Sentences with phrase «in alk»

However, the activation status of the mTOR pathway in ALK + ALCL is unknown.

Of note, AKT activation in ALK + ALCL tumors, determined as Ser473p - AKT expression (20), significantly correlated with p - mTOR and p - rpS6 (P = 0.037 and 0.002, respectively, χ2 test) as well as with total 4E - BP1 and total eIF4E (P = 0.001 and 0.003, respectively, χ2 test).

In ALK + ALCL, the chimeric protein nucleophosmin - ALK has been shown to activate PI3K and its downstream effector AKT (4).

mTOR pathway is frequently activated in ALK + ALCL tumors and cell lines.

However, the activation status of the mTOR pathway has not been investigated in ALK + ALCL.

We also show that inhibition of mTOR with rapamycin, as well as silencing mTOR gene product expression using mTOR - specific small interfering RNA, decreased phosphorylation of mTOR signaling proteins and induced cell cycle arrest and apoptosis in ALK + ALCL cells.

Inhibition of mTOR induces apoptosis in ALK + ALCL cells.

Alectinib provides longer symptom improvement than crizotinib in ALK - positive non-small-cell lung cancer (NSCLC), according to results from the ALEX trial (1) presented at the ELCC 2018 (European Lung Cancer Congress) in Geneva, Switzerland.

We observed that the phosphorylation level of AKT significantly correlated with the phosphorylation level of mTOR and rpS6 as well as with expression of total 4E - BP1 and eIF4E in ALK + ALCL tumors.

A subset of ALCL tumors carries chromosomal aberrations involving the anaplastic lymphoma kinase (alk) gene on chromosome 2p23 resulting in ALK overexpression (2).

Inhibition of the mTOR pathway interferes with essential proliferation and survival pathways in ALK + ALCL and might form the basis for a novel therapeutic strategy.

To investigate if AKT activation is sufficient to activate the mTOR pathway in ALK + ALCL cells, we infected the Karpas 299 and SU - DHL1 cell lines with an adenoviral vector, adeno - myrAkt, expressing constitutively active AKT (23).

These results suggest that inhibition of mTOR - raptor complex or silencing mTOR gene expression induced cell cycle arrest at G1 phase in ALK + ALCL cells.

We also provide evidence that activation of the mTOR pathway in ALK + ALCL depends, at least in part, on PI3K / AKT.

mTOR signaling in ALK + ALCL oncogenesis.

We also show that rapamycin and total mTOR silencing induces cell cycle arrest and apoptosis interfering with proliferation and survival pathways in ALK + ALCL.

Our results confirm that rapamycin inhibits activation of the mTOR pathway in ALK + ALCL cells.

These findings suggest that activation of mTOR signaling contributes to tumor cell survival in ALK + ALCL, thus providing a potential therapeutic target in this lymphoma type.

Because treatment with rapamycin also led to decreased AKT phosphorylation in ALK + ALCL cells in our in vitro study, it is tempting to speculate that an effector protein downstream of mTOR - raptor may contribute directly or indirectly to AKT activation.

In this study, we hypothesized that the mammalian target of rapamycin (mTOR) pathway, which functions downstream of AKT, mediates the oncogenic effects of activated PI3K / AKT in ALK + ALCL.

Here, we show that the mTOR pathway is activated in ALK + ALCL.

Here, we provide evidence that mTOR signaling phosphoproteins, including mTOR, eukaryotic initiation factor 4E — binding protein - 1, p70S6K, and ribosomal protein S6, are highly phosphorylated in ALK + ALCL cell lines and tumors.

Next came the test to see if Martensen's tumor contained the ALK mutation, which occurs when a section of DNA in the ALK gene, located on chromosome 2, breaks apart.

The NIH and Mass General are at the vanguard of a major effort to identify and treat cancer based on causative gene mutations like the one found in ALK.

Commenting on the trial, Dr Alice Shaw, director of thoracic oncology at the Massachusetts General Hospital Cancer Centre in Boston, US, said: «This is the first randomised study to examine how a second generation ALK inhibitor compares to standard second line chemotherapy in ALK positive patients who failed the standard first line therapy, which currently is crizotinib.»

The abnormality in ALK that arises in NSCLC is not, strictly speaking, a mutation (a change in the sequence of DNA within a gene).

Now, through an unexpected observation and a meticulous study of patients seen at Brigham and Women's Hospital, BWH investigators have added a fourth cause to the list: a genetic rearrangement in the ALK gene, observed in three patients with peritoneal mesothelioma.

«Rare genetic cause of peritoneal mesothelioma points to targeted therapy: Genetic rearrangement in the ALK gene found in young women with mesothelioma may be targetable with FDA - approved drugs.»

Not exact matches

In the UK, two rival products are approved for sale from Danish drugmaker ALK - Abello and from Valeant's Bausch and Lomb division.

In the United Kingdom, two rival products are approved for sale from Danish drugmaker ALK - Abello and from Valeant's Bausch and Lomb division.

Stifel analyst Joseph DeNardi argued in a research note that if Sprint (S) and T - Mobile (TMUS) merger gets a green light from the Trump administration, there would likely be a «bidding war» unseen before in the airline industry as the «Big 4» would have significant interest in acquiring Alaska Air (ALK) or JetBlue (JBLU) if they think they could.

And remember, I'm not alking about the religion of Christianity, but the aspect of my life where I believe in Jesus for eternal life, and try to follow His leading and His example.

For example, a fusion of ALK with EML4 occurs in about 5 % of cancers and is linked to strong patient response to treatment with crizotinib.

They also looked in samples collected from patients with pleural mesothelioma — the more common form of the diseases — but none of those samples were positive for ALK.

The ALK gene is important during embryonic development of the nervous system but should be inactive later in life.

Chirieac and colleagues hope to extend their study of ALK - positive mesotheliomas in a global patient population.

In his own practice, Chirieac is routinely examining for the presence of ALK rearrangements for patients with mesothelioma and educating his residents about this new finding.

Previous studies of genetic alterations in lymphoma and lung cancer have found that certain genetic mutations — specifically when part of a gene breaks off and gets fused to another — can inappropriately switch on ALK, driving cancer cells to grow and divide.

They identified ALK - positive mesotheliomas by immunohistochemistry; confirmed with fluorescence in situ hybridization; and performed targeted next - generation sequencing of tumor DNA and RNA to get a full picture of the exact genetic rearrangement underpinning the disease.

After enriching for CTCs, the researchers analyzed the samples for ALK rearrangements and for an increase in the number of copies of the ALK gene.

Median progression - free survival for the 13 patients who had a decrease in the number of CTCs with ALK copy number gain was 14.0 months, while the median progression - free survival for the 16 patients who had stable or increased numbers of CTCs with ALK copy number gain was 6.1 months.

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.

Analysis of CTC numbers at the different time points showed that the one measurement that was statistically significantly associated with progression - free survival was a change in the number of CTCs with ALK copy number gain over time.

These results are among the best in the field, offering a lot of hope to people with ALK - positive lung cancer,» says D. Ross Camidge, MD, PhD, director of thoracic oncology at the University of Colorado Cancer Center and the trial's principal investigator.

«Although still only in an early phase trial, brigatinib is showing an objective response rate in approximately 70 percent of ALK - positive patients post-crizotinib and it's showing about a year of progression - free survival.

«We look forward to conducting further research through the STARTRK - 2 phase II trial and are hopeful that treatment with entrectinib in patients with a range of advanced or metastatic solid tumors harboring NTRK1 / 2/3, ROS1, or ALK gene fusions will result in very meaningful benefit.»

Multiplexed genetic screening for epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) gene rearrangements and subsequent biomarker - guided treatment is cost - effective compared with standard chemotherapy treatment without any molecular testing in the metastatic non-small cell lung cancer (NSCLC) setting in the United States.

Some patients with non-small cell lung cancer (NSCLC) have changes in the anaplastic lymphoma kinase (ALK) gene, which can drive the development of their cancer.

Dorothy Romanus, lead author of the study, states «this analysis supports the value of multiplexed testing for EGFR and ALK gene rearrangements followed by molecularly - guided therapy in decisions surrounding coverage of related testing and targeted therapy.

«Testing for EGFR mutations, ALK rearrangements is cost - effective in NSCLC..»