The technology has been demonstrated in animal models and also
in human breast tumors.
They identified an alkylphenol leaching from the plastic as the culprit, having «estrogen - like properties when tested
in the human breast tumor cells.»
Not exact matches
The researchers «deserve a lot of credit» for testing the approach
in the mice that spontaneously develop
breast tumors, he says, which more closely mimic how cancer arises
in humans.
Oncologists William Hahn, Robert Weinberg, and colleagues at the Whitehead Institute for Biomedical Research
in Cambridge, Massachusetts, mutated the gene for one part of the enzyme and inserted it into cultured
human cells from colon, ovary, and
breast tumors.
Researchers have isolated exosomes from
tumors and from blood of patients with
breast cancer, and from blood of mice with
human tumors grown after
breast implantation
in mice, called ortoxenogratfs.
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.
«We knew ZMYND11 was a candidate
tumor - suppressor because it's down - regulated
in a number of
human cancers, including
breast cancer,» Shi said.
Aiding their new research, Semenza says, was the knowledge that whereas the air we breathe is 21 percent oxygen, oxygen levels average around 9 percent
in healthy
human breast tissue but only 1.4 percent
in breast tumors.
Horvath and Tell's research is the first reported study to compare
breast cancer subtypes and gene expression patterns associated with STAT3
in the
tumors of
human patients.
In earlier studies involving animal models and human cancer cell lines, researchers found that breast cancer spreads when three specific cells are in direct contact: an endothelial cell (a type of cell that lines the blood vessels), a perivascular macrophage (a type of immune cell found near blood vessels), and a tumor cell that produces high levels of Mena, a protein that enhances a cancer cell's ability to sprea
In earlier studies involving animal models and
human cancer cell lines, researchers found that
breast cancer spreads when three specific cells are
in direct contact: an endothelial cell (a type of cell that lines the blood vessels), a perivascular macrophage (a type of immune cell found near blood vessels), and a tumor cell that produces high levels of Mena, a protein that enhances a cancer cell's ability to sprea
in direct contact: an endothelial cell (a type of cell that lines the blood vessels), a perivascular macrophage (a type of immune cell found near blood vessels), and a
tumor cell that produces high levels of Mena, a protein that enhances a cancer cell's ability to spread.
The title of the paper is «Bioinformatic analysis reveals a pattern of STAT3 - associated gene expression specific to basal - like
breast cancers
in human tumors.»
In tumors formed by
human breast cancer cells, DNA damage (brown staining) is increased by simultaneous Olaparib treatment and PGAM1 suppression (right) when compared to either Olaparib treatment (left) or PGAM1 suppression (center) alone.
In this study, the researchers tested the effects of Olaparib on the
tumors formed by
human breast cancer cells injected into mice.
Their study, published
in the ACS journal Chemical Research
in Toxicology, found that triclosan, as well as another commercial substance called octylphenol, promoted the growth of
human breast cancer cells
in lab dishes and
breast cancer
tumors in mice.
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.
Using cultured cells derived from
human tumors of the
breast and prostate gland, they confirmed that the IL6R / STAT3 / miR -34 a feedback loop is also activated
in other
tumor types.
The researchers grafted
breast or lung
tumors in mice, allowed the
tumors to grow to small size and removed these
tumors surgically — essentially mimicking the situation
in a
human tumor patient
in which the
tumor is surgically removed as soon as possible after diagnosis.
As a next step, Guha, Avadhani and colleagues plan to extend this study to
in vivo mouse models and will also investigate these mechanisms
in tumor samples from
human breast cancer patients.
Humans have an ortholog of the murine Nrk gene, and considering that the gene expression pattern
in breast tumor in Nrk mutant mice was similar to that
in human luminal B
breast cancer, the findings of this study may lead to further understanding of the mechanisms of
human breast cancer suppression and to advances
in its diagnosis and therapy.
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).
Further research uncovered a broad spectrum of cell surface stem cell markers (e.g., CD133, CD44, and CD24) that allow the identification of CSCs
in human solid
tumors, including brain,
breast, prostate, pancreas, liver, ovary, skin, colon cancers, and melanoma (3 - 6)(Figure 1 based on 7).
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 researchers then injected AAV2 into
human breast cancer cell line - derived
tumors in mice without functioning immune systems.
It has been reported that
human breast CSCs and normal
human mammary stem / progenitor cells showed decreased expression of miR200c and other miR200 members and that restoring miR200c
in breast CSCs inhibits their ability to expand clonally and form
tumors in vivo [38].
Rudensky's team compared Tregs
in normal
human breast tissues with those found
in untreated
breast tumors, and found that Tregs
in tumors were capable of more potent and aggressive immunosuppressive action.
[i] Gutterman JU, Blumenschein GR, Alexanian R, Yap HY, Buzdar AU, Cabanillas F, Hortobagyi GN, Hersh EM, Rasmussen SL, Harmon M, Kramer M, Pestka S. Leukocyte interferon - induced
tumor regression
in human metastatic
breast cancer, multiple myeloma, and malignant lymphoma.
Flavopiridol inhibits several cellular kinases and has demonstrated cytostatic and cytotoxic activity
in vitro and
in vivo
in numerous
human tumor cell lines and xenograft models (including
human breast, prostate, and lung carcinoma) at clinically achievable concentrations.
: This study evaluated the effects of an antagonistic analog of growth hormone - releasing hormone, MIA - 602, on
tumor growth, response to doxorubicin, expression of drug resistance genes, and efflux pump function
in human triple negative
breast cancers.
Introduction: This study evaluated the effects of an antagonistic analog of growth hormone - releasing hormone, MIA - 602, on
tumor growth, response to doxorubicin, expression of drug resistance genes, and efflux pump function
in human triple negative
breast cancers.
We also demonstrate that immunoglobulin - secreting NSCs exhibit preferential tropism to
tumor cells
in vivo, and can deliver antibodies to
human breast cancer xenografts
in mice.
Dr. Mack's research has focused primarily on the use of novel antitumor agents
in human estrogen receptor negative
breast tumor cells, and more recently, on the use of bioflavonoids
in the regulation of estrogen receptor positive (ER +) and estrogen receptor negative (ER --RRB-
breast tumor cell proliferation.
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.
And we confirmed that the growth of the
tumors formed by the
human BCSCs transfected with the anti-miR-142-expressing lentivirus was significantly slower than those of the control
tumors formed by the control lentivirus transfected BCSCs (Major points raised by the editors and the reviewers # 3) These data suggest that the regulation of APC and the Wnt signaling is at least one of the important pathways targeted by miR - 142
in human breast cancer cells and BCSCs.
Considering that miR - 142 is highly expressed
in human BCSCs, but weakly expressed or undetectable
in the stem / progenitor population of the mammary epithelial cells, our result suggest that the upregulation of miR - 142 and its enhancement of the miR - 150 expression seem to be especially relevant
in the
breast tumor progression
in vivo.
The most frequent
tumors in human — cancer of the colon,
breast, lung, and prostate — all involve mutations
in tumor suppressor genes.
These molecular subtypes have recently been confirmed
in a comprehensive characterization of
human breast tumors at the genomic, epigenetic, transcriptomic, and proteomic levels (Cancer Genome Atlas Network, 2012).
Many women are «triple negative» No one yet knows precisely why, but African - American women are roughly twice as likely as white women to have triple - negative
breast cancer — so called because
tumor cells
in this particularly aggressive form of the disease test negative for estrogen receptor (ER), progesterone receptor (PR), and
human epidermal growth factor receptor 2 (HER - 2).
We know that the lemony aura of limonene is more than just a scent, as it can be found
in our blood after exposure.8 Furthermore, several anticancer cellular pathways appear to be affected by the terpene limonene, leading some to suggest it has anticancer, or chemopreventative, benefits.9 While feeding it to rats
in studies has revealed some efficacy against
breast tumors, 10 we have a ways to go before we can make such bold claims
in humans.
Studies of Gluts
in human tumors have shown a significant increase
in the abundance of Glut1 and Glut3 mRNA
in cancers of the esophagus, colon, and pancreas, overexpression of Glut1 and Glut3 mRNA and Glut1 protein expression
in head and neck
tumors and Glut1 protein overexpression
in breast and renal cell carcinomas
As a result,
breast cancer cell growth is blocked One study
in mice concluded that flaxseed inhibited the growth of
human estrogen - dependent
breast cancer, and strengthened the
tumor - inhibitory effect of tamoxifen.
According to another study on mice, the
human equivalent of just two handfuls of walnuts a day cut
breast cancer risk
in half, and slowed
tumor growth by 50 percent as well.
According to Lise Alschuler, author of the Definitive Guide To Cancer: An Integrative Approach to Prevention, Treatment, and Healing, studies on flax lignans demonstrate safety and efficacy
in their use against
breast cancer, «inhibiting the growth of
human estrogen - dependent
breast cancer cells
in mice and strengthening the
tumor - inhibitory effect of tamoxifen».
They help block the ability of cancer cells to produce the
tumor invasion enzyme
in the first place,
in both
human colon cancer cells, and
human breast cancer.
Veterinary oncologists working with a program at the University of Pennsylvania are treating mammary
tumors in shelter dogs with the hope of learning about the progression of
breast cancer
in humans.
There are many differences between mammary
tumors in animals and
breast cancer
in humans, including
tumor type, malignancy, and treatment options