Future studies will test and compare the efficacy of imatinib and allosteric compounds
in mouse models of breast cancer.
Working
in mouse models of breast cancer and breast tumor samples from patients, Longmore and his colleagues showed that a protein that sits on the surface of tumor cells, called DDR2, binds to collagen and activates a multistep pathway that encourages tumor cells to spread.
When the team used the retinoid fenretinide along with anti-estrogen therapy
in mouse models of breast cancer, they did not see the expansion of CK5 + cells previously seen with anti-estrogen therapy alone.
Then they removed the protein
in a mouse model of breast cancer and discovered the cancer's ability to spread was significantly reduced.
Similar results were observed
in a mouse model of breast cancer.
T - cells (red, yellow, and blue) attack a tumour
in a mouse model of breast cancer following treatment with radiation and a PD - L1 immune checkpoint inhibitor, as seen by transparent tumour tomography.
Moreover, ablation of a STAT5A allele reduces tumor incidence
in a mouse model of breast cancer in which mammary epithelial cells express T antigen (48).
Not exact matches
The researchers tested their drug compound, Targapremir - 210,
in mouse models of triple negative
breast cancer.
«Indeed,
in a second tumor
model of metastatic
breast cancer, we demonstrated that
mice treated with the EphA2 - targeting paclitaxel conjugate presented nearly no lung metastases, while a large numbers
of lesions were observed
in both untreated
mice and
in mice treated with just paclitaxel.»
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.
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 astrocyte
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 astrocyte
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.
The research, conducted
in cell lines and
mouse models, explored enhancing the
cancer - killing effects
of PARP inhibitors not only
in regard to AML but also triple - negative
breast cancer.
In a
mouse model of triple - negative
breast cancer,
mice injected with
cancer cells that over-express ZMYND11 had tumor volumes
of less than 50 cubic millimeters while control
mice and those injected with cells expressing ZMYND11 deficient for binding to the methyl group had tumor volumes ranging from 150 to 400 cubic millimeters at eight weeks.
Treatment
in a
mouse model of metastatic
breast cancer with two
of the down - regulated miRNAs (miR - 141 and miR - 219) suppressed bone metastases, suggesting that these miRNAs may have therapeutic utility.
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.
Witt - Enderby at Duquesne is using her expertise
in molecular pharmacology to study the effects
of melatonin on a
mouse breast cancer model.
In a four - year study conducted on the mouse model in advanced breast cancer metastasis in the eye's anterior chamber, Petty and colleagues found that the new nanoparticle not only killed tumor cells in the eye, but also extended the survival of experimental mice bearing 4T1 tumors, a cell line that is extremely difficult to kil
In a four - year study conducted on the
mouse model in advanced breast cancer metastasis in the eye's anterior chamber, Petty and colleagues found that the new nanoparticle not only killed tumor cells in the eye, but also extended the survival of experimental mice bearing 4T1 tumors, a cell line that is extremely difficult to kil
in advanced
breast cancer metastasis
in the eye's anterior chamber, Petty and colleagues found that the new nanoparticle not only killed tumor cells in the eye, but also extended the survival of experimental mice bearing 4T1 tumors, a cell line that is extremely difficult to kil
in the eye's anterior chamber, Petty and colleagues found that the new nanoparticle not only killed tumor cells
in the eye, but also extended the survival of experimental mice bearing 4T1 tumors, a cell line that is extremely difficult to kil
in the eye, but also extended the survival
of experimental
mice bearing 4T1 tumors, a cell line that is extremely difficult to kill.
Human
breast tumors transplanted into
mice are excellent
models of metastatic
cancer and are providing insights into how to attack
breast cancers that no longer respond to the drugs used to treat them, according to research from Washington University School
of Medicine
in St. Louis.
«Unusual drug generates exciting results
in mouse models of metastatic
breast cancer.»
The team's next steps are to test coibamide A
in a
mouse model for triple negative
breast cancer and
in a
mouse model for brain
cancer in which the glioblastoma cells are grown
in the brain instead
of the flank.
A new study shows coibamide A has potent anti-
cancer activity
in mice and cell cultures that
model brain tumors and triple negative
breast cancer, two
of the most aggressive and difficult - to - treat types
of cancer.
After confirming
in mouse models that cells from HER2 - positive
breast cancers became resistant to anti-HER2 treatment when implanted into the brain but not into other tissues, the investigators found that HER3 is overexpressed
in brain metastases
of HER2 - positive
breast cancers from both
mice and human patients.
Additionally, the study showed that genetic knockdown
of RASAL2 gene can lead to reduced metastasis
in breast cancer mouse model.
2) The two repeated experiments analyze the source
of POSTN expression
in the lung and whether it affects the number / size
of primary and secondary tumor formation
in a spontaneous
mouse model of breast cancer (MMTV - PyMT).
Tagged therapeutic stem cells (green) are targeting
breast cancer metastases (red)
in the brain
of a
mouse model.
We'll test this
in other
models — with other classes
of drug and
in mice with a
cancer that mimics metastatic
breast cancer, for example.»
Therefore, we have explored the role
of the alpha2 beta1 integrin
in cancer initiation and progression using a clinically - relevant, spontaneous
mouse model, the MMTV - Neu
model of breast cancer progression and metastasis.
Now,
in Stem Cells Translation Medicine, the group
of Shu Wang at the National University
of Singapore describe the derivation
of EPCs from human iPSCs, their therapeutic modification, and their ability to inhibit tumor growth
in a
mouse breast cancer model [4].
Unlike previous MRI studies
of tumors
in mice, the researchers were able to detect very small naturally occurring
cancers, which were excellent
models for human
breast cancer; the tumors the
mice developed were «realistic
models of the most frequently detected human
cancers,» the authors wrote.
The authors then tested the tumor targeting capability
of iPSC - EPCs labelled with the near - infrared fluorescent dye DiR
in two established
mouse breast cancer models.
We found that allosteric inhibition
of the ABL kinases effectively impaired
breast cancer bone metastasis and blocked tumor - induced osteolysis
in mouse models.
Together, our findings suggest that ABL kinases activate the TAZ and STAT5 pathways and that coactivation
of their downstream targets promote the bone metastasis
of breast cancer cells
in mouse models.
The King lab is currently testing these novel
cancer therapies
in mouse models of metastatic
breast and prostate
cancer through the use
of whole body luminescence imaging.
Deletion
of the amino acid transporter Slc6a14 suppresses tumour growth
in spontaneous
mouse models of breast cancer
In the present study, we interrogated the role of this transporter in breast cancer by deleting Slc6a14 in mice and monitoring the consequences of this deletion in models of spontaneous breast cancer (Polyoma middle T oncogene - transgenic mouse and mouse mammary tumour virus promoter - Neu - transgenic mouse
In the present study, we interrogated the role
of this transporter
in breast cancer by deleting Slc6a14 in mice and monitoring the consequences of this deletion in models of spontaneous breast cancer (Polyoma middle T oncogene - transgenic mouse and mouse mammary tumour virus promoter - Neu - transgenic mouse
in breast cancer by deleting Slc6a14
in mice and monitoring the consequences of this deletion in models of spontaneous breast cancer (Polyoma middle T oncogene - transgenic mouse and mouse mammary tumour virus promoter - Neu - transgenic mouse
in mice and monitoring the consequences
of this deletion
in models of spontaneous breast cancer (Polyoma middle T oncogene - transgenic mouse and mouse mammary tumour virus promoter - Neu - transgenic mouse
in models of spontaneous
breast cancer (Polyoma middle T oncogene - transgenic
mouse and
mouse mammary tumour virus promoter - Neu - transgenic
mouse).
These kind
of mice are an extraordinary resource for
modeling human disease; for instance, research has found that
mice that are genetically mutated to carry the BRCA1 gene (a human
breast cancer gene) behave more similarly to human
cancer patients than those
mice who have had a tumor physically transplanted
in.
Last year, Mandriota and collaborators demonstrated that
in a
cancer mouse model, concentrations
of aluminum
in the amount
of those measured
in the human
breast are able to transform cultured mammary epithelial cells, allowing them to form tumors and to metastasize.
Our
mouse model data are not
in conflict with the epidemiological observation that a first pregnancy before age 22 greatly reduces
breast cancer risk (MacMahon et al., 1970), because at this young age, the chance
of having already accumulated precancerous cells is small.