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Prof Greaves says one implication of the research is that therapies need to be developed which target the trunk of the tumour and that current targeted therapies being researched may not tackle advanced cancers.
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Subsequent bispecifics have been developed which target both EGFR and the apoptosis regulating protein bcl-2.
In recent years, different molecules have been developed which target this pathway at various steps.
Recently, novel pharmacological and genetic therapeutic strategies were developed which target abnormal intracellular Ca2+ cycling in HF and arrhythmias [ 5, 13, 22].
Highly efficient medicaments have already been developed which target cancer driving oncogene mutations in a number of defined human malignancies (Verweij et al., 2008).
Many novel therapeutics have been developed which aim to target this process by acting as either angiogenesis inhibitors (e.g. by blocking the action of vascular endothelial growth factor) or as vascular disrupting agents, which target the extracellular matrix [2],[3].
Based on these epigenetic changes, drugs against different types of tumors were developed, which mainly target epimutations in the genome.
Methylation profiles are altered in many diseases, most notably cancer (Das and Singal, 2004; Sharma et al., 2010), and as such epigenetic therapies are being developed, which specifically target methylation (Yang et al., 2010).
For the diagnosis of human brucellosis, a PCR assay with one pair of primers was developed, which amplifies the target genomic sequence of Brucella species.
Furthermore, a mathematical model was developed which does the targeting and design simultaneously.
Indeed, several such agents have been developed, which include inhibitors targeting prosurvival Bcl-2 family members including Bcl-2, Bcl-xL, and Mcl-1.
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