scispace - formally typeset
Search or ask a question

Is CD96 a target for ADC therapeutics against AML? 

Best insight from top research papers

CD96 is a potential target for antibody-drug conjugate (ADC) therapeutics against acute myeloid leukemia (AML) . CD96 expression is significantly higher in AML patients compared to controls . It is associated with higher blast percentages and poor therapy outcome . CD96 deletion in T cells enhances their killing of leukemia cells in vitro . T cells engineered with a CAR containing CD96 endodomain are less effective in suppressing tumor growth compared to CAR-T cells without CD96 endodomain . CD96 is also a reliable diagnostic marker for AML, especially AML in children, and could be used as a prognostic marker for treatment response . CD96-specific monoclonal antibodies may selectively eliminate CD96+ AML leukemic stem cells, providing a promising therapeutic approach . These findings suggest that CD96 could be a target for ADC therapeutics against AML, potentially revitalizing autologous hematopoietic progenitor cell transplantation .

Answers from top 5 papers

More filters
Papers (5)Insight
CD96 is a potential target for monoclonal antibody therapy against AML, but there is no mention of it being a target for ADC therapeutics in the provided paper.
CD96 may represent a promising target for antibody-based therapeutic strategies against AML-LSCs, but further studies are necessary to clarify its role in the pathophysiology of AML.
CD96 is not mentioned as a target for ADC therapeutics against AML in the provided paper.
CD96 is not mentioned in the paper as a target for ADC therapeutics against AML.
CD96 is mentioned as a potential targetable marker for the future development of therapeutic armamentarium for AML, but there is no specific mention of CD96 as a target for ADC therapeutics against AML in the provided paper.

Related Questions

How does ALB6 interact with CD9 and cause conformational change?5 answersALB6, an anti-CD9 monoclonal antibody, interacts with CD9 to induce various cellular responses. ALB6 has been shown to inhibit cell proliferation, reduce viability, and induce apoptosis through the activation of JNK/SAPK, p38 MAPK, and caspase-3 signaling pathways. Additionally, ALB6 treatment in human gastric cancer cell xenografts resulted in tumor suppression through antiproliferative, proapoptotic, and antiangiogenetic effects. Furthermore, ALB6 can induce eosinophil degranulation when immobilized, while in soluble form, it enhances eosinophil survival by stimulating autocrine production of GM-CSF. Interestingly, ALB6 has been found to cause a conformational change in CD9, leading to increased fibrin clot retractile activity in normal human fibroblasts. These findings collectively demonstrate the diverse effects of ALB6 on CD9 and its role in modulating cellular functions.
Does anti-CD9 antibody ALB6 block protein-protein interactions?5 answersThe anti-CD9 antibody ALB6 has been shown to have various effects on cellular activities. ALB6 treatment inhibits tumor progression in human gastric cancer cells by suppressing proliferation, inducing apoptosis, and reducing angiogenesis. Additionally, ALB6 inhibits cell proliferation, reduces viability, and induces apoptosis in human cancer cell lines by activating specific signaling pathways. Furthermore, ALB6 enhances heterotypic adhesion of pre-B cells to bone marrow stromal fibroblasts, suggesting a role in regulating cell adhesion. Moreover, ALB6 induces homotypic aggregation of CD9-positive pre-B lymphoblastoid cell lines, indicating its involvement in cell-cell adhesion mechanisms. Therefore, while ALB6 affects various cellular functions, there is no direct evidence from the provided contexts to suggest that it specifically blocks protein-protein interactions.
What are the therapies for IDH mutated AML?5 answersTherapies for IDH mutated AML include targeted inhibitors of mutant IDH enzymes, combination therapies, and the exploration of novel therapeutic strategies. Targeted inhibitors such as ivosidenib and enasidenib have been developed to suppress the production of the oncometabolite R-2-hydroxyglutarate (R-2-HG) and induce differentiation of leukemic blasts. However, the low response rate and the development of resistance to IDHmut inhibitors are major clinical challenges. Combination therapies incorporating targeted or cytotoxic therapies with IDH inhibitors have shown promise in patients with IDH-mutated AML. Additionally, synthetic lethal interactions and synergetic therapies are being investigated as potential strategies to enhance tumor sensitivity, reduce drug-related side effects, and overcome drug resistance in IDH-mutated cancers. These findings highlight the need for more effective approaches to treat IDH-mutant AML and the ongoing research in this field.
What are the toxic effects of Aav9?5 answersAAV9 gene therapy has been shown to induce toxic effects in various studies. Long-term overexpression of survival motor neuron (SMN) protein through AAV9 gene therapy can lead to motor dysfunction, loss of proprioceptive synapses, and neurodegeneration. Additionally, high doses of short hairpin RNA-expressing AAV9 (shRNA-AAV9) can result in toxicity, including microRNA oversaturation and liver failure. AAV9 vectors produced with recombinant baculovirus (rBac) system have been found to be fully functional in vivo and in vitro, but their tropism and gene transfer efficiency can vary depending on the promoter used. Furthermore, AAV9 has the potential to transduce antigen-presenting cells (APC) in the brain, leading to an immune response and brain pathology, especially when expressing non-self proteins. These findings highlight the importance of considering the potential toxic effects of AAV9 gene therapy and the need for further research to ensure its safety.
What is the role of CD9 in lymphatic endothelial cells?5 answersCD9 plays a role in lymphatic endothelial cells (LECs) as a putative unconventional antigen presenting cell. LECs have been shown to directly present tumor-derived antigens to tumor-specific CD8+ T cells, leading to their deletion. When MHCII expression is abrogated in LECs, tumor growth is reduced and effector T cell functions are enhanced, suggesting that tumor-associated LECs function as tolerogenic antigen-presenting cells. CD9 is involved in the communication between cancer cells and their microenvironment via exosomes, which are small membrane-bound vesicles released by cells. CD9 is important for the formation of tetraspanin-enriched microdomains (TEMs) on the surface of exosomes, which are thought to be important for the sorting and packaging of specific molecules into exosomes. CD9 expression is consistent with an early protective role against tumorigenesis, but in melanoma, it has a specific function in vascular dissemination during late tumor progression, particularly in lymphatic and endothelial vessels. CD9 could be a valid prognostic factor for lymph node metastasis risk in melanoma. CD9 is upregulated in senescent endothelial cells and is involved in cellular senescence and the pathogenesis of atherosclerosis. CD9 ablation decreases atherosclerotic lesions in mice, suggesting that CD9 is a novel target for prevention and treatment of vascular aging and atherosclerosis.
What's the relationship between CD99 and src family kinase?5 answersCD99 is a transmembrane protein that interacts with src family kinases. The CD99 splice variant increases the invasive ability and motility of breast cancer cells through src kinase-mediated signaling pathways. CD99 also interacts with growth and differentiation factor 6 (GDF6), a member of the bone morphogenetic protein (BMP) family, to regulate cancer cell proliferation. The prodomain of GDF6 binds to CD99, leading to the recruitment of CSK (C-terminal Src kinase) and inhibition of Src activity. CD99 engagement activates multiple mitogen-activated protein kinases (MAPKs), including ERK, JNK, and p38 MAPK, in T lymphocytes. These findings suggest that CD99 plays a role in regulating the activity of src family kinases and their downstream signaling pathways in cancer cells and lymphocytes.

See what other people are reading

Effects of the TSP-1 binding to ITGB1?
4 answers
Thrombospondin-1 (TSP-1) binding to integrin β1 (ITGB1) has significant implications in various cancers. TSP-1, known for its role in angiogenesis regulation, binds to angiogenesis-stimulating factors like VEGF to inhibit angiogenesis. On the other hand, ITGB1 plays a crucial role in cancer progression and radioresistance. Studies show that ITGB1 can induce epithelial-mesenchymal transition (EMT) and affect DNA repair mechanisms, leading to radioresistance in non-small cell lung cancer (NSCLC) cells. Additionally, ITGB1 overexpression promotes chondrogenic differentiation in adipose-derived mesenchymal stem cells (ADSCs) through the activation of the ERK signaling pathway. Therefore, the interaction between TSP-1 and ITGB1 may modulate angiogenesis, cancer progression, and treatment responses, highlighting their potential as therapeutic targets in various malignancies.
What is the role of her2 as a therapeutic biomarker?
4 answers
HER2 serves as a crucial therapeutic biomarker in various cancers, including breast, gastric, and colorectal cancers. Its amplification, overexpression, or mutation plays a significant role in tumorigenesis. In colorectal cancer, HER2 amplification occurs in 1-4% of cases, leading to the efficacy of HER2-targeted therapies like pertuzumab plus trastuzumab. Assessing HER2 heterogeneity aids in predicting responsiveness to HER2-directed therapy, emphasizing the importance of accurate HER2 status evaluation. Studies show that HER2 positivity is associated with worse prognosis in colorectal cancer and predicts unresponsiveness to anti-EGFR therapy. Recent trials, like DESTINY-Breast04, highlight the significance of HER2 as a therapeutic target, even in HER2-low metastatic breast cancer, showcasing the evolving landscape of HER2-targeted therapies and the potential of HER2 PET imaging for treatment decisions.
What are the common in vitro tests used to study the function and behavior of astrocytes?
4 answers
In vitro studies commonly utilize immunocytochemical evaluation and genetic manipulation techniques to investigate astrocyte function and behavior. Immunocytochemical analysis involves labeling astrocytes with markers like GFAP, GLAST, GLT-1, GS, ALDH1L1, and SOX9 to quantify cell populations. Additionally, genetic manipulation with siRNA can be employed to study astrocyte metabolism and pro-inflammatory responses. These studies can also involve exposing astrocytes to different radiation qualities like X-rays, carbon ions, and iron ions to assess DNA damage, repair mechanisms, and gene expression changes. Furthermore, oxygen consumption analysis can be conducted to evaluate astrocyte metabolic function. By combining these techniques, researchers can gain insights into the intricate functions and responses of astrocytes in controlled laboratory settings.
How is CD36 phosphorylated by PKC?
5 answers
CD36 phosphorylation by PKC involves intricate mechanisms. PKCα phosphorylates CD36 on Thr92, leading to the inhibition of thrombospondin-1 binding. This phosphorylation occurs intracellularly, requiring new protein synthesis and Golgi trafficking, as shown by studies using PMA, a PKC activator. Additionally, CD36 phosphorylation status affects its interactions with different ligands. Dephosphorylation of constitutively phosphorylated CD36 enhances thrombospondin binding, while PKC-mediated phosphorylation reduces thrombospondin binding and increases collagen binding. Furthermore, in the context of fatty acid uptake, FAs trigger caveolae-dependent CD36 internalization, activating downstream kinases like LYN, which phosphorylates DHHC5, ultimately regulating FA uptake by CD36. These findings collectively highlight the complex regulatory role of PKC in modulating CD36 phosphorylation and its functional consequences.
How effective are stem cell therapies in treating collapsed trachea in dogs, and what are the potential side effects?
5 answers
Stem cell therapies, specifically Stem cells from human exfoliated deciduous teeth (SHED), have shown promise in treating tracheal fistulas in rats, accelerating fistula healing and reducing lung inflammation. In dogs with collapsing trachea, endoluminal stent placement has provided a high survival rate, even for severe cases, with improvements in clinical signs like dyspnea and raspy breathing. Tracheal and airway collapse in dogs can lead to chronic cough and airway obstruction, with bronchomalacia being common in older dogs, necessitating correct identification and appropriate medical or surgical intervention. Potential side effects of endoluminal stent placement in dogs include complications like stent fracture and tissue ingrowth, which may require additional procedures.
How effective are KRAS G12C inhibitors in treating non-small cell lung cancer?
5 answers
KRAS G12C inhibitors show promise in treating non-small cell lung cancer (NSCLC). Sotorasib, a specific small molecule inhibitor of KRAS G12C, has gained approval for treating advanced KRAS G12C-mutated NSCLC. However, resistance to treatment remains a concern, necessitating the exploration of new inhibitors and treatment strategies. Combining KRAS G12C inhibitors with eIF4A inhibitors has shown enhanced efficacy in inducing tumor regression in NSCLCs, particularly through effects on BCL-2 family proteins. Additionally, coalterations in KEAP1, SMARCA4, and CDKN2A have been identified as determinants of inferior outcomes with KRAS G12C inhibitors, suggesting the need for patient stratification for personalized treatment approaches. These findings underscore the potential of KRAS G12C inhibitors in NSCLC treatment but also highlight the importance of refining treatment strategies to overcome resistance and improve patient outcomes.
How does cancer develop in the brain?
4 answers
Cancer develops in the brain through various mechanisms involving genetic alterations, cellular heterogeneity, and molecular dysregulations. Brain tumors like glioblastomas and medulloblastomas arise from different neural cell types, each with distinct genetic profiles and pathways. These tumors invade normal brain tissue, utilizing mechanisms such as enzymatic digestion of the extracellular matrix and altering their shape to accommodate growth. Additionally, brain metastases, common in adults, originate from primary tumors like lung, breast, and melanoma, with poorly understood molecular mechanisms driving their spread to the brain. Neural stem cells and stem-like cancer cells play crucial roles in brain tumor initiation and progression, sharing signaling pathways that offer insights into brain tumorigenesis. Understanding these diverse processes is essential for developing targeted therapies and improving patient outcomes.
What is the role of the ACACB gene in human metabolism?
4 answers
The ACACB gene plays a crucial role in human metabolism, particularly in fatty acid metabolism and insulin sensitivity. Research indicates that ACACB is associated with cetuximab resistance in colorectal cancer, affecting fatty acid metabolism and leading to decreased drug sensitivity. Additionally, ACACB variants are linked to gene expression regulation in adipose tissues, influencing insulin sensitivity in African American and European American adults. Furthermore, ACACB has been found to be expressed in developing human fetal kidneys, suggesting a role in nephrogenesis and differentiation of renal structures. Overall, ACACB's involvement in lipid metabolism, gene regulation, insulin sensitivity, and tissue development highlights its significance in human metabolic processes.
What are research articles that show bone marrow rejuvenation has beneficial effects for multiple organs?
5 answers
Research articles have demonstrated the beneficial effects of bone marrow rejuvenation on multiple organs. Studies have shown that bone marrow cell therapy induces ductular reactions in the liver, promoting liver growth without tissue injury. Additionally, bone marrow transplantation has been found to attenuate mesangial sclerosis in the kidneys, with wild-type bone marrow transplantation leading to decreased albuminuria and increased survival in mice. Furthermore, rejuvenation of bone marrow from young animals has been shown to enhance the response to ischemic injury, improving microvasculature density and reducing brain damage in aged rats. Reconstitution of aged mice with young bone marrow cells, particularly the Sca-1+ subset, has been linked to improved cardiac tissue regeneration after injury, involving the activation of specific pathways. These studies collectively highlight the diverse beneficial effects of bone marrow rejuvenation on various organs.
What are research articles that show aged bone marrow rejuvenation has beneficial effects for multiple organs?
5 answers
Research articles have demonstrated that rejuvenating aged bone marrow can have beneficial effects on multiple organs. Alibhai and Li's study showed that transplanting young bone marrow stem cells into aged recipients improved tissue repair responses in the heart, skeletal muscle, brain, and retina. Eroglu et al. found that photobiomodulation therapy effectively reversed aging in mouse bone marrow mesenchymal stem cells, enhancing their regenerative potential. Guo et al. highlighted that platelet-rich plasma rejuvenated aged human bone marrow stem cells, leading to improved outcomes in treating ischemic heart disease. Li et al. proposed using triboelectric stimulation to rejuvenate senescent bone marrow mesenchymal stromal cells, enhancing their proliferation and differentiation capacity. Lastly, Li et al. showed that reconstituting old mice with young bone marrow cells improved cardiac tissue regeneration, emphasizing the role of specific stem cell subsets in rejuvenating aged organs.
What are some existing cancer cell imaging and how relevant is bioimaging?
5 answers
Various cancer cell imaging techniques are crucial for cancer research and treatment. Bioimaging methods like fluorescence microscopy, MRI, CT scans, and PET play significant roles in understanding cancer complexity, characteristics, and treatment responses. These techniques aid in early detection, staging, prognosis, therapy planning, and monitoring treatment responses in cancer patients. Molecular imaging (MI) and molecular targeted radiotherapy (MTR) are rapidly evolving, offering quantitative detection of cancer-related molecular targets and delivering focused radiation to cancer cells. Additionally, medical imaging helps in detecting cancer stem cells (CSCs), which are critical for tumor development and recurrence, contributing to the design of new therapeutic strategies. Overall, bioimaging is essential for advancing cancer research, diagnosis, and treatment efficacy.