«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.»
In this study, we explored the antitumor potential of prostate stem cell antigen (PSCA)- redirected CAR T and mucin 1 (MUC1)- redirected CAR T cells in
tumor models of NSCLC.
Not exact matches
Capsaicin additionally produced a significant deceleration
of the development
of prostate
tumors created simply by those human cell lines grown in mouse
models.
«We also confirmed a role in PDAC
tumor maintenance as inhibition
of PRMT1 in patient - derived mouse
models significantly inhibited
tumor growth and extended survival,» said Giuliani.
In December 2017, writing in Computer Methods in Applied Mechanics and Engineering, Yankeelov and collaborators at UT Austin and Technical University
of Munich, showed that they can predict how brain
tumors (gliomas) will grow and respond to X-ray radiation therapy with much greater accuracy than previous
models.
In October 2016, writing in Mathematical
Models and Methods in Applied Sciences, the team used a study of cancer in rats to test 13 leading tumor growth models to determine which could predict key quantities of interest relevant to survival, and the effects of various ther
Models and Methods in Applied Sciences, the team used a study
of cancer in rats to test 13 leading
tumor growth
models to determine which could predict key quantities of interest relevant to survival, and the effects of various ther
models to determine which could predict key quantities
of interest relevant to survival, and the effects
of various therapies.
Model of tumor growth in a rat brain before radiation treatment (left) and after one session
of radiotherapy (right).
Over the years, many different mathematical
models of tumor growth have been proposed, but determining which is most accurate at predicting cancer progression is a challenge.
«We're trying to build
models that describe how
tumors grow and respond to therapy,» said Yankeelov, director
of the Center for Computational Oncology at The University
of Texas at Austin (UT Austin) and director
of Cancer Imaging Research in the LIVESTRONG Cancer Institutes
of the Dell Medical School.
According to ICES Director J. Tinsley Oden, mathematical
models of the invasion and growth
of tumors in living tissue have been «smoldering in the literature for a decade,» and in the last few years, significant advances have been made.
They implemented this principle through the development and application
of something they call the «Occam Plausibility Algorithm,» which selects the most plausible
model for a given dataset and determines if the
model is a valid tool for predicting
tumor growth and morphology.
«This approach will hopefully lead to better mechanistic predictive
modeling of response and future design
of therapies that further take advantage
of how the immune system recognizes
tumors.»
PDX
models are created by implanting cancerous tissue from a human primary
tumor directly into immunodeficient mouse or rat
models, enabling acceleration
of oncology research or drug discovery and development programs.
A raft
of studies in laboratory animals, molecular
models and cancer patients suggest that pain drugs given during and after cancer surgery stimulate the growth and spread
of certain
tumors.
The researchers then induced melanoma
tumors in their
model and evaluated the effects
of a battery
of immunotherapies.
«Particularly in such patients with underlying CKD, our
modeling results support the integration
of renal
tumor anatomic features at cross-sectional imaging into decision making for treatment
of small renal masses and may be used to provide a patient - centered framework for selection
of optimal candidates for ablative therapy,» Kang said.
«This
model was trained on genetic data from human
tumors in The Cancer Genome Atlas and was able to predict response to certain inhibitors that affect cancers with overactive Ras signaling in an encyclopedia
of cancer cell lines,» Greene said.
Traditional genetic approaches together with the new wealth
of genomic information for both human and
model organisms open up strategies by which drugs can be profiled for their ability to selectively kill cells in a molecular context that matches those found in
tumors.
In this new study published in Nature, Alexandra Van Keymeulen and colleagues used state
of the art genetic mouse
models to identify the cellular origin
of PIK3CA and p53 induced breast
tumors.
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.
«Lower - carb diet slows growth
of aggressive brain
tumor in mouse
models.»
«We know that 70 - 75 percent
of glioblastoma patients undergo surgery for
tumor debulking, and we have previously shown that MSCs encapsulated in biocompatible gels can be used as therapeutic agents in a mouse
model that mimics this debulking,» he continued.
«It's very difficult to produce a mouse
model of a solid
tumor of the type we see in most women who are diagnosed with cervical cancer.
Again, using mouse
models of glioblastoma — this time created from brain
tumor cells that were resistant to the herpes virus — the therapy led to increased animal survival.
For this study, Guttridge, first author David J. Wang, who developed many
of the study's concepts, and their colleagues monitored NF - kB activity during
tumor development using mouse embryonic fibroblasts and two mouse
models.
Moreover, experiments on an ovarian cancer murine
model that investigated the effects
of orally administered ONA resulted in longer lifespans and inhibited ovarian cancer
tumor development.
Testing each
of these factors for their ability to return differentiated
tumor cells to a stem - like state, identified a combination
of four — POU3F2, SOX2, SALL2 and OLIG2 — that was able to reprogram differentiated
tumor cells back into glioblastoma stem cells, both in vitro and in an animal
model.
Engineered human immune cells can vanquish a deadly pediatric brain
tumor in a mouse
model, a study from the Stanford University School
of Medicine has demonstrated.
This treatment prevented the formation
of polyps, showing that bacteria are essential for early
tumor development in this
model.
The researchers confirmed these findings in a mammary carcinoma mouse
model — treatment with dasatinib just a few days after administering two high doses
of chemotherapy prevented
tumor growth and increased survival rates.
The researchers took this discovery and, in an animal
model, identified a drug that is able to re-activate those immune cells and reduce brain
tumor growth, thereby increasing the lifespan
of mice two to three times.
The next step for the researchers is to demonstrate the viability
of this approach to the production and delivery
of an anticancer molecule in a whole
tumor model system.
Kilian said his team's synthetic microenvironment lies somewhere in the middle
of two extremes in the field
of modeling biology: the hard plastic plate, and expensive mouse avatars that are created by injecting human
tumor cells into mice.
Kuang is also involved in efforts to
model various aspects
of tumor growth and management as part
of ASU's efforts on cancer research.
Weeraratna's team used an artificial skin reconstruct
model to recreate the interactions
of melanoma cells with either a young or aged
tumor microenvironment.
He and his co-investigators analyzed 66 ultrasound images
of tumors (32 pictures
of a single
tumor and 34
of multiple
tumors) inside a plastic
model of a breast to determine the augmented - reality system's accuracy
of measuring
tumor volume.
BPTES has been used in animal
models for a variety
of cancers but has not substantially reduced
tumor sizes, probably because the drug concentration in
tumor tissue is not high enough when using conventional drug formulation methods, say the scientists.
One form
of pancreatic cancer has a new enemy: a two - drug combination discovered by UF Health researchers that inhibits
tumors and kills cancer cells in mouse
models.
Last fall, Bergö's group reported that ingestion
of extra antioxidants drove the metastasis
of melanoma in a mouse
model, though they didn't have any effect on the primary
tumor.
«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 Diseases.
Its research includes a cluster
of related interdisciplinary projects that examine disparities in breast cancer mortality between African - American and Caucasian women using animal
models, molecular characterization
of tumors, and behavioral research focused on social - environmental factors.
In the current study, Dr. Xu and colleagues gave radiation therapy to a mouse
model of human pancreatic cancer to eradicate the bulk
tumors, while only the cancer stem cells remained in the residual scars.
«The effective immune response didn't happen in every
tumor model we tested, so we still need to figure out exactly what triggered the
tumor shrinkage and how to predict which
tumors will shrink in response to virotherapy,» said Leddon, who is also working toward her medical and doctoral degrees at the University
of Cincinnati.
In collaboration with the group
of Valerian Kagan, Ph.D., D.Sc., at the University
of Pittsburgh, Gabrilovich and colleagues analyzed in great detail the events that take place in the DCs from
tumor - bearing mice
models and found that impaired cross-presentation, which occurred in the presence
of tumor - derived factors, was associated with defective trafficking
of the antigen - MHC complex to the cell surface.
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.
Previous work on cartilage
tumors has been done using
models based on genetic mutations that occurred only rarely in enchondromas; however, IDH mutations are present in a high percentage
of enchondromas.
Desgrosellier said the team will follow up with mouse
models containing
tumor fragments from patients to better reflect the diversity
of cell types present in human disease.
A team
of researchers, led by Ross Cagan, PhD, developed a multi-gene lung cancer
model in the fruit fly Drosophila to better understand the mechanisms that promote
tumors in NSCLC.
The mouse
model could also contribute to the further development
of immunotherapies — a method in which the body's immune system is stimulated, so that it intensifies its fight against
tumor cells.
However, when the researchers switched on KRAS in the preclinical
models, an entirely different kind
of tumor formed, called angiosarcoma.