scispace - formally typeset
Search or ask a question

What is the alk gene? 


Best insight from top research papers

The anaplastic lymphoma kinase (ALK) gene is a crucial gene involved in various cancers, including anaplastic large cell lymphoma, lung cancer, and neuroblastoma. It encodes a transmembrane receptor tyrosine kinase that, when activated by fusion with partner genes or through mutations, leads to oncogenic protein production and downstream signaling activation . ALK activation occurs through dimerization and autophosphorylation of its intracellular kinase domain upon ligand binding to its extracellular domain . The gene is a hotspot for chromosomal translocations, resulting in fusion proteins that drive various malignancies . ALK inhibitors like crizotinib and alectinib have shown effectiveness in treating ALK-positive cancers, particularly non-small cell lung cancer, although resistance mechanisms are being studied for improved treatment strategies .

Answers from top 5 papers

More filters
Papers (5)Insight
The ALK gene encodes a transmembrane tyrosine kinase receptor involved in various cancers due to fusion with oncogenes or gene alterations, making it a target for specific inhibitors in treatment.
The ALK gene encodes the anaplastic lymphoma kinase, a receptor tyrosine kinase linked to neuroblastoma development due to genetic alterations, impacting cell behavior in neuroblastoma.
The ALK gene encodes the anaplastic lymphoma kinase receptor, a receptor tyrosine kinase crucial for CNS functions and implicated in various malignancies due to fusion proteins and mutations.
The ALK gene is a tumor driver gene found in non-small cell lung cancer, with various fusion partners like CLIP1-ALK. It plays a role in cancer development and treatment response.
The ALK gene encodes a transmembrane receptor tyrosine kinase. It forms oncogenic fusion proteins with partner genes due to chromosomal translocation, found in various hematological neoplasms like ALCL and AML.

Related Questions

What causes alk NSCLC?4 answersALK-positive non-small cell lung cancer (NSCLC) is primarily caused by rearrangements of the anaplastic lymphoma kinase (ALK) gene, accounting for approximately 5-6% of NSCLC cases. These ALK rearrangements drive the development of NSCLC and make the cancer sensitive to ALK tyrosine kinase inhibitors (TKIs) but also prone to drug resistance. The most common fusion variant observed in ALK-positive NSCLC is the EML4-ALK fusion, accounting for the majority of cases, while other rare fusion forms have also been identified. The identification of ALK rearrangements in NSCLC is typically done through techniques like fluorescence in situ hybridization (FISH) and immunohistochemistry, which detect ALK translocations and overexpression, respectively, aiding in predicting response to TKIs.
What are the ERK related genes?5 answersThe ERG gene is a member of the ETS transcription factor family and is consistently overexpressed in about half of patients with clinically significant prostate cancer (PCa). ERG plays a central role in PCa progression by enhancing tumor growth, promoting inflammatory and angiogenic responses, and increasing the ability of cancer cells to metastasize. In endothelial cells (EC), ERG is a positive regulator of genes involved in EC function and a negative regulator of genes involved in inflammation. ERG also plays a pivotal role in regulating EC barrier function and is involved in the regulation of CLDN5 gene expression. Additionally, ERG has been identified as a novel class of eukaryotic GTPases in plants, with a crucial role in plant growth and development, possibly by influencing mitochondrial division.
What is the role ALPK3 gene in cardiovascular disease?5 answersALPK3 gene has been found to play a role in cardiovascular disease. A study by Caglayan et al. identified a novel homozygous frameshift mutation in ALPK3 in a male infant with primary dilated cardiomyopathy, which progressed to hypertrophic cardiomyopathy after birth. This mutation was not present in heterozygous family members who were normal. Another study by van den Akker et al. found that persons homozygous for haplotype 3 of the glucocorticoid receptor gene, which is a common variant of ALPK3, had an increased risk of myocardial infarction and coronary heart disease compared to nonhomozygous persons. These findings suggest that genetically determined cortisol sensitivity, regulated by ALPK3, is involved in the pathogenesis of cardiovascular disease.
How many genes in the human have a kinase domain?5 answersThe human genome contains approximately 500 genes that have a kinase domain. These genes encode for proteins known as protein kinases, which play important roles in various cellular processes such as proliferation, maintenance of cell shape, and apoptosis. The protein kinases are characterized by the presence of a common kinase catalytic domain, and some members of this family also have additional non-kinase domains that contribute to their specialization. The kinase gene family is diverse and includes both well-known genes and genes that have been identified more recently through computational studies. The kinome, which refers to the protein kinase component of the human genome, was exhaustively compiled in 2002 and identified 478 eukaryotic protein kinase (ePK) genes and 40 atypical protein kinases.
The expression of which genes is regulated by TGFb-ALK1 signalling?5 answersTGF-β-ALK1 signaling regulates the expression of several genes. One of these genes is Serum/glucocorticoid-regulated kinase 1 (SGK1). Another gene regulated by TGF-β-ALK1 signaling is alk1, which is involved in proper vascular development. Additionally, TGF-β1-ALK1 signaling induces the expression of Id3, HAMP, and PLAUR genes in macrophages.
What is the function of anaplastic lymphoma kinase?5 answersAnaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase that plays important roles in various cancers, including anaplastic large cell lymphoma (ALCL), non-small cell lung cancer (NSCLC), and neuroblastomas. ALK gene alterations, such as gene rearrangements and mutations, are key drivers in the development of these tumors. Targeted therapy with ALK inhibitors has transformed the treatment paradigm for ALK-positive tumors, leading to improved outcomes for patients. ALK inhibitors, such as crizotinib, ceritinib, alectinib, brigatinib, and lorlatinib, have been approved by the U.S. Food and Drug Administration (FDA) for the treatment of ALK-positive NSCLCs. The function of ALK is to activate signaling pathways that promote cell growth and survival, and its constitutive activation in ALK-fused cancers can be inhibited by ALK tyrosine kinase inhibitors (TKIs). The development of next-generation ALK inhibitors and combination therapies targeting ALK and alternative signaling pathways are being explored to overcome resistance and improve treatment outcomes.

See what other people are reading

What is the future of brentuximab? use multiple citations?
4 answers
The future of brentuximab vedotin looks promising across various hematologic malignancies. Studies highlight its efficacy and safety in treating CD30-positive lymphomas like anaplastic large cell lymphoma (ALCL), classic Hodgkin lymphoma (cHL), and relapsed and refractory Hodgkin lymphoma. Brentuximab vedotin has shown high response rates in heavily pretreated patients, leading to FDA approvals for relapsed/refractory ALCL and cHL. Ongoing clinical trials explore its use in combination therapies and as a bridge to stem cell transplant, indicating a growing role for brentuximab vedotin in both frontline and salvage settings. The drug's targeted activity, limited toxicity, and potential synergistic effects with other chemotherapy agents position it as a valuable treatment option for various CD30-expressing malignancies, paving the way for further advancements in its clinical applications.
Why are gd T cells attractive for allotherapy?
5 answers
Gamma/delta (gd) T cells are attractive for allotherapy due to their unique characteristics. Unlike conventional alpha/beta T cells, gd T cells can recognize antigens independently of MHC molecules, exhibit innate NK-cell-like reactivities, and possess the ability to act as professional antigen-presenting cells. Additionally, gd T cells have shown promising antitumor potential and can be engineered for chimeric antigen receptor (CAR) immunotherapy, targeting tumor-associated antigens like GD2. Studies have also indicated that immune checkpoint inhibitors can enhance the antitumor effects of gd T cells by reversing their dysfunctional state in the tumor microenvironment, making them a valuable component of immunotherapeutic interventions. Furthermore, gd T cells provide a platform for allogeneic cell therapies, offering a potential solution to the challenges of ex vivo expansion and donor variability in adoptive cell therapy.
What is neuroendocrine transformation of epithelial cancers?
5 answers
Neuroendocrine transformation (NET) refers to the process where epithelial cancers, such as non-small cell lung cancer (NSCLC) and colorectal cancer, acquire neuroendocrine characteristics. This transformation involves the development of neuroendocrine components in the tumor, leading to changes in histology and behavior. In NSCLC, NET can occur as a resistance mechanism to targeted therapies like EGFR/ALK tyrosine kinase inhibitors. Similarly, in colorectal cancer, histological transformation to large cell neuroendocrine carcinoma has been observed during antiangiogenesis and anti-PD-1 combination therapy, impacting treatment response and overall survival. Understanding and identifying NET is crucial for predicting disease course, treatment responses, and patient outcomes in various epithelial cancers. Monitoring dynamic changes in tumor markers and conducting sequential tumor biopsies are essential for detecting such transformations.
What is MAGIC syndrome?
4 answers
MAGIC syndrome, short for Mouth and Genital Ulcer with Inflamed Cartilage syndrome, is a rare autoinflammatory disorder that combines features of Behcet's disease (BD) and relapsing polychondritis (RP). It presents with clinical manifestations such as oral aphthae, uveitis, polyarthritis, and chondritis, resembling both BD and RP. The syndrome's pathogenesis remains unclear, with debates on whether it is a distinct entity or a mere association of BD and RP. Some cases have shown a potential link to an increased risk of aortic aneurysms. Management typically involves a combination of medications like colchicine and prednisolone, tailored to the specific symptoms presented by the patient. Further research and accumulation of data are necessary to enhance the understanding and management of MAGIC syndrome.
What are the genetic or race based risk factors for brain metastasis?
4 answers
Genetic risk factors for brain metastasis in lung cancer patients include mutations in driver genes like epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), and rearranged during transfection (RET). Additionally, a novel copy number event centered around the MCL1 gene was identified in 75% of brain metastasis samples, indicating a potential role in promoting metastasis. Race-based risk factors include black race being a risk factor for brain metastasis in small-cell lung carcinoma (SCLC) patients. Furthermore, disparities in medical care, including racial differences in treatment, have been observed, with minorities and economically disadvantaged groups receiving fewer supportive medications following brain metastasis diagnosis compared to non-Hispanic whites. These findings underscore the importance of considering both genetic and racial factors in assessing the risk of brain metastasis in lung cancer patients.
How much cell death occur in lung cancer 3D models after transfection with CD47 siRNA?
5 answers
Transfection with CD47 siRNA in lung cancer 3D models induces significant cell death. Studies have shown that CD47 siRNA effectively suppresses cell proliferation and promotes apoptosis in lung cancer cells, as observed in Hep-2 cells transfected with CD47 siRNA lentiviral plasmid. Furthermore, targeting CD47 in resistant ALK-positive lung cancer cell lines resulted in distinct subpopulations, with the CD47 high subpopulation exhibiting high tumorigenicity and sphere formation ability, while CD47 inhibition reduced sphere formation. Additionally, simultaneous disruption of the CD47-SIRPα axis in refractory NSCLC models led to macrophage-mediated elimination of relapsed tumor cells, enhancing the anti-tumor effect and sensitizing NSCLC to therapy. These findings collectively suggest that CD47 siRNA transfection induces significant cell death in lung cancer 3D models, highlighting its potential as a therapeutic strategy.
What are the current advancements in 3D virtual modeling technology for neuroblastoma surgery?
5 answers
Recent advancements in 3D virtual modeling technology for neuroblastoma surgery include the integration of 3D bioprinting with neuroblastoma spheroid technologies to create in vitro vascular models of neuroblastoma. Additionally, the development of perfused bioreactor-based 3D models using neuroblastoma cell lines and tissue slice-culture has enabled the evaluation of drug responses in a 3D structure, showcasing the potential for preclinical drug testing in neuroblastoma. Moreover, innovative imaging reconstruction techniques like Cinematic Rendering, Volume Rendering, 3D modeling, Virtual Reality, Augmented Reality, and 3D printing are increasingly utilized to plan complex pediatric oncological cases, including neuroblastoma surgeries, offering new insights for surgical planning and therapeutic decisions. These advancements hold promise for enhancing surgical outcomes and treatment strategies for neuroblastoma patients.
Willian H.J norton (2012) and Gregoryet al., 2016 zebrafish
4 answers
William H.J. Norton in 2012 and Gregory et al. in 2016 conducted research involving zebrafish. Norton's study focused on the spontaneous tumor spectrum and frequency in adult zebrafish, identifying specific mutant alleles linked to neuroblastoma-like tumors originating from neural precursors due to the up-regulation of the fibroblast growth factor 8 gene. On the other hand, Gregory et al. investigated the impact of pycr1 gene knockout in zebrafish, leading to progeria-like phenotypes, reduced locomotion activity, aggression, and dysregulated circadian rhythm, providing insights into aging-related behavioral alterations. Both studies highlight the diverse applications of zebrafish as a model organism in understanding various biological processes, from cancer susceptibility to aging-related phenotypes, offering valuable insights into human health and disease mechanisms.
What are the molecular mechanisms underlying TERT promoter methylation in cancer cells?
5 answers
TERT promoter methylation in cancer cells involves complex molecular mechanisms. Studies reveal that TERT promoter methylation patterns differ between wild-type and mutant cancers, impacting gene expression levels. In urothelial carcinomas, TERT promoter mutations and aberrant methylation activate TERT transcription, crucial for telomerase activation in cancer progression. Neuroblastoma shows hypomethylation of the TERT promoter, affecting telomere maintenance mechanisms. Small cell lung cancer studies suggest that abnormal methylation of the hTERT promoter enhances tumor progression and radiotherapy resistance through upregulation of EZH2 expression. Additionally, epigenetic regulation of TERT expression in various cell lines indicates that hypermethylation of promoter sequences in cancer cells leads to transcriptional repression, influencing TERT activation levels.
How does the microenvironment of cancer cells influence the maintenance of TERT promoter hypomethylation?
5 answers
The microenvironment of cancer cells plays a crucial role in influencing the maintenance of TERT promoter hypomethylation. In cancer, TERT promoter methylation status is intricately linked to gene expression regulation. Hypermethylation of TERT promoter alleles is associated with transcriptional repression, leading to the attenuation of TERT activation in cancer cells. Interestingly, in wild-type cancer cell lines, epialleles with hypomethylated proximal and core promoters exhibit active histone marks, while methylated epialleles show repressive histone marks. This differential methylation pattern and histone modifications influence TERT expression levels, highlighting the impact of the tumor microenvironment on epigenetic regulation of TERT in cancer cells. Additionally, DNA methylation alterations can modulate the tumor immune microenvironment, further emphasizing the intricate interplay between epigenetic modifications and cancer progression.
Can CD8a be expressed by non-T cells?
4 answers
CD8A expression is primarily associated with CD8+ cytotoxic T lymphocytes (CTLs). However, studies have shown that CD8A can also be expressed by non-T cells in certain contexts. For example, in anaplastic lymphoma kinase-positive anaplastic large cell lymphoma, non-common subtypes express CD8 more frequently, with CD8 expression being associated with a poorer outcome. This indicates that CD8A can indeed be expressed by non-T cells in specific pathological conditions. While its role as a biomarker for T-cell responses is well-established, the expression of CD8A by non-T cells highlights its potential versatility in different cellular environments and disease states.