Search or ask a question

What are tofacitinib target in lung?

PI3K/AKT/mTOR pathway

Median follow-up

Progression-free survival

Best insight from top research papers

Tofacitinib targets were not mentioned in any of the provided abstracts.

Answers from top 4 papers

PDF

Open Access

More filters

Papers (4)	Insight
Open access•Journal Article•DOI Alectinib in RET-rearranged non-small cell lung cancer-Another progress in precision medicine? Robert Pirker, Martin Filipits - Show less +1 more 20 Apr 2015-Translational lung cancer research 10 Citations	The provided paper is about alectinib as a potential therapeutic option for RET fusion-positive non-small cell lung cancer. It does not mention anything about tofacitinib or its targets in the lung.
Open access•Journal Article [Gefitinib target treatment in non-small cell lung cancer]. Yi-Long Wu, Jin-Ji Yang, Jiaying Lin, Yujuan Huang, Ri-Qiang Liao, Yi-Sheng Huang, Qing Zhou, Chong-Rui Xu, Zhen Wang - Show less +8 more 01 Feb 2007-Chinese Journal of Tuberculosis and Respiratory Diseases 8 Citations	The provided paper is about Gefitinib target treatment in non-small cell lung cancer. It does not mention anything about tofacitinib or its targets in the lung.
Open access•Journal Article•DOI Mammalian Target of Rapamycin: A Target for (Lung) Diseases and Aging Brian K. Kennedy, Juniper K. Pennypacker - Show less +1 more 22 Dec 2016-Annals of the American Thoracic Society 15 Citations	The provided paper does not mention tofacitinib or its targets in the lung. The paper discusses the involvement of the mammalian target of rapamycin (mTOR) signaling pathway in lung diseases and aging.
Open access•Journal Article•DOI Target therapy of gefitinib in advanced adenocarcinoma of the lung Hua Zheng, Jingping Wang, Qiyi Meng, Zan Liu, Baolan Li, Yunzhong Zhu - Show less +5 more 20 Jun 2007-Chinese Journal of Lung Cancer 1 Citations	The provided paper is about the target therapy of gefitinib in advanced adenocarcinoma of the lung. It does not mention anything about tofacitinib or its targets in the lung.

My columns

Related Questions

Is pembrolizumab effective for lung cancer?4 answersPembrolizumab has shown effectiveness in the treatment of lung cancer. It is a humanized monoclonal antibody that targets the PD-1/PD-L1 pathway in T cells, and it has been used in combination with chemotherapy or as monotherapy. Studies have shown that pembrolizumab, when used in combination with chemotherapy, significantly improves event-free survival, major pathological response, and pathological complete response in patients with resectable, early-stage non-small cell lung cancer (NSCLC). In patients with advanced or metastatic NSCLC, pembrolizumab-based therapy has been found to improve overall survival and progression-free survival compared to chemotherapy alone. Additionally, pembrolizumab has been found to be similar to sintilimab in terms of efficacy and safety for the first-line treatment of advanced squamous lung cancer. However, it is important to note that the efficacy of pembrolizumab may be influenced by certain factors such as age, sex, smoking history, and PD-L1 expression status.

What are the most promising treatment for lung cancer?4 answersNovel treatment strategies for lung cancer include combination therapies with programmed death ligand 1 inhibitors, targeting alternative immune checkpoints, and the use of novel immunomodulatory therapies. The microbiome plays a role in the initiation and progression of lung cancer, and understanding its relationship with clinical characteristics can contribute to treatment management. Inhibitors of Aurora kinases, such as Aurora-A and Aurora B, show potential in targeted therapies for lung cancer. Multiple therapeutic options are available for the management of nonsmall cell lung cancer (NSCLC), including chemotherapy, immunotherapy, targeted therapy, and combination therapy. Immunotherapy, particularly immune checkpoint inhibitors, has shown positive responses in NSCLC patients. Targeted therapies that focus on specific oncogenic drivers, such as EGFR and ALK gene mutations, are being investigated. Combination therapies, such as radiotherapy combined with immunotherapy, have shown improved survival outcomes for lung cancer patients.

How effective is tofacitinib in treating psoriasis?4 answersTofacitinib has shown effectiveness in treating psoriasis, particularly in cases that are refractory or have not responded well to conventional treatments. It has been used successfully in patients who have exhausted other treatment options, including biologicals, and have experienced no side effects with tofacitinib.Additionally, a topical formulation of tofacitinib has been developed for the treatment of nail psoriasis, with preliminary data suggesting its potential use in this condition.In a study assessing the improvement in quality of life in patients with moderate-to-severe psoriasis, tofacitinib demonstrated a significant improvement in disease severity and symptoms after 12 weeks of therapy.Real-life data from patients with psoriatic arthritis treated with tofacitinib also showed that it is well tolerated and leads to a significant reduction in inflammatory markers.Furthermore, tofacitinib has been used effectively to treat psoriasiform dermatitis caused by IL-17 inhibitors.

Is Tofacitinib associated with nephrotic syndrome?5 answersTofacitinib has been associated with nephrotic-range proteinuria and acute worsening of renal function in a 75-year-old female patient.

In the ever-evolving field of TB therapeutics, what novel molecular targets emerge as promising candidates for future exploration?4 answersNovel molecular targets that emerge as promising candidates for future exploration in TB therapeutics include multitargeting compounds against Mycobacterium tuberculosis (Mtb) survival pathways, promiscuous compounds from natural products or repurposed drugs, gene targets for rapid molecular drug susceptibility assays, and previously discarded compounds and programs from the "golden age of antibiotics". Additionally, the aspartate metabolism pathway in M. tuberculosis has shown potential as a target for drug development, as it is essential for the bacteria's survival and absent in humans. These targets offer opportunities for the development of new therapeutic regimens and host-directed therapies to combat drug-resistant TB.

What are the most innovative targets in lung cancer?5 answersThe most innovative targets in lung cancer include mutations in genes such as EGFR, ALK, ROS1, BRAF, MET, RET, NTRK, KRAS, PIK3CA, and HER2, as well as immune checkpoints CTLA-4 and PD-1/PD-L1. Long non-coding RNAs (LncRNAs) have also emerged as potential targets, with their dysregulation playing a role in lung cancer development and therapy resistance. Additionally, Myc amplification and overexpression have been associated with lung cancer progression and therapeutic resistance, making it a promising target for inhibition. These innovative targets offer opportunities for personalized therapies and immunotherapy in lung cancer treatment.

See what other people are reading

How to measure PI3K/AKt activity?

To measure PI3K/Akt activity, various methods have been proposed in the literature. One approach involves utilizing a genetically-encoded fluorescent kinase translocation reporter to visualize and quantify Akt activity in live cells over time. Another method suggests using specific antibodies conjugated with quantum dots to assess the phosphorylation states of proteins in the AKT signaling pathway, particularly in colorectal cancer patients with PTEN loss. Additionally, a test has been developed to provide a quantitative PI3K pathway activity score based on measuring FOXO transcription factor target gene mRNA levels, offering a way to predict drug response and resistance to targeted therapies. Furthermore, a multiplex immunoassay has been described to quantitate isoform-specific phosphorylation of proteins in the PI3K/AKT pathway, allowing for the assessment of pharmacodynamic changes in response to targeted agents.Can FOXO1 suppress NFkB signaling?

Yes, FOXO1 can suppress NF-κB signaling. Research indicates that FOXO1 activation inhibits NF-κB in various contexts. In gastric cancer, FOXO1 was found to be a negative upstream regulator of NF-κB, with overexpression of FOXO1 suppressing NF-κB activation. Additionally, in a study on bone marrow-derived mesenchymal stem cells, it was shown that FOXO1 plays a role in defending against oxidative damage, and its decline due to estrogen deficiency led to NF-κB activation, contributing to oxidative damage and stem cell dysfunction. Furthermore, FOXO1 agonists were found to promote osteogenesis by inhibiting NF-κB activation under inflammatory conditions, suggesting a protective effect on bone formation by modulating multiple signaling pathways. These findings collectively support the notion that FOXO1 can indeed suppress NF-κB signaling in different biological contexts.What is the incidence of squamous cell carcinoma of the pancreas?

The incidence of primary squamous cell carcinoma (SCC) of the pancreas is rare, ranging from 0.5% to 5% of all pancreatic malignancies. This form of pancreatic cancer is particularly challenging due to its scarcity and lack of well-understood diagnostic and treatment protocols. Primary SCC of the pancreas is typically diagnosed after excluding other primary sources of the tumor and confirming the absence of a glandular component. The prognosis for patients with SCC of the pancreas is generally poor, with a median overall survival time ranging from 6 to 12 months and a 5-year survival rate estimated at around 10%. Surgical resection is considered the only potentially curative treatment for SCC of the pancreas, emphasizing the importance of early diagnosis and intervention.What is the current understanding of the molecular mechanisms linking osteosarcopenia and cellular senescence?

Current research suggests that cellular senescence plays a crucial role in the development of osteosarcopenia, a condition characterized by the simultaneous loss of bone and muscle mass. Senescent cells, which accumulate with age, contribute to disrupted tissue homeostasis and inflammation, leading to age-related diseases like osteosarcopenia. Mechanisms such as the TRIM21/HSP90/CHIP axis have been identified to regulate senescence in osteosarcoma cells, impacting the expression of senescence markers like p21. Additionally, targeting senescent cells through autophagy and senotherapies has shown promise in alleviating stem cell dysfunction and improving bone and muscle formation in chronic diseases like osteosarcopenia. Understanding these molecular pathways could lead to novel therapeutic strategies for managing osteosarcopenia by targeting cellular senescence mechanisms.What is the role of PI3K delta in the development and progression of cholangiocarcinoma?

PI3K delta plays a crucial role in the development and progression of cholangiocarcinoma (CCA). Univariate and multivariate analyses have identified PI3K delta as a significant factor associated with survival in CCA patients, indicating its importance in the disease process. Additionally, Supplementary Figures S1-S18 provide further insights into the mechanisms through which PI3K delta influences CCA progression, potentially highlighting its potential as a therapeutic target. Understanding the impact of PI3K delta on CCA pathogenesis is essential for developing targeted therapies that can effectively intervene in the disease's progression and improve patient outcomes.What is the long-term survival for Grade II/III oligodendriglioma?

The long-term survival for Grade II/III oligodendroglioma varies based on treatment strategies. Studies show that patients with oligodendroglioma can have a favorable clinical outcome, with survival ranging between 10 and 20 years, especially for those with anaplastic oligodendroglioma (AO). Surgical resection plays a crucial role in improving overall survival, with an extent of resection above 50% being necessary for better outcomes. Additionally, complete surgical resection and stable lesions before pregnancy have been associated with longer post-pregnancy survival in female patients with Grade II glioma. Furthermore, greater extent of resection is linked to improved survival in both low-grade and anaplastic oligodendroglioma subgroups. These findings support the importance of tailored treatment approaches in enhancing long-term survival for patients with Grade II/III oligodendroglioma.What casein are people using in atpase assays with clp protein?

Researchers are utilizing casein as a substrate in ATPase assays with Clp proteins. Clp proteins, such as ClpA and ClpP, form complexes like ClpAP that degrade proteins in an ATP-dependent manner. These complexes interact with casein, a model substrate, to study the order of events during substrate binding, unfolding, and degradation. The oligomeric state of the ClpAP complex remains stable during multiple catalytic cycles, allowing for the turnover of multiple casein molecules before significant dissociation occurs. Mutations in the ATP binding sites of ClpA affect the rates of dissociation of ClpA and ClpAP complexes, highlighting the importance of ATP binding in stabilizing the oligomeric state and influencing the dynamics of interaction with substrates.What is the mechanism of action of ATRA in treatment of Leukemia?

The mechanism of action of All-trans retinoic acid (ATRA) in treating leukemia involves inducing differentiation and apoptosis in leukemia cells. ATRA suppresses global translation and protein synthesis in acute myeloid leukemia (AML) cells, requiring translational regulatory functions for cell growth arrest and differentiation induction. In non-APL AML, sensitizing cells to ATRA can be achieved by combining it with enzastaurin, which enhances ATRA-induced differentiation by modulating protein levels of key transcription factors. Additionally, combining ATRA with agents that inhibit DNA methyltransferase, such as 5-azacytidine, improves its activity against AML by targeting epigenetic changes blocking differentiation. These findings highlight the diverse pathways through which ATRA exerts its therapeutic effects in different subtypes of leukemia.What's the significance of Type.1.phosphatidylinositol.4.5.bisphosphate.4.phosphatase in endolysosomes within the context of AD amyloid pathology.?

Type 1 phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) plays a crucial role in Alzheimer's disease (AD) amyloid pathology by modulating amyloid-β (Aβ) production. PI(4,5)P2 is generated by phosphatidylinositol 4-phosphate 5-kinases (PIP5Ks) and influences membrane composition. Alterations in PI(4,5)P2 levels impact Aβ production, with overexpression of PIP5K1A leading to reduced Aβ secretion. Additionally, PI(4,5)P2's presence in endomembranes influences the distribution of endosomes and lysosomes, affecting cellular processes. The intricate functions of PI(4,5)P2 in membrane dynamics, signaling, and protein recruitment underscore its significance in AD pathology, highlighting a potential therapeutic target for modulating Aβ production and potentially ameliorating AD progression.What's the role of PDK1 in alzheimer's?

PDK1 plays a crucial role in Alzheimer's disease (AD) by influencing neuropathological features, genetics, Aβ aggregation, Tau protein hyperphosphorylation, neuroinflammation, and aging in the AD brain. Inhibition of PDK1 in neurons has been shown to affect AD-like pathology in animal models, indicating its significance in the disease's progression. Studies have demonstrated that early inhibition of PDK1 can effectively prevent AD-like neuropathology, reducing plaque pathology and gliosis in AD mouse models. Additionally, the activation of PDK1 through molecules like PS48 has shown promising results in improving insulin signaling, mitigating Aβ peptide toxicity, and enhancing synaptic plasticity in AD models, suggesting a potential therapeutic target for AD treatment.What is the major mechanism for mechanotransduction in bone?

The major mechanism for mechanotransduction in bone involves the activation of connexin 43 (Cx43) hemichannels through a unique pathway that includes integrin molecules, particularly integrin α5 and αV, in osteocytes. Osteocytes, being the primary cells involved in force adaptation due to mechanical stimulation, play a crucial role in sensing and responding to mechanical cues in bone tissue. Alterations in lacunar-canalicular (LC) structure can affect fluid flow patterns and impact osteocytes' ability to sense and translate mechanical signals, thus influencing bone remodeling processes. Additionally, osteocytes sense mechanical loading through various sensing proteins, transducing these signals into different signaling molecules that initiate biochemical responses, ultimately regulating bone remodeling and adaptation. Understanding these complex mechanotransduction pathways in osteocytes is essential for developing strategies for bone tissue regeneration and potential therapeutic interventions for conditions like osteoporosis.