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Draft:Cancer relapse

From Wikipedia, the free encyclopedia

Cancer relapse is a condition that occurs when a cancer patient experiences recurrence of cancer after a previous treatment succeeded in eradicating detectable malignant disease.[1][2][3][4]

In a variety of cancer types relapse poses a substantial obstacle to therapy, and often brings a poor prognosis; relapse may be accompanied by a metastasis, which is the appearance of malignant tumor that is related to the primary tumor, in a different organ of the patient's body.[5][6][7] Relapse may occur even after a patient has received hematopoietic cell transplantation.[8]

Causes

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Cancer recurrence (relapse) is ascribed to malignant cells that evade therapy. Small numbers of cancer cells may remain undetected, and dormant, pausing their proliferation for long time.[9][10] In fact, the effects of therapy that kills most cancer cells, may cause a few of them to pause proliferation instead of dying.[11] While the precise mechanism of growth arrest is not entirely clear and may not be uniform across cancer cases, malignant cells that survive chemotherapy make several metabolic adaptations and possess altered configuration of key positions of their chromatin, the material that packages their DNA. This has as result that certain conditions can trigger expression of genes that reignite cancer cell growth, causing proliferation, and additionally these conditions may trigger aberrant expression of genes that cause changes in the host tissue, which help cancer growth.[12]

References

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  1. ^ Gong, J; Salgia, R (Jun 2018). "Managing Patients With Relapsed Small-Cell Lung Cancer". J Oncol Pract. 14 (6): 359–366. doi:10.1200/JOP.18.00204. PMC 6002253. PMID 29894664.
  2. ^ Smid, M; el, al (1 May 2008). "Subtypes of breast cancer show preferential site of relapse". Cancer Res. 68 (9): 3108–14. doi:10.1158/0008-5472.CAN-07-5644. PMID 18451135.
  3. ^ Sun, Y; el, al (21 Jan 2021). "Single-cell landscape of the ecosystem in early-relapse hepatocellular carcinoma". Cell. 184 (2): 404–421.e16. doi:10.1016/j.cell.2020.11.041. PMC 3756368. PMID 33357445.
  4. ^ Egan, G; Tasian, SK (1 Sep 2023). "Relapsed pediatric acute myeloid leukaemia: state-of-the-art in 2023". Haematologica. 108 (9): 2275–2288. doi:10.3324/haematol.2022.281106. PMC 10483345. PMID 36861399.
  5. ^ Kast, K; el, al (Apr 2015). "Impact of breast cancer subtypes and patterns of metastasis on outcome". Breast Cancer Res Treat. 150 (3): 621–9. doi:10.1007/s10549-015-3341-3. PMID 25783184.
  6. ^ Huang, X; el, al (22 Aug 2024). "Protocol for a systematic review and meta-analysis of recurrence and metastasis of different surgical techniques for non-small cell lung cancer". BMJ Open. 14 (8): e086503. doi:10.1136/bmjopen-2024-086503. PMID 39179278.
  7. ^ Amansyah, F; el, al (2024). "The relationship of changes in molecular subtypes with metastases and progression-free survival in breast cancer". Breast Dis. 43 (1): 71–78. doi:10.3233/BD-249000. PMC 11091556. PMID 38669518.
  8. ^ Dimitriou, M; Mortera-Blanco, T; et, al (14 Mar 2024). "Identification and surveillance of rare relapse-initiating stem cells during complete remission after transplantation". Blood. 143 (11): 953–966. doi:10.1182/blood.2024025371. PMC 10950475. PMID 38096358.
  9. ^ Truskowski, K; et, al (Mar 2023). "Dormant cancer cells: programmed quiescence, senescence, or both?". Cancer Metastasis Rev. 42 (1): 37–47. doi:10.1007/s10555-022-10073-z. PMC 10014758. PMID 36598661.
  10. ^ Tamamouna, V; et, al (11 Nov 2022). "Regulation of Metastatic Tumor Dormancy and Emerging Opportunities for Therapeutic Intervention". Int J Mol Sci. 23 (22): 13931. doi:10.3390/ijms232213931. PMC 9698240. PMID 36430404.
  11. ^ Aleksandrova, KV; et, al (28 Feb 2024). "mTOR pathway occupies a central role in the emergence of latent cancer cells". Cell Death Dis. 15 (2): 176. doi:10.1038/s41419-024-06547-3. PMC 10902345. PMID 38418814.
  12. ^ Vlahopoulos, SA (2024). "Divergent Processing of Cell Stress Signals as the Basis of Cancer Progression: Licensing NFκB on Chromatin". International Journal of Molecular Sciences. 25 (16): 8621. doi:10.3390/ijms25168621. PMID 39201306.