rather than a medical professional. When I found an article by
David Railton, called “ Cancer Research from August 2018”, I realized I had found the perfect
article that could summarize this past months research and include deeper research.
The author breaks down the article into a couple of new ideas that have been found to
combat cancer and how they all aim to either fix, suppress, or end cancer cells. The first section
of the article was concerning research that focused on the​ natural process called “autophagy,
wherein damaged components of metastatic cancer cells are broken down and recycled" directly
by the body. During this section I learned how scientist tried turning off the activity of lysosomes
used in autophagy. When they did so, they found that the cancerous cells were unable to survive
the process of metastasis. While this was a very promising way to suppress and destroy cancer
cells, I did have some concerns. For example, if this body process was manipulated in order to
target cancer cells, how would the scientists stop the lysosomes from secreting enzymes that
would destroy other healthy cells as well. And this is where I believe my focus in ISM comes
into play. I want to conduct research into the physicians side of oncology but more relevantly, I
want to research CRISPR, which is a gene editing technology. I believe that through proper
CRISPR manipulation, we can truly make the target cells only cancer cells and no other for
lysosomes.
The next topic he goes into is Wnt Signaling and protrusions from cells called cytocemes.
Scientists believe that from stopping cytocemes, we can effectively stop cancer cells from
signaling and dividing. While this is a really good idea and there is much hope in it, I believe the
scientists still do not have a definitive way of how they want to achieve this. And because of this,
I do have some questions regarding this treatment. How will the scientists target individual cells
or will they cluster the cells together? Has there been any specific research done in order to use
the cytocemes and stop their signaling? Is it safe for the body and the host? There is not much
research done into the specific way the researchers want to achieve this and this is apparent from
the article. The author, David Railton, lets us know that scientists are hoping for a therapy that
can help them achieve this and then implies that they don’t really know much about actually
bringing this idea into fruition. However, I had not heard of Wnt Signaling and Cytocemes as a
way of treating cancer before reading this article so I was glad to have learned a new way that
metastatic cancer can be put to a stop. This will no doubt help me in the near and distant future
when I want to actually perform real research in a lab as this will be a choice for me to research
deeper into with a mentor.
The last and most surprising topic that the author goes into is instead of killing cancer
cells or suppressing them, is how to put cancer cells to sleep, indefinitely. This was the most
interesting part of the article because I had never before heard about a cancer treatment that did
not focus on killing cancer cells. This was a major discovery for me because one of my goals
was to find a way to help cancer treatments go from painful routes like chemotherapy and
radiation technology to less harmful ones, such as this. This discovery, I believe is the next step
in cancer treatment as it allows the patient to feel healthy and be healthy while effectively ending
cancer. I learned so much from this section of the article such as how new compounds inhibit
KAT6A and KAT6B proteins within the cancer cells and effectively puts all affected cells into a
deep and permanent sleep. Because of how important this kind of treatment is to me, I was very
critical of it. I had many questions and concerns about the research. For example, how ready will
patients be in accepting a treatment that will keep cancer cells within their body with a promise
of “permanent sleep” when there are other routes which kill cancer cells? Also, will these cells
ever mutate and come back from “permanent sleep” and begin hurting the patient? These were
some questions I had concerning this treatment and the article but I also had some concerns. As
human nature proves, we are more likely to choose a solution that guarantees a 100% efficiency
and success. I am concerned that many investors and grants will realize this and think that there
is not a future in a technology where it is not a 100% guarantee, which I believe will stop them
from giving money to this very important research. I think that if the scientists can find a 100%
guaranteed success rate that all cancer cells will go to permanent sleep, this can be not only
profitable but a godsend for patients. This section was truly important for me because it made me
understand that this topic not only concerns patients and healthcare but all fields, such as
psychology, business, and politics. I will definitely keep that as a caution when delving deeper
into my topic this year.
Reading this article has not only made me more knowledgeable about current events and
research into my topic but also aware that medicine and treatment is not as simple as just a
relationship between the producer and patient. It made me question human psychology, politics,
and business and truly how complex the world of pharmaceuticals is. I wonder if many
wonderful innovations and medicine that can change the face of healthcare are being suppressed
due to the pressures of politics and finance. This article, while just about research, has opened
my eyes to the real world, and because of that, I am ready to tackle cancer problems as well as
the other “non-medicinal” problems that will come out of it. In conclusion, this article has
improved my knowledge and helped me turn into a more realistic individual who is more than
ever ready to better the world of oncology.

(Article begins on next page)


Article :

Cancer never rests — and neither do those who have devoted their lives to finding new ways to
battle this deadly disease. In this Spotlight, we look at some of the most promising cancer studies
from the past month. ​Researchers continue to attack cancer from all sides.

Many of the most promising investigations into novel ​cancer​ therapies focus on the cellular
mechanisms at play in cancer formation and progression, and how they can be manipulated in a
way that ultimately benefits the patient. We have looked at several such studies over the past
month, including​ one​ that examined how metastatic cancer cells can be both created and
destroyed. Metastasis occurs when cancer cells break away, traveling through the body and
multiplying in new areas. This spreading of cells creates significant challenges for oncologists
attempting to locate and destroy tumors. The researchers behind the new study examined a
natural process called autophagy, wherein damaged components of metastatic cancer cells are
broken down and "recycled." The scientists tried turning off the activity of cellular structures
called lysosomes that are implicated in autophagy. When they did so, they found that the
cancerous cells were unable to survive the process of metastasis.

Acidity matters

A Spanish-American team that used a computer model to investigate how the metabolic
pathways in cancer cells are affected by variations in their environment has recently identified
another method for weakening cancer cells. The study ​reports​ that cancer cells need an alkaline
environment to function optimally and that they function less well in more acidic environments.
"This work is still very academic," admits study co-author Miquel Duran-Frigola, "but we
believe that some of the targets identified are ready to be tested in animals, thus allowing us to
move into more advanced preclinical trial stages." Another recent study identified a cellular
mechanism that the authors hope might contribute to a major change in cancer treatment. This
study​ investigated the role that Wnt proteins — proteins that control the proliferation of cells —
play in cancer development. Researchers already know that a process involving these proteins
called Wnt singaling enables cells to divide, and that when this process goes wrong, it can cause
malignant cells to divide, resulting in cancer. ​The researchers found that protrusions on cells
called cytonemes are involved in Wnt signaling, and that the process can be interrupted by
preventing cytonemes from forming. They believe that new therapies targeting the formation of
cytonemes may then be effective against cancer.

Putting cancer to bed

Would putting cancer cells "to sleep" work? Apparently so, according to researchers from
Australia, who developed a ​new class​ of compounds that appear to block the activity of cancer
cells.Could we put cancer cells to sleep permanently? Study author Anne Voss, from the Walter
and Eliza Hall Institute in Parkville, Australia, explained how the compounds inhibit KAT6A
and KAT6B, which are two proteins associated with certain cancers. ​"Rather than causing
potentially dangerous DNA damage," she says, "as ​chemotherapy​ and ​radiotherapy​ do, this new
class of anticancer drugs simply puts cancer cells into a permanent sleep."​ "This new class of
compounds stops cancer cells dividing by switching off their ability to 'trigger' the start of the
cell cycle. The technical term is cell senescence." ​"The cells are not dead, but they can no longer
divide and proliferate. Without this ability, the cancer cells are effectively stopped in their
tracks." ​She continues, "There is still a lot of work to be done to get to a point where this drug
class could be investigated in human cancer patients. However, our discovery suggests these
drugs could be particularly effective as a type of consolidation therapy that delays or prevents
relapse after initial treatment."

What are Sprouty 1 and 2?

As well as finding ways to exploit weaknesses in cancer at a cellular level, some cancer studies
we reported on this month have looked at how the body's natural defense mechanisms might be
primed to better fight cancer.​ One ​study​, for instance, found that immune cells are more effective
at attacking cancerous cells if two delightfully named key molecules called Sprouty (Spry) 1 and
Spry 2 are deleted. ​Deleting the genes responsible for these molecules improved the survivability
of CD8 T cells, which are a potent weapon of the immune system for dealing with viruses and
bacteria.

Primary breast cancer can 'shut down its own spread'

New findings may help "freeze" cancer cells before they can move to distant parts of the body.
As well as making CD8 T cells stronger in the face of cancerous cells, the removal of these
genes also allowed the CD8 T cells to "memorize" their cancerous adversities. So, if the body
encounters these cells again in the future, the immune system is quicker and more effective at
reacting to the threat. As the authors say, "Our findings could provide an opportunity to improve
future engineering of CAR T cells against tumors. This could potentially be used in combination
with a genome-editing technique like CRISPR that would remove the Sprouty 1 and 2 molecules
from the cells to make them more effective." Scientists from the University of California, San
Diego also ​recently​ investigated how some genes support cancer development. They discovered
that shards of DNA called enhancer RNAs (eRNAs) — which had previously been considered by
scientists to have no functional purpose — contain "instructions" for making molecules that help
cancer spread. The study found that eRNAs keep tumor-promoting genes "turned on at high
levels," but that these genes became less expressive when eRNAs were depleted. "Taken
together," the authors conclude, "our findings are consistent with the emerging notion that
eRNAs are functional molecules, rather than merely reflections of enhancer activation or simply
transcriptional noise."

Causing cancer to self-destruct

We have looked at studies that tried to stop cancerous cells from dividing, weaken cancer, and
put cancer to sleep, but ​one study​ investigated how to cause brain cancer to "self-destruct," as its
authors put it. Researchers attack cancer cells' power source. The team identified a chemical
compound that cut off the energy supply of malignant cells in mice with a highly aggressive type
of brain cancer called glioblastoma. Cancerous cells' energy supply consists of tiny organelles
called mitochondria.​ Scientists found that a compound called KHS101 prevented the
mitochondria from turning nutrients into energy, effectively killing the glioblastoma cells.
Importantly, the researchers found that this approach was effective at treating the full range of
genetic variations of glioblastoma cells. "This is the first step in a long process, but our findings
pave the way for drug developers to start investigating the uses of this chemical, and we hope
that one day it will be helping to extend people's lives in the clinic," explain the authors. Why are
elephants less susceptible to cancer? It is a valid question. Elephants are less susceptible to
cancer than us humans, and a ​new study​ suggests an explanation. Scientists previously
discovered that elephants each have at least 20 copies of a gene called p53 that suppresses
tumors, compared with the sole copy of this gene that humans and most other animals carry. In
the new study, researchers found that p53 contains a "pseudogene" called ​leukemia​ inhibitory
factor 6 (LIF6), which has the ability to "come back to life" and reactivate. ​When it is
reactivated, LIF6 ceases to be a pseudogene and starts to attack and kill damaged DNA. Similar
to the previous study that we looked at, LIF6 does this by puncturing the membranes of the
mitochondria of the affected cells, starving them of energy, and preventing them from potentially
becoming cancerous.​ The authors refer to LIF6 as a "zombie gene," as this once-defunct gene's
origins in elephants seem to date back to 30 million years ago. According to them, "This dead
gene came back to life. This is beneficial because it acts in response to genetic mistakes, errors
made when the DNA is being repaired. Getting rid of that cell can prevent a subsequent cancer."

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