The result was a highly selective drug they named SBI - 0206965, which successfully killed a number of cancer cell types, including human and
mouse lung cancer cells and human brain cancer cells, some of which were previously shown to be particularly reliant on cellular recycling.
Not exact matches
The researchers confirmed this hypothesis by showing that if they blocked YAP1 they could inhibit stem
cells from undergoing self - renewal, forming blood vessel - like structures, and reduce
lung cancer cell growth in
mice.
In the
Cell study, Dr. Massagué, with Fellow Manuel Valiente, PhD, and other team members, found that in
mouse models of breast and
lung cancer — two tumor types that often spread to the brain — many
cancer cells that enter the brain are killed by astrocytes.
Compared to a control (left), epalrestat treatment (right) reduces the number of metastatic tumors (arrowheads) in the
lungs of
mice injected with human basal - like breast
cancer cells.
Loss of either GSTO1 or RYR1, the researchers report, decreased the number of
cancer stem
cells in the primary tumor, blocked metastasis of
cancer cells from the primary tumor to the
lungs, decreased the duration of chemotherapy required to induce remission and increased the duration of time after chemotherapy was stopped that the
mice remained tumor - free.
To test this idea, the researchers utilized two
mouse models of human breast
cancer metastasis and found dormant disseminated tumor
cells residing upon the membrane microvasculature of
lung, bone marrow and brain tissue.
By using molecular genetic tools to reduce the amount of PC in human
lung cancer cells, the team observed decreased
cell growth, a compromised ability to form colonies in soft agar (a gelatinous material specifically used to grow bacteria and other
cells), and a reduced rate of tumor growth in
mice.
Both the number and activity of osteoblasts —
cells that produce and reshape bone tissue — were increased within the bone marrow of
mice with
lung tumors compared with
cancer - free animals; and reducing the number of osteoblasts in
mice not only limited neutrophil infiltration of tumors but also interrupted tumor progression.
The
cells exhibited many functions associated with tumor progression; their presence within
mouse tumors substantially accelerated
cancer growth, and in human
lung tumors, a SiglecFhigh neutrophil signature was associated with poor patient survival.
«For example,
mouse mammary tumors shared a signaling pathway that is found in human
lung cancer and controls how
cells reproduce and move from one location to another.»
The Manchester researchers tested a new drug that targets one of these molecules, MCT1, in
lung cancer cells and in
mouse models.
Mice injected with breast
cancer cells making lots of a long strand of RNA called HOTAIR developed 10 times as many
lung tumors as controls (left) did.
In a study appearing in Science Translational Medicine, the researchers report they have effectively and safely employed this stem
cell - targeting system in
mice to treat metastatic breast
cancer that had spread to the
lung.
Using
lung cancer cells and
mice the scientists showed that the combination of two drugs, called TRAIL and a CDK9 inhibitor, altered the molecular switches in the
cell suicide process — forcing the
cancer cells to self - destruct.
They showed that it slowed the growth of human
lung cancer cells but not kidney
cancer cells in these
mice.
As a result, the
mice had twice as many
cancer cells zipping through their bloodstream and in their
lungs compared with
mice not treated with paclitaxel.
Now, in a new study in the journal
Cancer Cell, Shaw and a team of scientists at the Salk Institute for Biological Studies found that phenformin, a derivative of the widely - used diabetes drug metformin, decreased the size of
lung tumors in
mice and increased the animals» survival.
The dual - drug therapy — with analogs already in use for other diseases — doubled the survival rate of
mice with
lung cancer and halted
cancer in pancreatic
cells.
To better understand how these normally helpful components of the immune system are put to nefarious tasks in
cancer cells, Verma and his colleagues developed a new method of inducing non-small-cell
lung cancer in
mice.
Verma has successfully developed lentiviral vector - mediated
mouse models for glioblastoma,
lung adenocarcinoma and small
cell lung cancer (SCLC).
The experimental metastasis assay we detail here includes tail - vein injection of
cancer cells into the
mouse and determination of the resulting secondary organ colonization, primarily in the
lung, 10 d post dosing.
In this study, human
lung cancer cells with additional copies of the opioid receptor grew more than twice as fast as tumor
cells that lacked extra receptors when transplanted into
mice.
Bench and
mouse studies have shown that the Notch1 gene is a crucial contributor to tumorigenesis in non — small -
cell lung cancer (NSCLC).
One study presented in the journal — from a group led by Patrick Singleton, PhD, assistant professor of medicine at the University of Chicago Medicine — shows how opioids already present in the body can enhance the malignant tendencies of human
lung cancer cells transplanted into
mice, even without the addition of morphine.
Finally, to determine whether LARP7 KD also results in an increase in breast
cancer metastasis in vivo, the T47D control or shLARP7 - 2
cells were injected intravenously into the nude
mice, and
lung metastasis was examined 12 weeks later.
In Wisconsin, a group of researchers conducted a study using
mice to see if adding pomegranate juice to their diet made a significant impact on
lung cancer cells.