She anticipates that her research will lead to a better understanding the role of CCR7 (+)
breast tumor metastasis to the lymph nodes, and how oncologists treat these tumors.
Not exact matches
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.
«The result was an extensive inhibition of
tumor growth and prevention of
metastasis to the lung in HER2 - positive animal models of
breast cancer,» notes Navasona Krishnan, Ph.D., a postdoctoral investigator in the Tonks lab who performed many of the experiments and is lead author on the paper reporting the results.
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 kill.
They showed that the iKnife could distinguish normal and
tumor tissues from different organs, such as
breast, liver, and brain, and could even identify the origin of a
tumor that was a
metastasis, a secondary growth seeded by a primary
tumor elsewhere in the body.
«We determined that it was specifically fructose, in table sugar and high - fructose corn syrup, ubiquitous within our food system, which was responsible for facilitating lung
metastasis and 12 - HETE production in
breast tumors.»
The team also found that these genes had different functions in promoting
metastasis: One group encouraged growth of
tumor cells in both
breast and lungs, whereas the other only helped the new
tumor thrive in the lungs.
The study team believes that the mechanism by which dietary sucrose or fructose affects
breast tumor growth and
metastasis, especially through the 12 - LOX pathways, warrants further investigation.
Houston Methodist researchers led by Dario Marchetti, PhD, have developed a blood test that can identify circulating
tumor cells to predict
breast cancer patients at risk for developing brain
metastasis.
Additionally, overexpression of POSTN in human mammary epithelial and
breast cancer cells resulted in enhanced
tumor growth and
metastasis (Wang et al., 2013), which is similar to a colon cancer cell model where overexpression of POSTN resulted in an increase in the number and size of liver metastases (Bao et al., 2004).
To further validate the clinical significance of miR - 7 and KLF4 in brain
metastasis of
breast cancer, we microdissected
tumor tissues from both primary and brain metastatic lesions followed by conducting TaqMan qRT - PCR.
On a brighter note, not all
breast cancer patients have the kind of
tumor microenvironment in which pre-op chemo can promote
metastasis.
Abstract 466: Systemic early immune priming via
tumor - secreted cytokines facilitates
breast cancer
metastasis in syngeneic mouse model
CXCR4 peptide antagonist inhibits primary
breast tumor growth,
metastasis and enhances the efficacy of anti-VEGF treatment or docetaxel in a transgenic mouse model.
May 12, 2016 Stopping cancer in its tracks Researchers from the University of Chicago have shown that inhibiting autophagy, a self - devouring process used by cells to degrade large intra-cellular cargo, effectively blocks
tumor cell migration and
breast cancer
metastasis in
tumor models.
Metastasis of
Breast Tumor Cells to Brain Is Suppressed by Phenethyl Isothiocyanate in a Novel In Vivo
Metastasis Model.
A CXCR4 antagonist CTCE - 9908 inhibits primary
tumor growth and
metastasis of
breast cancer.
Oral delivery of PND - 1186 FAK inhibitor decreases
tumor growth and spontaneous
breast to lung
metastasis in pre-clinical models.
More recently, he has focused on triple - negative
breast cancer, the role of micro-RNAs in cancer growth and
metastasis,
tumor heterogeneity and novel approaches to targeting therapy - resistant
breast cancers.
Injections of iPSC - EPCs did not however have significant effect on
tumor growth or on overall survival, but transducing cells with a baculovirus expressing CD40L, a member of the TNF gene family which can induce apoptosis [6, 7], and injection into the
breast cancer lung
metastasis, increased levels of pro-apoptotic cytokines in lung tissues, indicating the induction of apoptosis by CD40L carried by the EPCs (See figure).
Review BRCA 1/2
Tumors and Gene Expression Therapy for
Breast Cancer Development and
Metastasis Anup P. Challa, Chikezie O. Madu, Yi Lu Oncomedicine 2017; 2: 132 - 137.
Tags: aspirin, Bezos, bioengineering,
Breast Cancer, Cameron Turtle, Cancer etiology - prevention - outcomes, CAR t - cell, Clinical Research, Colorectal Cancer, genome, hiv, hiv vaccine, hiv vaccine trials network, Human Biology, immunology, Jason Bielas, Lawrence Corey, Matthias Stephan, merkel cell carcinoma,
metastasis, Molecular basis of cancer, mylotarg, Obliteride, Paul Nghiem, philanthropy, Polly A Newcomb, Public Health Sciences, RNA, Ruth Etzioni, Soheil Meshinchi, Steven Henikoff, Transplant and Immunotherapy,
Tumor specific translational research, Vaccine and Infectious Disease, Vaccine development - Viral cancers
To evaluate whether altered expression of the ABL genes is associated with
breast cancer progression and
metastasis, we examined the expression of ABL1 and ABL2 in normal and invasive
breast tumor specimens using published TCGA (The Cancer Genome Atlas) data sets (14 — 16).
These findings reveal a function for ABL kinases in the regulation of
breast cancer bone
metastasis and
tumor - induced osteolysis in vivo.
Here, we uncovered a role for the ABL kinases in promoting
breast cancer bone
metastasis through the regulation of distinct pathways required for
tumor colonization and survival in the bone microenvironment.
Similar to IL - 6 and MMP1, TNC is abundant in some
breast tumors and promotes
metastasis in mouse models (49).
We found that allosteric inhibition of the ABL kinases effectively impaired
breast cancer bone
metastasis and blocked
tumor - induced osteolysis in mouse models.
These data suggest that ABL kinases promote
breast cancer
metastasis to bone in part by increasing
tumor cell survival within the bone microenvironment.
Tumor hypoxia is often linked to decreased survival in patients with
breast cancer and has been shown to induce specific molecular changes in cells including changes that confer a more malignant phenotype such as increased proliferation (3), survival (4), invasion (5), and
metastasis (6).
Importantly, NSCs can target
breast cancer
metastasis in the brain [9] and can penetrate deep and hypoxic regions of solid
tumors [7].
Haihui Lu, Ph.D., a CRI fellow at the Whitehead Institute for Biomedical Research, has identified a surface marker that distinguishes a population of
breast cancer cells that are more prone to
metastasis and demonstrate higher levels of «stemness,» the ability to seed other
tumors.
We report that ABL kinases promoted
metastasis of
breast cancer cells to bone by regulating the crosstalk between
tumor cells and the bone microenvironment.
It is these same lymph vessels that carry
tumor cells from
breast tumors to the lungs or to other organs in a process called
metastasis.