Not exact matches
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.
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 scar
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 scar
in the residual scars.
In mice with
pancreatic tumors, Kalbasi and other members of the team found relatively high levels of inflammatory compounds including CCL2, the signaling molecule that activates CCR2 on monocytes and macrophages to make these cells migrate to
tumors.
The study, conducted
in mice and including analyses of human cancers, found very high levels of two proteins — dectin - 1 and galectin - 9 —
in pancreatic tumors.
Recently, teaming up with co-investigator Associate Professor Dr. Rolf A. Brekken, they looked into its possible involvement
in Pancreatic Ductal Adenocarcinoma (PDA), the most common form of pancreatic cancer, in a mouse model with an early onset aggressive form of tumor de
Pancreatic Ductal Adenocarcinoma (PDA), the most common form of
pancreatic cancer, in a mouse model with an early onset aggressive form of tumor de
pancreatic cancer,
in a
mouse model with an early onset aggressive form of
tumor development.
In two mouse models of pancreatic cancer, a single treatment consisting of intravenous delivery of the PMILs followed by localized delivery of near - infrared light to the tumor site via optical fibers resulted in significantly greater reduction in tumor size than did either treatment with XL184 or PDT with BPD alon
In two
mouse models of
pancreatic cancer, a single treatment consisting of intravenous delivery of the PMILs followed by localized delivery of near - infrared light to the
tumor site via optical fibers resulted
in significantly greater reduction in tumor size than did either treatment with XL184 or PDT with BPD alon
in significantly greater reduction
in tumor size than did either treatment with XL184 or PDT with BPD alon
in tumor size than did either treatment with XL184 or PDT with BPD alone.
With the help of various
mouse models for
pancreatic cancer, they have succeeded
in elucidating the molecular pathways of
tumor development
in detail and have gained a better understanding of how various characteristics of the disease arise.
Meng and Nel also collaborated with Dr. Timothy Donahue, chief of gastrointestinal and
pancreatic surgery and a Jonsson Comprehensive Cancer Center member, to demonstrate that treatment with the iRGD peptide can enhance
tumor cell killing for patient - derived
pancreatic cancers, growing subcutaneously
in a
mouse model.
The combination was significantly toxic to
pancreatic cancer cells and disrupted
tumor growth and extended survival
in several types of advanced
pancreatic cancer
mouse models.
When antibodies and other methods were used to dramatically deplete the supply of Tregs
in mice, the researchers saw a dramatic jump
in the numbers of activated dendritic cells and CD8 + T cells
in pancreatic tumor tissue, as well as a slowing of
tumor growth.
In this study, samples were taken from patients»
tumors during surgery and transplanted into
mice to grow new
pancreatic cancer
tumors.
We chose this model because 1) it more closely recapitulates features of human
pancreatic cancer than do s.c. - implanted
tumors, 2) it can be used
in immunocompetent
mice to permit assessment of immune responses, and 3) the cells grow
in vivo with predictable kinetics (34).
To evaluate
tumor growth
in mice of each genotype, we used an orthotopic implant model derived from a spontaneous
pancreatic tumor arising
in a C57BL / 6 KPC
mouse (33), which expresses mutant forms of K - Ras and p53 selectively
in pancreatic tissue.
The KPC1242 cell line, derived from a spontaneous
pancreatic tumor that arose
in a KPC
mouse, was a generous gift of David Tuveson (Cold Spring Harbor Laboratories, Cold Spring, NY).
In a paper appearing online November 9, 2008 in the journal Nature, David Cheresh, Ph.D., professor and vice chair of pathology at the UC San Diego School of Medicine and the Moores UCSD Cancer Center and his co-workers mimicked the action of anti-angiogenesis drugs by genetically reducing VEGF levels in mouse tumors and inflammatory cells in various cancers, including pancreatic cance
In a paper appearing online November 9, 2008
in the journal Nature, David Cheresh, Ph.D., professor and vice chair of pathology at the UC San Diego School of Medicine and the Moores UCSD Cancer Center and his co-workers mimicked the action of anti-angiogenesis drugs by genetically reducing VEGF levels in mouse tumors and inflammatory cells in various cancers, including pancreatic cance
in the journal Nature, David Cheresh, Ph.D., professor and vice chair of pathology at the UC San Diego School of Medicine and the Moores UCSD Cancer Center and his co-workers mimicked the action of anti-angiogenesis drugs by genetically reducing VEGF levels
in mouse tumors and inflammatory cells in various cancers, including pancreatic cance
in mouse tumors and inflammatory cells
in various cancers, including pancreatic cance
in various cancers, including
pancreatic cancer.
To study how the modified virus attacks
tumors, researchers
in the McDonald lab injected it intravenously into
mice genetically modified to develop neuroendocrine
pancreatic cancer.
Bottom Line: Bacterial load was significantly higher
in pancreatic tumor samples from patients with
pancreatic ductal adenocarcinoma compared with
pancreatic tissue from normal individuals, and
in studies using
mice, eliminating certain «bad» bacteria slowed the growth of
pancreatic cancer, reversed immune suppression, and upregulated the immune checkpoint protein PD1.
This approach has led to the finding that activated fibroblasts
in the
tumor stroma mediate immune suppression
in several
mouse models of cancer, including the autochthonous model of
pancreatic ductal adenocarcinoma of the Tuveson lab.