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Tips on passing the exam
Published in Aalia Khan, Ramsey Jabbour, Almas Rehman, nMRCGP Applied Knowledge Test Study Guide, 2021
Aalia Khan, Ramsey Jabbour, Almas Rehman
Start preparing in good time. We think that 3 months’ preparation is more than adequate for the AKT. Begin by making a note of challenging consultations, either those that you did not feel confident about or those in which you had to look things up. This is a good method of identifying areas of weakness.
Cognition Enhancers
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Ramneek Kaur, Rashi Rajput, Sachin Kumar, Harleen Kaur, R. Rachana, Manisha Singh
Even though the synthesis of BDNF is controlled by PKC, the actions of TrkB receptors and BDNF receptors seem to depend on ERK/Ras, phospholipase Cγ (PLCγ), and phosphatidylinositol-3 kinase (PI3K)/Akt pathways (Xia et al., 2010; Leal et al., 2014). Akt (also called protein kinase B) is a kinase which is concerned in a range of inhibiting pathways related to apoptosis. Environmental enrichment increases BDNF, number of dendritic spines, and Akt levels thereby, enhancing neurogenesis and cognition (Ramirez-Rodriguez et al., 2014).
Spinal Physiology Recovery or Russian Alternative to Chinese Acupuncture
Published in Anne George, Snigdha S. Babu, M. P. Ajithkumar, Sabu Thomas, Holistic Healthcare. Volume 2: Possibilities and Challenges, 2019
When Bekhterev’s disease is early diagnosed, with the use of AKT (the patient is 16), it is possible to receive regress of the disorder. Adult patients can stop the disease and prevent its development, at that, creatinine remains on normal parameters. Regular use of AKT helps to improve essentially the quality of life of the patients, which is unobtainable with other treatment methods including drug treatment.
Transcription factors TP63 facilitates malignant progression of thyroid cancer by upregulating KRT17 expression and inducing epithelial-mesenchymal transition
Published in Growth Factors, 2023
AKT is a serine/threonine protein kinase that appears in biological control such as cell survival, invasion, proliferation, glucose metabolism, and apoptosis (Revathidevi and Munirajan 2019). Many studies have confirmed that the AKT signaling pathway is involved in tumor invasion and metastasis (Shariati and Meric-Bernstam 2019). As reported, KRT17 activates AKT signaling and induces EMT in esophageal squamous cell carcinoma (Liu et al. 2020). Silenced KRT17 represses cell proliferation in osteosarcoma via constraining the AKT/mTOR/HIF1α signaling pathway (Yan et al. 2020). In gastric cancer, silencing KRT17 represses gastric cancer cells’ malignant progression via inhibiting the AKT/mTOR signaling pathway (Chivu-Economescu et al. 2017). In summary, AKT signaling pathway regulated by KRT17 was crucial in cancer development and progression. EMT is where cells acquire intercellular properties like enhanced motility and lose epithelial properties like cell polarity (Hao et al. 2019). EMT plays a crucial role in cancer cell invasion and migration, and AKT can induce EMT (Larue and Bellacosa 2005; Yan et al. 2009). Here, we confirmed through molecular experiments that KRT17 facilitated the EMT process of TC cells via regulating the AKT signaling pathway, consistent with the results of present publications. Further rescue experiments confirmed that TP63 promoted KRT17 level to initiate AKT signaling pathway and induced EMT to push the malignant progression of TC cells.
Gnetum montanum extract induces apoptosis by inhibiting the activation of AKT in SW480 human colon cancer cells
Published in Pharmaceutical Biology, 2022
Xianglong Pan, Xiaotao Hou, Fan Zhang, Peiling Tang, Wanruo Wan, Zixia Su, Yeguo Yang, Wei Wei, Zhengcai Du, Jiagang Deng, Erwei Hao
AKT is an important regulator of several cellular functions such as cell growth, apoptosis, and survival (Shin et al. 2017; Zeng et al. 2019). Overexpression of AKT has been found to associate with various human malignancies. Thus, inhibiting the AKT pathway could be an effective way to prevent and treat malignancies (Debatin 2004). In the present study, the inhibition of AKT activation is potentially one of the underlying mechanisms of GME in inducing apoptosis in the SW480 human colon cancer cells. Further, GME is derived from a natural plant which possesses multi-target and multi-channel regulatory effects. This is a preliminary study to explore the regulation of AKT signalling pathway by GME. Further study to determine the mechanism of antitumor action of GME is needed for detailed pharmacodynamic study in the future.
The landscape of systemic therapy for early stage triple-negative breast cancer
Published in Expert Opinion on Pharmacotherapy, 2022
Jin-Yu Lu, Alvaro Alvarez Soto, Jesus D Anampa
PI3K/AKT pathway activation is associated with tumor evolution and resistance to chemotherapy. Dysregulation of the PI3K/AKT signaling pathway occurs in about 25% of primary TNBC, and it is even more common in metastatic TNBC [61]. Two phase 2 trials, the LOTUS [62] and PAKT [63] trial, evaluated paclitaxel in combination with AKT inhibitors ipatasertib and capivasertib, respectively, in advanced/metastatic TNBC. Addition of AKT inhibitor to first-line paclitaxel in treating metastatic TNBC significantly increased PFS in both trials and OS in PAKT trial [62,63]. The efficacy of AKT inhibitors was subsequently tested in phase 3 trials. The IPATunity130 trial (NCT03337724) [64] randomized patients with metastatic TNBC and mutations in the PI3K/AKT signaling pathway to receive first-line paclitaxel with or without ipatasertib. The study showed no significant improvement in PFS. Analysis of OS and correlative biomarkers is ongoing [65]. Capivasertib, in combination with taxane, is currently being tested in CAPItello-290 (NCT03997123), pending future report [66]. These results reflect the challenges in targeting the P13k/AKT pathway in TNBC. AKT pathway inhibition was also assessed in early breast cancer by the phase 2 I-SPY team. Addition of the pan-AKT inhibitor MK-2206 to NACT in TNBC (NCT01042379) was associated with an increase in the estimated pCR rate (22.2% vs. 39.8%) [67].