Splicing DNA Damage Adaptations for the Management of Cancer Cells
Copyright© Bentham Science Publishers; For any queries, please email at epubbenthamscience.net..
Maintaining a tumour cell's resistance to apoptosis (organized cell death) is essential for cancer to metastasize. Signal molecules play a critical function in the tightly regulated apoptotic process. Apoptosis may be triggered by a wide variety of cellular stresses, including DNA damage, but its ultimate goal is always the same: the removal of damaged cells that might otherwise develop into tumours. Many chemotherapy drugs rely on cancer cells being able to undergo apoptosis as a means of killing them. The mechanisms by which DNA-damaging agents trigger apoptosis, the interplay between pro- and apoptosis-inducing signals, and the potential for alteration of these pathways in cancer are the primary topics of this review.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2024 |
|---|---|
| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:24 |
|---|---|
| Enthalten in: |
Current gene therapy - 24(2024), 2 vom: 17., Seite 135-146 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Singh, Arun Kumar [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Apoptosis |
|---|
| Anmerkungen: |
Date Completed 30.01.2024 Date Revised 30.01.2024 published: Print Citation Status MEDLINE |
|---|
| doi: |
10.2174/0115665232258528231018113410 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM367728567 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM367728567 | ||
| 003 | DE-627 | ||
| 005 | 20240130232213.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 240129s2024 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.2174/0115665232258528231018113410 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1275.xml |
| 035 | |a (DE-627)NLM367728567 | ||
| 035 | |a (NLM)38282448 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Singh, Arun Kumar |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Splicing DNA Damage Adaptations for the Management of Cancer Cells |
| 264 | 1 | |c 2024 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 30.01.2024 | ||
| 500 | |a Date Revised 30.01.2024 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright© Bentham Science Publishers; For any queries, please email at epubbenthamscience.net. | ||
| 520 | |a Maintaining a tumour cell's resistance to apoptosis (organized cell death) is essential for cancer to metastasize. Signal molecules play a critical function in the tightly regulated apoptotic process. Apoptosis may be triggered by a wide variety of cellular stresses, including DNA damage, but its ultimate goal is always the same: the removal of damaged cells that might otherwise develop into tumours. Many chemotherapy drugs rely on cancer cells being able to undergo apoptosis as a means of killing them. The mechanisms by which DNA-damaging agents trigger apoptosis, the interplay between pro- and apoptosis-inducing signals, and the potential for alteration of these pathways in cancer are the primary topics of this review | ||
| 650 | 4 | |a Review | |
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Apoptosis | |
| 650 | 4 | |a DNA damage | |
| 650 | 4 | |a cancer | |
| 650 | 4 | |a extrinsic pathway | |
| 650 | 4 | |a genetic therapy. | |
| 650 | 4 | |a p38 signaling | |
| 700 | 1 | |a Yadav, Deepika |e verfasserin |4 aut | |
| 700 | 1 | |a Malviya, Rishabha |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Current gene therapy |d 2001 |g 24(2024), 2 vom: 17., Seite 135-146 |w (DE-627)NLM119780747 |x 1875-5631 |7 nnns |
| 773 | 1 | 8 | |g volume:24 |g year:2024 |g number:2 |g day:17 |g pages:135-146 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.2174/0115665232258528231018113410 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 24 |j 2024 |e 2 |b 17 |h 135-146 | ||