The result was a highly selective drug they named SBI - 0206965, which successfully killed a number of cancer cell types, including
human and mouse lung cancer cells and human brain cancer cells, some of which were previously shown to be particularly reliant on cellular recycling.
All of these findings were supplemented with several other experiments that were designed to learn how CHI3L1 interacts with other cells involved in the tissue repair response in both
human and mouse lungs.
Not exact matches
In experiments conducted on
human lung endothelial cells
and in
mice, the researchers showed that NS1 caused permeability of the endothelium, which lines the walls of blood
and lymph vessels.
Similar to
humans, the
mice developed tumors at secondary sites including the liver,
lung, peritoneum,
and diaphragm.
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.
Researchers developed a new type of cell transplantation to treat
mice mimicking a rare
lung disease that one day could be used to treat this
and other
human lung diseases caused by dysfunctional immune cells.
By using molecular genetic tools to reduce the amount of PC in
human lung cancer cells, the team observed decreased cell growth, a compromised ability to form colonies in soft agar (a gelatinous material specifically used to grow bacteria
and other cells),
and a reduced rate of tumor growth in
mice.
«This association is important for
lung development in
mouse embryos,
and at least for one of these long non-coding RNAs, important for
human lung function.»
This factor is the first
lung molecular marker during
mouse and human development
and is essential for
lungs to mature properly in an embryo.
The cells exhibited many functions associated with tumor progression; their presence within
mouse tumors substantially accelerated cancer growth,
and in
human lung tumors, a SiglecFhigh neutrophil signature was associated with poor patient survival.
In the study, the fungal infection Candida albicans was introduced to
mice or
human models of the
lung vasculature
and as blood was pumped over that system, researchers recorded what happened using highly sophisticated microscopes.
They demonstrated that, similar to
mouse, Rac1 inhibition resulted in impaired branching
and decreased expression of AXIN2
and FGFR2b in
human lung cultures.
The findings, now published in PLOS Genetics, reveal how
mice can actually mimic
human breast cancer tissue
and its genes, even more so than previously thought, as well as other cancers including
lung, oral
and esophagus.
«For example,
mouse mammary tumors shared a signaling pathway that is found in
human lung cancer
and controls how cells reproduce
and move from one location to another.»
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.
The 19 NIH institutes, centers
and offices contributing to the Knockout
Mouse Project are: the NIH Office of Strategic Coordination / Common Fund; NCRR; the National Eye Institute; NHGRI; the National Institute of Allergy
and Infectious Diseases; the National Heart,
Lung and Blood Institute; the National Institute on Aging; the National Institute of Alcohol Abuse
and Alcoholism; the National Institute of Arthritis
and Musculoskeletal
and Skin Diseases; the Eunice Kennedy Shriver National Institute of Child Health
and Human Development; NIDCD; the National Institute of Dental
and Craniofacial Research; the National Institute of Environmental Health Sciences; the National Institute of General Medical Sciences; the National Institute of Mental Health; the National Institute of Neurological Disorders
and Stroke; the National Institute of Diabetes
and Digestive
and Kidney Diseases; the National Cancer Institute;
and the Office of AIDS Research.
Using studies in both
mice and humans, they found that exposure to farm dust increases expression of a protective protein that suppresses the inflammatory immune system by modifying the communication between the lining of the
lungs and the immune system.
E-cigarette smoke damages DNA
and reduces repair activity in
mouse lung, heart,
and bladder as well as in
human lung and bladder cells, reports a new study, published in PNAS.
In recent years, researchers have developed so - called «senolytic» drugs that wipe out senescent cells in aging
mice and mouse models of age - related disease, exploiting the high dependence of these cells on specific biochemical survival pathways.9, 10 In these studies, senolytic drugs have restored exercise capacity9
and formation of new blood
and immune precursor cells11 in aging
mice to near youthful norms,
and prevented or treated
mouse models of diseases of aging like osteoarthritis, 12 fibrotic
lung disease, 13 hair loss, 14 atherosclerosis, 15,16
and age - related diseases of the heart itself.9 UNITY Biotechnology is leading a growing charge toward the clinic, with
human clinical trials expected to begin in 2019.
«We developed a new method of initiating
lung cancer in
mice, which has properties associated with
human lung cancer,
and used this model to identify the role of this enzyme in cancer proliferation.
Studies in animals
and humans have shown that dietary glutathione increases blood levels of glutathione, but one study in
mice suggested that under ordinary conditions, dietary glutathione can not boost its own concentration in other tissues except in the
lung, where large amounts of glutathione are needed to maintain the fluidity of mucus.
1) that the rate of mutations increase in
mice exposed to SHS
and 2) that the spectra of mutations in the SHS exposed
mice is the same as in non - smoker
humans with
lung cancer.