Factors and molecular mechanisms of radiation resistance in cancer cells

Alamilla-Presuel, Juan; Burgos-Molina, Antonio Manuel; González-Vidal, Alejandro; Portero, F. Sendra; Ruiz-Gómez, Miguel J

doi:10.1080/09553002.2022.2047825

Cited by 23 publications

(13 citation statements)

References 79 publications

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“…The dose-dependent increase in AHH-1 radioresistance further suggests the inactivation of p53 in AHH-1 cells. The increased cellular radioresistance can be attributed to a number of factors, one of which is apoptosis resistance [ 49 ]. Cancer cells with mutant p53 have been shown to evade apoptosis via the expression of anti-apoptotic genes within the BCL family, and the suppression of pro-apoptotic genes BAX, PUMA (BBC3) and NOXA (PMAIP1) [ 42 , 48 , 50 ].…”

Section: Discussionmentioning

confidence: 99%

“…Apoptosis resistance also has been attributed to expression of microRNAs. such as miR-34a in head and neck cancer [ 51 ], or the expression of activating transcription factor 3 (ATF3) in breast cancer cell lines [ 49 ]. Improved DNA repair capacity also increases the cellular radioresistance, as shown in lung cancer extracellular signal-regulated kinase 5 (ERK5), also known as MAPK7, which improved DNA repair via the homologous recombination repair pathway via the activation of Chk1 [ 52 ].…”

Section: Discussionmentioning

confidence: 99%

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Cell Type-Specific Patterns in the Accumulation of DNA Damage Following Multifractional Radiation Exposure

Akuwudike

Tartas

López-Riego

et al. 2022

IJMS

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Predicting the risk of second malignant neoplasms is complicated by uncertainties regarding the shape of the dose–response relationship at high doses. Limited understanding of the competitive relationship between cell killing and the accumulation of DNA lesions at high doses, as well as the effects of other modulatory factors unique to radiation exposure during radiotherapy, such as dose heterogeneity across normal tissue and dose fractionation, contribute to these uncertainties. The aim of this study was to analyze the impact of fractionated irradiations on two cell systems, focusing on the endpoints relevant for cancer induction. To simulate the heterogeneous dose distribution across normal tissue during radiotherapy, exponentially growing VH10 fibroblasts and AHH-1 lymphoblasts were irradiated with 9 and 12 fractions (VH10) and 10 fractions (AHH-1) at 0.25, 0.5, 1, or 2 Gy per fraction. The effects on cell growth, cell survival, radiosensitivity and the accumulation of residual DNA damage lesions were analyzed as functions of dose per fraction and the total absorbed dose. Residual γH2AX foci and other DNA damage markers (micronuclei, nuclear buds, and giant nuclei) were accumulated at high doses in both cell types, but in a cell type-dependent manner. The competitive relationship between cell killing and the accumulation of carcinogenic DNA damage following multifractional radiation exposure is cell type-specific.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cell Type-Specific Patterns in the Accumulation of DNA Damage Following Multifractional Radiation Exposure

Akuwudike

Tartas

López-Riego

et al. 2022

IJMS

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“…Previous cancer treatment could be a marker of radioresistance and/or rapid repopulation, which would explain lower LC. 19 …”

Section: Discussionmentioning

confidence: 99%

Interval From Simulation Imaging to Treatment Delivery in SABR of Lung Lesions: How Long is Too Long for the Lung?

Gilles

Selma²,

Jansen³

et al. 2023

Advances in Radiation Oncology

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“…Radiation therapy (RT) is considered as a standard in the treatment of most of solid tumors ( 97 ). Radioresistance is a key factor for RT failure, and development of locoregional relapse and distant metastases are the major obstacles for the success of the treatment ( 98 – 101 ). The involvement of TME in radioresistance was demonstrated in several studies ( 102 , 103 ).…”

Section: Effects Of Treatment On Circulating Monocytesmentioning

confidence: 99%

Monocyte programming by cancer therapy

et al. 2022

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Monocytes in peripheral blood circulation are the precursor of essential cells that control tumor progression, that include tumor-associated macrophages (TAMs), dendritic cells (DCs) and myeloid-derive suppressor cells (MDSC). Monocytes-derived cells orchestrate immune reactions in tumor microenvironment that control disease outcome and efficiency of cancer therapy. Four major types of anti-cancer therapy, surgery, radiotherapy, chemotherapy, and most recent immunotherapy, affect tumor-associated macrophage (TAM) polarization and functions. TAMs can also decrease the efficiency of therapy in a tumor-specific way. Monocytes is a major source of TAMs, and are recruited to tumor mass from the blood circulation. However, the mechanisms of monocyte programming in circulation by different therapeutic onsets are only emerging. In our review, we present the state-of-the art about the effects of anti-cancer therapy on monocyte progenitors and their dedifferentiation, on the content of monocyte subpopulations and their transcriptional programs in the circulation, on their recruitment into tumor mass and their potential to give origin for TAMs in tumor-specific microenvironment. We have also summarized very limited available knowledge about genetics that can affect monocyte interaction with cancer therapy, and highlighted the perspectives for the therapeutic targeting of circulating monocytes in cancer patients. We summarized the knowledge about the mediators that affect monocytes fate in all four types of therapies, and we highlighted the perspectives for targeting monocytes to develop combined and minimally invasive anti-cancer therapeutic approaches.

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Factors and molecular mechanisms of radiation resistance in cancer cells

Cited by 23 publications

References 79 publications

Cell Type-Specific Patterns in the Accumulation of DNA Damage Following Multifractional Radiation Exposure

Cell Type-Specific Patterns in the Accumulation of DNA Damage Following Multifractional Radiation Exposure

Interval From Simulation Imaging to Treatment Delivery in SABR of Lung Lesions: How Long is Too Long for the Lung?

Monocyte programming by cancer therapy

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