Our group studies
how normal cell behaviour is altered by mutation in the early stages of cancer evolution.
«You have to understand
how normal cells work.»
«This calls for a systems level approach, and network analysis techniques, to really understand
how normal cells are transformed into cancer cells at the molecular level.»
When studying
how normal cells change into cancer cells, dos Santos and other cancer researchers pay close attention to gene expression.
Christofk studies the genes and proteins behind the way cancer cells use sugars to live and grow, which is different from
how normal cells do.
Not exact matches
And, perhaps most strikingly, a team at a gaggle of New York research institutions published a paper showing
how they'd used hPSCs to cook up — in just days, rather than several months — cortical neurons (critical central nervous system
cells) that had
normal electrophysiological signaling properties.
Joe W. Ramos, PhD, deputy director of the UH Cancer Center and collaborators focused on investigating
how these oncogenes and related signals lead to dysregulation of
normal processes within the
cell and activate highly mobile and invasive cancer
cell behavior.
Using a mathematical model known as the Ising model, invented to describe phase transitions in statistical physics, such as
how a substance changes from liquid to gas, the Johns Hopkins researchers calculated the probability distribution of methylation along the genome in several different human
cell types, including
normal and cancerous colon, lung and liver
cells, as well as brain, skin, blood and embryonic stem
cells.
In this latest advance reported in PNAS, the Wyss team showed that the human gut - on - a-chip's unique ability to co-culture intestinal
cells with living microbes from the
normal gut microbiome for an extended period of time, up to two weeks, could allow breakthrough insights into
how the microbial communities that flourish inside our GI tracts contribute to human health and disease.
The metabolism of bone
cells determines
how much sugar they use; if the bone
cells consume more sugar than
normal, this can lower the glucose level in the blood.
A Biophysical Journal study published September 1 reveals exactly
how the venom's toxin — called MP1 (Polybia - MP1)-- selectively kills cancer
cells without harming
normal cells.
How it hides: In a
normal cell, genes encode instructions for surface proteins known as the major histocompatibility complex (MHC).
How it spreads: Unlike
normal cancers, where the disease - causing mutation is confined to one organism, devil facial tumor disease (DFTD)
cells have evolved the ability to spread from devil to devil.
Most of the time, let - 7 effectively communicated to the gene exactly
how much KRAS protein was needed for
normal cell turnover.
It is unclear
how the entire body is affected because Spector looked only at telomeres, nucleotides on the ends of chromosomes that slowly erode as
cells copy themselves during
normal aging.
Like Medieval alchemists who searched for an elixir that could turn base metals into gold, biology's modern alchemists have learned
how to use oocytes to turn
normal skin
cells into valuable stem
cells, and even whole animals.
These genes are believed to be essential for the
normal function of nerve
cells, and previous studies have linked these mutations to problems with synaptic function —
how neurons communicate with each other.
Pathologists classify tumors by
how far their
cells deviate from their
normal forms, while hematologists identify and count different leukocytes by sight.
Now, thanks to the new mouse model, it will be possible to study
how renal tumors are able to develop in an environment with a
normal immune system, and
how cancer
cells manage to evade the immune system's attacks.
One possibility for
how that happens, says Hekimi, is that slow cellular metabolism delays the
normal buildup of metabolic byproducts, such as reactive compounds known as free radicals, that are toxic to
cells.
«We need to know
how taste
cells grow and work in
normal situations before we can harness this knowledge to help people.»
Breast cancer researchers have mapped early genetic alterations in
normal - looking
cells at various distances from primary tumours to show
how changes along the lining of mammary ducts can lead to disease.
At the core of this
cell behavior is
how the loss of that single gene changes activation levels of dozens of other genes, suppressing genes associated with metastatic disease and increasing activity of genes linked to
normal tissue.
For the first time ever, we could make a really comprehensive comparison of individual
normal and tumour
cells from the exact same type of tissue, taken at the same time, from the same person, and see
how the cancer had developed.»
Ballabio and his colleagues studied the role of the pathway in two
normal cellular activities;
how cells respond to physical exercise and
how they respond to nutrient availability.
«We know that the pathway is important for
normal cells to carry their activities as it is involved in regulating metabolism, that is,
how cells process nutrients to obtain energy and
how cells use energy to grow.
In this webinar we will explore
how cancer
cells are able to reprogram their metabolic pathways to enable energy production under conditions that are disabling to most
normal cells.
The researchers now want to find out exactly
how Tregs interact with fat tissue and whether the immune
cells accumulate in other organs during
normal aging.
He is trying to identify the molecules with which the klotho protein interacts in tissues and to figure out
how cells with defective klotho behave differently from
normal cells.
Jamieson's team wanted to understand
how RNA might change with the aging of
normal blood stem
cells compared with sAML stem
cells.
Endocytosis is not
normal in cancer
cells but
how dysregulated the process is in cancer
cells has just been revealed by Sarah Elkin and colleagues in the University of Texas (UT) Southwestern Medical Center lab of Sandra Schmid.
Kipnis and his colleagues wondered
how smart mice would be if they had a
normal supply of T
cells everywhere in their bodies except the meninges, so he injected a compound into mice that prevented T
cells from reaching the meninges.
«The potency of these engineered macrophages is relatively clear, but the crucial issue is
how to maximize the anti-cancer effects while minimizing side effects, namely the engulfment of
normal cells.»
If the egg were indelibly etched with asymmetric information that unequivocably determines development, the argument went,
how could two embryonic
cells be separated and still produce whole, intact,
normal individuals?
For the first time, researchers have been able to grow, in a lab, both
normal and primary cancerous prostate
cells from a patient, and then implant a million of the cancer
cells into a mouse to track
how the tumor progresses.
A novel mechanism — similar to
how normal tissue stem
cells respond to wounding — might explain why bladder cancer stem
cells actively contribute to chemo - resistance after multiple cycles of chemotherapy drug treatment.
Although this human Gut Chip recreated the villus epithelium of
normal intestine and enabled new insights into
how flow and cyclic peristalsis affects intestinal differentiation and function, it could not be used to study processes that relied on
normal intestinal
cells from individual donors, which, for example, is crucial for studying patient - specific responses for personalized medicine.
C1q also plays a positive role in the brain by clearing out dead
cells and helping target harmful materials, so learning
how to manipulate its presence to prevent debilitating synapse loss while maintaining its
normal functions will require further research.
«This is a significant example of
how knowing details of potential mechanisms and the basic science of redox active compounds in cancer versus
normal cells can be leveraged clinically in cancer therapy,» says co-senior author Douglas Spitz, who focused on the biochemical studies.
«This difference in metabolism is a key part of
how cancer
cells have a competitive advantage over
normal cells.
Working with Bhaduri, who has a background in statistics and bioinformatics, Pollen and Nowakowski began exploring
how specific classes of neurons and stem
cells in the developing brain contribute to
normal brain growth as well as to neurodevelopmental disease, and have begun to build a comprehensive, open - source atlas of gene expression across the developing brain, which they hope will serve as a resource for other scientists.
«Typical food triggers creation of regulatory T
cells: Researchers document
how normal diet establishes immune tolerance conditions in the small intestine.»
«This information yields new insights into
how sperm stem
cells function and develop under
normal circumstances,» says the study's lead author Bradley Cairns, PhD, senior director of basic science at HCI and professor and chair of oncological sciences at the U of U. «We have built a very important framework we can now use to help us understand what happens when things go wrong, resulting in issues like infertility and cancer in men.»
«The cancer stem
cells actively regrow and respond to the induced damage or apoptosis (
cell death) caused by chemotherapy in between the different cycles, similar to
how normal tissue stem
cells respond to wound - induced damages.»
This shows
how a
normal process of tissue development produces a
cell type that is predisposed to acquire cancer - causing mutations.
Knowing the origin of each
cell and which genes control their
normal function are the foundations for scientists to decipher the disease process and eventually to find out
how to guide the
cells to self - repair or even to build up a brand new organ using amended
cells from the patients.»
The RNA molecules direct which proteins the
cell produces, so the RNA sequences show
how tumor
cells behave differently to
normal cells.
The new study combined two methods: So - called «patch recording» of tiny voltages in single frog brain
cells and
how the voltages change in response to sounds of different lengths, and the administration of drugs that block neurotransmitters — a way to learn
how brain
cells respond to sound with and without the
normal neurotransmitters.
Dr. David Gilley's laboratory at the Indiana University School of Medicine in Indianapolis and Dr. Connie Eaves» laboratory at the BC Cancer Agency's Terry Fox Laboratory in Vancouver, Canada, collaborated to determine
how telomeres are regulated in different types of
normal breast
cells.
New research provides critical insights into
how normal breast precursor
cells may be genetically vulnerable to develop into cancer.