Timothy Wang at Columbia recently published
work in Cancer Cell (DOI: 10.1016 / j.ccell.2016.11.005) that showed that recruitment of nerves into the tumor microenvironment is necessary and sufficient for stomach cancer progression, and that blocking a neurotransmitter in the nerves that line the stomach could represent a novel therapy.
The Herlyn Laboratory seeks to further define the various signaling pathways that
work in cancer cells in order to discover new opportunities to inhibit cancer growth through targeted therapeutics.
A drug that prevents myosin from
working in cancer cells could keep them from invading other cells or metastasize into different organs.
Not exact matches
Chemotherapy
works by killing
cancer cells by targeting fast - dividing
cells, and
in most cases, kills off some healthy
cells along the way, including nerve
cells in the brain.
BioNTech, which has around 700 employees at sites
in Germany — more than any other unlisted biotech firm
in Europe — is also
working on other
cancer - fighting technologies, including antibodies,
cell therapies and small molecules.
The lab that I
work in is primarily interested
in understanding how and why certain
cancers are more likely to spread to the skeleton, and my personal project has focused on uncovering new mechanisms that the
cancer cells use to communicate with other
cells in the bone.
In one respect the first look is unnerving, because the chemical mechanisms that seem to drive the cancer cell astray are not different in kind from mechanisms at work in the normal cel
In one respect the first look is unnerving, because the chemical mechanisms that seem to drive the
cancer cell astray are not different
in kind from mechanisms at work in the normal cel
in kind from mechanisms at
work in the normal cel
in the normal
cell.
Recent collaborative
work between UCR and Cedars - Sinai Medical Center
in Los Angeles demonstrated that
in animal models of human breast
cancer, mice treated with 123B9 that was conjugated with paclitaxel had significantly fewer circulating
cancer cells in the blood compared to mice that were not treated or even treated with paclitaxel alone.
The compound (right panel) has a scorpion - like shape with two arms grabbing EphA2 - expressing
cancer cells, and a tail (brown) constituted by a cytotoxic chemotherapeutic agent (paclitaxel used
in this
work).
«The fine particles of this drug allow for it to be released slowly and stay
in the abdomen,» said Katherine Roby, Ph.D., research associate professor
in the Department of Anatomy and
Cell Biology at KU Medical
Cancer, who started her pre-clinical
work on Nanotax more than a decade ago.
Previous
work in Weinberg's lab had shown that after a tumor forms
in one part of the body, some of the
cancer cells undergo EMT, Mani explains.
For some years now, a new class of drugs called antibody - drug conjugates (ADCs) have been used, which
work in two ways: they consist of an antibody that binds selectively to the tumor
cell receptor and interrupts the signal to propagate; they also act as a transport vehicle for a chemical substance that enters the
cancer cells with the antibody and triggers their death.
Working in cell cultures and mice, researchers at Johns Hopkins have found that an experimental drug called fostamatinib combined with the chemotherapy drug paclitaxel may overcome ovarian
cancer cells» resistance to paclitaxel.
Skin
Cancer cells work together to spread further and faster, according to a new study published
in Cell Reports.
«Our
work strongly supports that
cancer stem
cells are the main source of growth
in these tumors and, as such, should be considered promising targets for treatment,» says Mario Suvà, MD, PhD, of the MGH Department of Pathology, co-senior author of the Nature paper.
While researchers have long
worked with nanoparticles for drug delivery, the findings put forth by He and his team represent a crucial breakthrough
in addressing multidrug resistance
in cancer cells.
In addition to using healthy
cells to do their
work for them,
cancer cells also slowly destroy the skin's immune defence mechanism.
For some
cancer patients, viruses engineered to zero
in on tumor
cells work like a wonder drug.
Recent
work shows the biggest ones are abundant
in many
cancer cells but not healthy
cells and that these circles may aid the
cancer's evolution and recurrence.
Previous
work in the lab of CU
Cancer Center investigator, Carol Sartorius, PhD, and others shows that progesterone aids the expansion of CK5 +
cells.
She was on her way out to a pub after a scientific conference when she spotted Paul Nurse, who was
working on
cell - cycle regulation at Imperial
Cancer Research Fund
in London.
However, along with this seemingly linear storyline
in which retinoids block progesterone's promotion of CK5 +
cells, previous
work in the lab of CU
Cancer Center investigator Peter Kabos, MD, and others shows that breast
cancers treated with anti-estrogen drugs like tamoxifen or aromatase inhibitors show an increased population of CK5 +
cells — it is as if these therapies remove the roadblock of estrogen - dependent
cells, leaving CK5 +
cells to proliferate.
Immunotherapy is an emerging field
in the global fight against
cancer, even though scientists and clinicians have been
working for decades to find ways to help the body's immune system detect and attack cancerous
cells.
«Different types of
cancer cells with different strengths and weaknesses are both present
in the tumor at the same time and can
work together to spread faster and more efficiently.
In a continuation of this work, Goldman is also using mathematical modeling to pursue the most effective dose of chemotherapy to induce the vulnerable transition state of the cancer cell demonstrated in this researc
In a continuation of this
work, Goldman is also using mathematical modeling to pursue the most effective dose of chemotherapy to induce the vulnerable transition state of the
cancer cell demonstrated
in this researc
in this research.
«Our
work suggests a mechanism for
cell lethality involving the regulation of BCAAs as crucial elements
in pancreatic
cancer by regulating ME3,» said Ronald DePinho, M.D., professor of Cancer Biology, senior author of the Nature paper and president of MD And
cancer by regulating ME3,» said Ronald DePinho, M.D., professor of
Cancer Biology, senior author of the Nature paper and president of MD And
Cancer Biology, senior author of the Nature paper and president of MD Anderson.
Although Coley couldn't explain precisely why or how his toxins
worked, modern immunotherapy treatments help T -
cells in the immune system to recognize specific
cancer cells and attack them.
He needed a stem
cell transplant, which is a normal treatment for leukemia, but his
cancer needed to be
in remission first, and the chemotherapy wasn't
working.
The biomarker panel, enabled by discovery
work of first author Jungsun Kim, PhD, a postdoctoral fellow
in Zaret's lab, builds on a first - of - its - kind human -
cell model of pancreatic
cancer progression the lab described
in 2013.
«As it has been shown to be selective to
cancer cells and non-toxic to normal
cells in the lab, this peptide has the potential to be safe, but further
work would be required to prove that.»
The findings were published recently
in the Journal of the National
Cancer Institute by a group that includes Rony A. François, an M.D. / Ph.D. student
working with Maria Zajac - Kaye, Ph.D., an associate professor
in the UF College of Medicine's department of anatomy and
cell biology.
But their overriding interest
in BPTES, says Slusher, was
in how it
works: by blocking the production of glutamine, an amino acid that acts as a building block of
cells and is used frequently by pancreatic
cancers to create more
cancer cells.
Maria Zajac - Kaye, Ph.D., an associate professor
in the College of Medicine's department of anatomy and
cell biology, and Rony François, an M.D. / Ph.D. student who
works with her, found a new drug combination that inhibits one form of pancreatic
cancer tumor and kills its
cells.
Using the same computer - based approach, the team has now been able to target the c - FLIP (cellular FLICE [FADD - like IL - 1β - converting enzyme]- inhibitory) protein, known to play a key role
in cancer stem
cell maintenance and survival, described
in previously published
work by the Institute.
CAR - T
cell therapy is particularly exciting because it
works well
in people whose
cancers haven't responded to other available treatments, says Renier Brentjens, an oncologist at Memorial Sloan Kettering
Cancer Center
in New York City.
This
work is being done
in collaboration with Dr. Hasan Korkaya, assistant professor, Biochemistry and Molecular Biology at the Medical College of Georgia, who has developed drug - resistant
cell lines, and with breast
cancer clinicians.
UT Southwestern Medical Center
cancer researchers have identified a protein critical to the spread of deadly
cancer cells and determined how it
works, paving the way for potential use
in diagnosis and eventually possible therapeutic drugs to halt or slow the spread of
cancer.
Cells suspended in a stiff matrix were more likely to work their way through the matrix to other side of a serum gradient, analogous to how metastasizing cancer cells break free from their tu
Cells suspended
in a stiff matrix were more likely to
work their way through the matrix to other side of a serum gradient, analogous to how metastasizing
cancer cells break free from their tu
cells break free from their tumors.
«The challenge is finding targets that exist on other types of
cancer cells but not on normal
cells,» says pediatric oncologist Stephan Grupp of the Children's Hospital of Philadelphia, who
worked with Porter on testing the treatment
in mice.
«Despite the low infection levels of mouse
cells with oHSV, we were able to cause a delay
in tumor growth
in one of the
cancer models and even cure many of the mice in a second model,» said first author Jennifer Leddon, who conducted much of the laboratory work during a research experience in the Center for Childhood Cancer and Blood Dis
cancer models and even cure many of the mice
in a second model,» said first author Jennifer Leddon, who conducted much of the laboratory
work during a research experience
in the Center for Childhood
Cancer and Blood Dis
Cancer and Blood Diseases.
Tom Misteli, a
cell biologist at the National
Cancer Institute
in Bethesda, Maryland, considers the map a «framework for future
work.»
Epigenetic therapies are thought to
work in two ways to fix these errors
in cancer cells — by correcting the «position» of the gene switches and by making the
cell appear as though it's infected by a virus, triggering the immune system.
In one, researchers working with mice at the Institute of Molecular and Cellular Biology in Singapore used antibodies to target proteins inside cancer cells — an impressive feat, since the antibodies were long considered too large to cross the cancer cell's outer membran
In one, researchers
working with mice at the Institute of Molecular and Cellular Biology
in Singapore used antibodies to target proteins inside cancer cells — an impressive feat, since the antibodies were long considered too large to cross the cancer cell's outer membran
in Singapore used antibodies to target proteins inside
cancer cells — an impressive feat, since the antibodies were long considered too large to cross the
cancer cell's outer membrane.
The
work published
in Cancer Cell complements previous research efforts from the CNIO Melanoma Group, which could lead to the development of novel drugs that selectively target the mechanism of cell autodigestion as a potential therapeutic strat
Cell complements previous research efforts from the CNIO Melanoma Group, which could lead to the development of novel drugs that selectively target the mechanism of
cell autodigestion as a potential therapeutic strat
cell autodigestion as a potential therapeutic strategy.
Working together, Johns Hopkins biomedical engineers and neurosurgeons report that they have created tiny, biodegradable «nanoparticles» able to carry DNA to brain
cancer cells in mice.
«We haven't held out much hope for immune therapy to
work in them because before you can enter
cancer cells to knock them down, you have to be able to get inside.
«Hodgkin lymphoma is unusual among
cancers in that it consists of a small number of tumor
cells in a sea of inflammatory
cells and immune system
cells, including T
cells that don't
work very effectively.»
Working with human breast
cancer cells and mouse models of breast
cancer, scientists identified a new protein that plays a key role
in reprogramming
cancer cells to migrate and invade other organs.
Working with human breast
cancer cells and mice, scientists at The Johns Hopkins University say new experiments explain how certain
cancer stem
cells thrive
in low oxygen conditions.
Batimastat does not
work this way: instead, it is designed to keep
cancers in check by preventing malignant
cells breaking away and forming secondary tumours elsewhere
in the body.