One study presented in the journal — from a group led by Patrick Singleton, PhD, assistant professor of medicine at the University of Chicago Medicine — shows how opioids already present in the body can enhance the malignant tendencies
of human lung cancer cells transplanted into mice, even without the addition of morphine.
They showed that it slowed the growth
of human lung cancer cells but not kidney cancer cells in these mice.
Not exact matches
Scientists at the Johns Hopkins Kimmel
Cancer Center say they have preliminary evidence in laboratory - grown, human airway cells that a condensed form of cigarette smoke triggers so - called «epigenetic» changes in the cells consistent with the earliest steps toward lung cancer develo
Cancer Center say they have preliminary evidence in laboratory - grown,
human airway
cells that a condensed form
of cigarette smoke triggers so - called «epigenetic» changes in the
cells consistent with the earliest steps toward
lung cancer develo
cancer development.
In their latest study, they tested compounds against
cells from nine different types
of human cancer, including common types affecting blood, colon, breast, prostate, ovaries, kidneys, and
lungs.
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.
Beyond
lung cancer, TiY is able to target TICs in 28 types
of human cell lines derived from the central nervous system, melanoma, breast, renal, ovarian, colon, and prostate
cancer.
Using both fruit fly and
human lung cancer cell lines, researchers targeted two
of the most common genetic mutations associated with NSCLC — Ras and PTEN (P13K).
Normal
human colon
cells, kidney
cells,
lung cancer cells and two strains
of colon
cancer cells didn't respond to the bacteria.
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.
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 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.
«We now know much more about metabolic reprogramming
of cancerous tissues in
human patients, particularly that the activation
of pyruvate carboxylase is important to
lung cancer cell growth and survival,» said Fan, UK professor of toxicology and faculty member of the Markey Cancer Center and CESB at the University of Ken
cancer cell growth and survival,» said Fan, UK professor
of toxicology and faculty member
of the Markey
Cancer Center and CESB at the University of Ken
Cancer Center and CESB at the University
of Kentucky.
In a letter published in the
cancer journal Annals
of Oncology, researchers led by Professor Jean - Philippe Spano, head
of the medical oncology department at Pitie - Salpetriere Hospital AP - HP in Paris, France, report that while treating an HIV - infected
lung cancer patient with the
cancer drug nivolumab, they observed a «drastic and persistent decrease» in the reservoirs
of cells in the body where the
human immunodeficiency virus (HIV) is able to hide away from attack by anti-retroviral therapy.
However, scientists at SFU, the University
of British Columbia and the B.C.
Cancer Agency have discovered that many non-coding RNAs are perturbed in cancerous
human cells, including breast and
lung, in a specific way.
Inclusion Criteria: • Eastern Cooperative Oncology Group (ECOG) performance status
of 0 or 1 • Have histologically or cytologically confirmed advanced or metastatic non-small
cell lung cancer (NSCLC)(Stage IIIb or greater) • Measurable disease, as defined by Response Evaluation Criteria in Solid Tumors (RECIST) 1.1 • Known PD - L1 tumor status as determined by an immunohistochemistry (IHC) assay performed by the central laboratory on tissue obtained at Screening • A woman
of childbearing potential must have a negative highly sensitive serum (beta -
human chorionic gonadotropin [beta - hCG]-RRB- at Screening within 14 days prior to study drug administration Inclusion Criteria for Crossover: • Participants must have been randomized to Arm A
of the study and had radiographic disease progression according to RECIST 1.1 • Participants must have a mandatory biopsy at the time
of disease progression according to RECIST 1.1 prior to crossing over.
Wang's team discovered that if
human lung cancer cells in a lab dish in the presence
of the receptor were treated with BCX, they migrated less than untreated ones.
Management
of chemotherapy - related anaemia with low - dose recombinant
human erythropoietin in patients with small
cell lung cancer.
In this fashion, they derive a signal from the tumor
cells proportional to tumor mass which arises spontaneously in vivo in the accurate setting
of the
lung and from the accurate genetic lesions found in
human non-small
cell lung cancer (NSCLC).
Miller's group, including postdoctoral fellow Dr. Sharath Rai, graduate student Vladimir Vigdorovich and collaborators at the National
Cancer Institute, identified the human version of the viral receptor, a cell - surface protein called HYAL2 that has been implicated in lung c
Cancer Institute, identified the
human version
of the viral receptor, a
cell - surface protein called HYAL2 that has been implicated in
lung cancercancer.
I wanted to inactivate the gene BRAF (a kinase implicated in several
human cancers) in A549
cells (a
human lung cancer cell line), armed only with viruses obtained through Addgene's viral service and the methods sections
of scientific articles (gasp).
(a kinase implicated in several
human cancers) in A549
cells (a
human lung cancer cell line), armed only with viruses obtained through Addgene's viral service and the methods sections
of scientific articles (gasp).
Cyclooxygenase -2-dependent expression
of angiogenic CXC chemokines ENA - 78 / CXC Ligand (CXCL) 5 and interleukin - 8 / CXCL8 in
human non-small
cell lung cancer.
«Study
of the pro-apoptotic effect
of molecules interfering with epigenetic mechanisms on
human lung cancer cells».
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.
8) Shah P, Lockwood WW, Saurabh K, Kurlawala M, Shannon S, Waigel S, Zacharias W, Beverley LJ (2014) Ubiquilin1 represses migration and epithelial to mesenchymal transition
of human non-small
cell lung cancer cells.
Title
of thesis: «Study
of the pro-apoptotic effect
of histones deacetylases inhibitors, used alone and concurrently with chemotherapeutic agents, on
human lung cancer cells».
In this study,
human lung cancer cells with additional copies
of the opioid receptor grew more than twice as fast as tumor
cells that lacked extra receptors when transplanted into mice.
Revealed that the loss
of the
human leukocyte antigen (HLA) locus in
lung cancers is a way these tumors evade the immune system and allow mutation expansion and branched evolution within tumor
cells