Splicing variants are generated owing to alternative splicing based on the interactions between trans-acting splicing regulators (ESRP1, ESRP2, SF3B1, SRSF1, SRSF2, SRSF3 and others) and cis-acting nucleotide sequences (intronic splicing enhancers, intronic splicing silencers, exonic splicing enhancers and exonic splicing silencers). Splicing variants are also generated owing to transcription from alternative first exons based on alternative promoters. Splicing variants regulate various aspects of cancer biology, including angiogenesis, drug resistance, epithelia-mesenchymal transition, immune evasion, proliferation and survival.
Treatments targeting splicing variants are largely classified into (i) small-molecule compounds targeting splicing regulators, (ii) antisense oligonucleotides (ASOs) targeting splice site mutations or interfaces between pre-mRNAs and splicing regulators, and (iii) monoclonal antibodies (mAbs), antibody–drug conjugates (ADCs), bispecific antibodies (bsAbs), trispecific antibodies (tsAbs), chimeric antigen receptor (CAR) T and CAR natural killer (NK) cells targeting tumor-specific splicing isoforms.
The aim of this Research Topic is to gather a collection of manuscripts exploring the different aspects of splicing variant-targeted therapeutics mentioned above. We welcome submissions of original research, reviews, mini-reviews, methods, perspectives, community case studies, conceptual analysis, data reports, policy briefs, brief research reports, general commentaries, and opinions.
Keywords:
Splicing Variants, FGFR2b, CLDN18.2, SF3B1, SRSF2
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Splicing variants are generated owing to alternative splicing based on the interactions between trans-acting splicing regulators (ESRP1, ESRP2, SF3B1, SRSF1, SRSF2, SRSF3 and others) and cis-acting nucleotide sequences (intronic splicing enhancers, intronic splicing silencers, exonic splicing enhancers and exonic splicing silencers). Splicing variants are also generated owing to transcription from alternative first exons based on alternative promoters. Splicing variants regulate various aspects of cancer biology, including angiogenesis, drug resistance, epithelia-mesenchymal transition, immune evasion, proliferation and survival.
Treatments targeting splicing variants are largely classified into (i) small-molecule compounds targeting splicing regulators, (ii) antisense oligonucleotides (ASOs) targeting splice site mutations or interfaces between pre-mRNAs and splicing regulators, and (iii) monoclonal antibodies (mAbs), antibody–drug conjugates (ADCs), bispecific antibodies (bsAbs), trispecific antibodies (tsAbs), chimeric antigen receptor (CAR) T and CAR natural killer (NK) cells targeting tumor-specific splicing isoforms.
The aim of this Research Topic is to gather a collection of manuscripts exploring the different aspects of splicing variant-targeted therapeutics mentioned above. We welcome submissions of original research, reviews, mini-reviews, methods, perspectives, community case studies, conceptual analysis, data reports, policy briefs, brief research reports, general commentaries, and opinions.
Keywords:
Splicing Variants, FGFR2b, CLDN18.2, SF3B1, SRSF2
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.