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Developments of Health Care: A Brief History of Medicine
Published in P. Mereena Luke, K. R. Dhanya, Didier Rouxel, Nandakumar Kalarikkal, Sabu Thomas, Advanced Studies in Experimental and Clinical Medicine, 2021
P. Mereena Luke, K. R. Dhanya, Tomy Muringayil Joseph, Józef T. Haponiuk, Didier Rouxel, S. Thomas
Targeted therapy another mode of cancer treatment it primarily assisted with is a drug. But it is distinct from traditional chemotherapy [71]. Targeted therapy operates by targeting the particular genes, proteins, or tissue environment of the cancer that contribute to the development and survival of cancer. These genes and proteins are discovered in cancer cells or cancer growth-related cells. Molecularly targeted therapy has enabling cancer cells to be destroyed and stopping the proliferation of tumor while saving healthy cells [72].
Effects of treatment on the thorax
Published in Anju Sahdev, Sarah J. Vinnicombe, Husband & Reznek's Imaging in Oncology, 2020
Dhakshina Moorthy Ganeshan, Herman I Libshitz, Revathy B Iyer
Drug-induced pneumonitis is also an important complication associated with various molecularly targeted therapies such as mammalian target of rapamycin (mTOR) inhibitors, epidermal growth factor receptor (EGFR) inhibitors, anaplastic lymphoma kinase (ALK) inhibitors, and anti-CD-20 monoclonal antibodies (103–106). The incidence and severity of drug-induced pneumonitis varies according to the type of molecularly targeted therapy. For example, mTOR inhibitors such as everolimus and temsirolimus have been reported to cause pneumonitis in 20%–30% of patients, although the incidence of severe pneumonitis is much lower (<2%) (101,107). The incidence of pneumonitis is around 5% for EGFR inhibitors such as gefitinib, erlotinib, and afatinib (108), and 4%–10% for anti-CD 20 monoclonal antibodies such as rituximab (109). CT imaging features of pneumonitis associated with these drugs are similar to those seen with immune checkpoint inhibitors, ranging from AIP/ARDS-like pattern to hypersensitivity pneumonitis patterns. While many patients may respond to corticosteroid therapy, severe pneumonitis (especially that resulting in CT features of diffuse alveolar damage and an AIP-like pattern) may be associated with high morbidity and mortality. Studies have reported fatality rates of 15% in rituximab-induced pneumonitis and 30%–35% with gefitinib- and erlotinib-induced pneumonitis, underlining the significance of this rare, but potentially fatal, complication (108,109).
History and future of IGRT in lung cancer
Published in Jing Cai, Joe Y. Chang, Fang-Fang Yin, Principles and Practice of Image-Guided Radiation Therapy of Lung Cancer, 2017
Image-guided RT (IGRT) is crucial to conformality. It has led to improved RT accuracy and clinical outcomes (1), particularly with the use of positron emission tomography (PET)/CT, four-dimensional (4D)-CT (for evaluating the tumor's location, motion, and anatomy before and during RT), and on-board image-guided adaptive RT. These techniques have enabled us to aim radiation precisely at the target and minimize the dose to surrounding critical structures (1, 2). IGRT makes it is possible to widely implement cutting-edge technologies such as stereotactic ablative RT/stereotactic body RT (SABR/SBRT), intensity-modulated RT (IMRT), volumetric modulated arc therapy (VMAT), and particle therapy in lung cancer, which typically presents as a moving target. Although we are entering a new era of molecular biology and immunology-based personalized medicine, it remains investigated about how to define the optimal RT dose and volume individually based on genomic profiling and how to combine RT with immunotherapy and molecularly targeted therapy in individual patients [3,4]. In this chapter, we review the history of IGRT (Table 2.1), as well as its status and future directions.
The role of autophagy in acute myeloid leukemia development
Published in Expert Review of Anticancer Therapy, 2023
Martyna Bednarczyk, Karolina Kociszewska, Olga Grosicka, Sebastian Grosicki
Nowadays conventional chemotherapy is the base of the clinical treatment of AML. Certain chemotherapeutic agents used in the treatment of AML (e.g. cytarabine and daunorubicin) have been shown to induce autophagy that overcomes cytotoxic stress and counteracts the effects of these drugs. In addition, pharmacological inhibition of autophagy in combination with traditional cytotoxic drugs has helped to overcome drug resistance, improve clinical outcomes, and ameliorate drug toxicity in AML therapy. Autophagy activity is also a cytoprotective adaptation mechanism in leukemia stem cells against cellular stress such as chemotherapy. Activation of autophagy by anti-leukemic drugs promotes cancer cell survival contributing to drug resistance in LSC AML [4,48]. In recent years, molecularly targeted therapy has been becoming more and more popular. Treatment of AML involves small molecule agents targeting altered proteins or signaling pathways, for example FLT3 (fms related receptor tyrosine kinase 3), IDH (isocitrate dehydrogenase) and BCL2 (BCL2 apoptosis regulator). Treatment failures due to limited clinical response and acquired resistance have limited the development and use of molecularly targeted agents. However, there are increasing reports that autophagy plays a key role in the development of AML and the response to targeted therapies, suggesting that regulation of autophagy may enhance the therapeutic benefits of AML treatment [6,85,86]. Bortezomib-induced autophagy has been demonstrated in some types of cancer, including AML [87].
Tackling metastatic triple-negative breast cancer with sacituzumab govitecan
Published in Expert Review of Anticancer Therapy, 2021
Anna R Schreiber, Michelle Andress, Jennifer R Diamond
Molecular subtypes of TNBC, represent another potential for targeted therapy. From gene analyses, it has been found that distinct subtypes of TNBC can predict cytotoxic susceptibility as well as prognosis [14]. As an example, mesenchymal (M) subtypes of TNBC were found to have some sensitivity to phosphatidylinositol-3 kinase/mechanistic target of rapamycin (PI3K/mTOR) inhibitors and basal-like-1 (BL1) subtypes of TNBC were found to be sensitive to genotoxic agents. In addition, BL1, immunomodulatory (IM), mesenchymal stem-like (MSL) subtypes, had nearly double median OS and disease-free survival (DFS) when compared to basal-like-2 (BL2), luminal androgen receptor (LAR), and M subtypes [14]. The unique biology associated with each subtype, offers another option for molecularly targeted therapy.
Gene fusions in vascular tumors and their underlying molecular mechanisms
Published in Expert Review of Molecular Diagnostics, 2021
Sheena L. M. Ong, Karoly Szuhai, Judith V.M.G. Bovée
The identification of gene fusions has not only improved the classification and diagnosis of vascular tumors, it also sheds light on the underlying molecular mechanisms involved in tumorigenesis. By exploring these molecular pathways, leads can be found to develop molecularly targeted therapy. Since some of these vascular tumors, despite their intermediate biologic behavior, can be very difficult to treat there is an urgent need to develop novel therapeutic strategies [61]. Functional studies are however hampered by the lack of model systems, as no cell lines or animal models are available. However, novel technologies like CRISPR-Cas9 can be used to create gene fusions in induced pluripotent stem cells which allows studying the effect of the specific gene fusion in an isogenic background and the identification of therapeutic vulnerabilities [62]. For instance, the inhibition of PI3K and MAPK signaling was identified as a therapeutic option in PHE [62], and indeed case reports describe the usability of mTOR and multi-tyrosine kinase inhibitor [58–61].