Not exact matches
Immune
cells modified by CRISPR - Cas9 were inserted into a
lung cancer patient at the West China Hospital in Chengdu in the hopes that they'll be able to fight
tumors, and 10 people total will receive injections of CRISPR re-engineered
cells in order to assess the method's safety.
However, the impact of the two methylation - regulating enzymes was still seen at 10 to 15 months, when scientists found decreased expression of hundreds of genes — many of which are key
tumor suppressor genes such as BMP3, SFRP2 and GATA4 — in the smoke - exposed
cells and a five - or - more-fold increase in the signaling of the KRAS oncogene that is known to be mutated in smoking - related
lung cancers.
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.
Potti and his colleagues began by testing chemotherapy drugs on cultured
cell lines from human
tumors, such as from the
lung, breast, or ovary.
Further preclinical work will be needed to use the herpes - loaded stem
cells for breast,
lung and skin cancer
tumors that metastasize to the brain.
A Yale Cancer Center research team conducted a study to determine how those
tumor cells manage to grow outside the
lungs.
Pembrolizumab, or pembro, an immunotherapy drug that unmasks cancer
cells and allows the body's own immune system to help destroy
tumors, appears to be safe in treating
lung cancers, according to a study by Cancer Treatment Centers of America ® (CTCA) at Western Regional Medical Center (Western) in Goodyear, Arizona.
There is currently a PD - 1 antibody on the market that blocks T
cell exhaustion in patients with solid
tumors, like
lung cancer and melanoma.
«We believe that small subsets of metastatic
tumor cells have the ability to adopt the mechanisms used by immune
cells to exit the blood vessels into the
lungs, the bone marrow, the brain, and other organs.
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.
They found out that TiY is capable of distinguishing TICs from non-TICs in various human
lung cancer
cell lines and patient - derived
lung tumors.
The substance vigorously inhibited the growth of cultured
tumor cells from colon,
lung, and breast cancers, the team reports in the 20 January issue of Angewandte Chemie.
Among patients with non-small
cell lung cancer (NSCLC) fueled by ALK gene alterations who were being treated with crizotinib (Xalkori), a decrease in the number of circulating
tumor cells (CTCs) harboring increased copies of the ALK gene over the first two months of treatment was associated with increased progression - free survival.
The study, «The nuclear transport receptor Importin - 11 is a
tumor suppressor that maintains PTEN protein,» which will be published online February 13 in The Journal of
Cell Biology, suggests that the loss of Importin - 11 may destabilize PTEN, leading to the development of
lung, prostate, and other cancers.
«FDG PET shows
tumor DNA levels in blood are linked to NSCLC aggressiveness: Insights derived from FDG PET could improve treatment selection for patients with advanced non-small
cell lung cancer.»
Loss of either GSTO1 or RYR1, the researchers report, decreased the number of cancer stem
cells in the primary
tumor, blocked metastasis of cancer
cells from the primary
tumor to the
lungs, decreased the duration of chemotherapy required to induce remission and increased the duration of time after chemotherapy was stopped that the mice remained
tumor - free.
Italian researches have demonstrated a better way of determining the aggressiveness of
tumors in patients with advanced non-small
cell lung cancer (NSCLC).
CCL5 attracts
tumor cells to the
lungs and lymph nodes, and VEGF increases the number of blood vessels and makes them more porous, allowing
tumor cells to metastasize and infiltrate the
lungs.
Nana - Sinkam and his colleagues examined
lung -
tumor samples from 81 patients with stage - 1 nonsmall -
cell lung cancer and
tumor -
cell lines.
One of those genes, K - Ras, which was discovered nearly 30 years ago, is mutated in 30 percent of human
tumors, including 90 percent of pancreatic cancers, 40 percent of colon cancers, and 20 percent of non-small
cell lung cancers.
New research shows that microRNA - 486 is a potent
tumor - suppressor molecule in
lung cancer, and that the it helps regulate the proliferation and migration of
lung - cancer
cells, and the induction of programmed
cell death, or apoptosis, in those
cells.
«High concordance between EGFR mutations from circulating - free
tumor DNA and
tumor tissue in non-small
cell lung cancer.»
Epidermal growth factor receptor (EGFR) mutations found in the circulating free
tumor DNA (ctDNA) from the plasma of advanced non-small
cell lung cancer (NSCLC) patients correlates well with the EGFR mutations from patient - matched
tumor tissue DNA.
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.
By blocking these in
lung endothelial
cells, the researchers were able to slow
lung tumor growth in mice and also reduce the spread of metastatic
tumors.
Given that breast cancer
cells traveling through the bloodstream on their way to secondary sites where breast
tumors metastasize most often —
lung, bone marrow, brain and liver — must first pass through the basement membrane microvasculature, Ghajar and Bissell suspected that the basement membrane could be a major component of the dormant niche in distant organs.
Partnering with the U.S. Food and Drug Administration allowed Doebele and colleagues to access clinical trial data describing initial
tumor response, PFS and OS for 305 patients with stage IIIb or IV non-small
cell lung cancer on trials of ALK inhibitors and 355 similar patients on trials of immunotherapies directed at PD - 1.
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.
Other studies have found that nutrients in dark, leafy greens may inhibit the growth of
tumor cells in breast, skin,
lung and stomach cancers and that green tea may thwart cancer development in colon, liver, breast and prostate
cells.
By contrast, 16 out of 17 mice that produced annexin A2 in their
cells developed metastatic
tumors in the liver,
lungs or abdominal cavity.
«We found that many more mice developed
tumors when given the
cells that we had engineered to have these stem
cell characteristics, and they had a much higher incidence of metastasis in the
lungs,» Kilian said.
«Communication between
lung tumors, bones contributes to
tumor progression: Study identifying interaction among
tumor cells, bone marrow and immune
cells opens new avenue for immunotherapy.»
This soluble factor was found at higher levels in the blood of animals with
lung tumors, could increase the activation of osteoblasts and contributed to the maturation of neutrophils in cultured
cells.
Examination of gene expression in patients with non-small
cell lung cancer (NSCLC) showed the area adjacent to
tumors is rich with cancer markers.
«Our findings indicate the existence of long - distance interactions between
lung tumors and bones:
lung tumors remotely activate osteoblasts, and those bone
cells, in turn, shape immunity by supplying
tumors with cancer - promoting neutrophils,» says Pittet, who is an associate professor of Radiology at Harvard Medical School.
Both the number and activity of osteoblasts —
cells that produce and reshape bone tissue — were increased within the bone marrow of mice with
lung tumors compared with cancer - free animals; and reducing the number of osteoblasts in mice not only limited neutrophil infiltration of
tumors but also interrupted
tumor progression.
In the Dec. 1 issue of Science, the team from the MGH Center for Systems Biology describes a «crosstalk» between
lung tumors and bone marrow, which leads to the generation of a type of immune
cell that travels to the
tumor and promotes its progression.
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.
A possible explanation may be that, according to prior research findings,
tumors of the
lung and bowel tend to be colonized by particularly high quantities of immune
cells.
Results of an initial study of
tumors from patients with
lung cancer or head and neck cancer suggest that the widespread acquired resistance to immunotherapy drugs known as checkpoint inhibitors may be due to the elimination of certain genetic mutations needed to enable the immune system to recognize and attack malignant
cells.
To investigate why checkpoint inhibitors so often stop working, Velculescu; Valsamo Anagnostou, M.D., Ph.D., instructor of oncology at the Johns Hopkins University School of Medicine; Kellie N. Smith, Ph.D., a cancer immunology research associate at the Johns Hopkins University School of Medicine; and their colleagues at the Bloomberg ~ Kimmel Institute for Cancer Immunotherapy studied
tumors of four patients with non-small
cell lung cancer and one patient with head and neck cancer who developed resistance to two different checkpoint inhibitors: a drug called nivolumab that uses an antibody called anti-PD-1, or nivolumab used alone or in combination with a second drug called ipilimumab, which uses an antibody called anti-CTLA4.
«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.»
Among
lung cancer patients; suicide SMR was higher in males (SMR = 8.8), Asians (SMR = 13.7), widowed patients (SMR = 11.6), older patients (70 - 75 years; SMR = 12), patients with undifferentiated
tumors (SMR 8.6) or small
cell lung carcinoma (SCLC) histology (SMR = 11.2), patients presenting with metastatic disease (SMR = 13.9) and in patients who refused to receive surgical treatment (SMR = 13).
Mice injected with breast cancer
cells making lots of a long strand of RNA called HOTAIR developed 10 times as many
lung tumors as controls (left) did.
Different types of
tumors show a preference for specific organs and tissues; circulating breast cancer
cells, for example, are likely to take root in bones,
lungs, and the brain.
The results from our new study suggest that entinostat may enhance the anti-tumor efficacy of PD - 1 targeted therapy through MDSC targeting, potentially providing an effective combination treatment approach for patients with solid
tumors, including
lung and renal
cell carcinoma.»
«Preclinical results support entinostat's role in targeting the
tumor microenvironment: Entinostat inhibits function of myeloid derived suppressor
cells resulting in enhanced antitumor effect in murine models of
lung and renal
cell carcinoma.»
The study's findings, published in the journal Cancer Research, are the first to use these combined agents as an immune stimulator and may have the potential to kill cancerous
cells in solid
tumors, including some of the most aggressive cancers that form in the
lung and pancreas.
In their previous work, the scientists suspected that C / EBPα may act as a
tumor suppressant in normal
cells, but the mechanism by which its absence promoted
lung cancer
tumors remained unclear.
In one, a liver and armpit
tumor that had developed from spreading melanoma
cells shrank, and in the other a
lung tumor disappeared.