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Relevant bibliographies by topics / Tumour repopulation

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Academic literature on the topic 'Tumour repopulation'

Author: Grafiati

Published: 3 June 2025

Last updated: 22 June 2025

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Journal articles on the topic "Tumour repopulation"

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Pang, Lisa Y., Emma A. Hurst, and David J. Argyle. "Cyclooxygenase-2: A Role in Cancer Stem Cell Survival and Repopulation of Cancer Cells during Therapy." Stem Cells International 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/2048731.

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Cyclooxygenase-2 (COX-2) is an inducible form of the enzyme that catalyses the synthesis of prostanoids, including prostaglandin E2 (PGE2), a major mediator of inflammation and angiogenesis. COX-2 is overexpressed in cancer cells and is associated with progressive tumour growth, as well as resistance of cancer cells to conventional chemotherapy and radiotherapy. These therapies are often delivered in multiple doses, which are spaced out to allow the recovery of normal tissues between treatments. However, surviving cancer cells also proliferate during treatment intervals, leading to repopulation of the tumour and limiting the effectiveness of the treatment. Tumour cell repopulation is a major cause of treatment failure. The central dogma is that conventional chemotherapy and radiotherapy selects resistant cancer cells that are able to reinitiate tumour growth. However, there is compelling evidence of an active proliferative response, driven by increased COX-2 expression and downstream PGE2release, which contribute to the repopulation of tumours and poor patient outcome. In this review, we will examine the evidence for a role of COX-2 in cancer stem cell biology and as a mediator of tumour repopulation that can be molecularly targeted to overcome resistance to therapy.

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Marcu, Loredana G., Mikaela Dell’Oro, and Eva Bezak. "Opportunities in Cancer Therapies: Deciphering the Role of Cancer Stem Cells in Tumour Repopulation." International Journal of Molecular Sciences 24, no. 24 (2023): 17258. http://dx.doi.org/10.3390/ijms242417258.

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Tumour repopulation during treatment is a well acknowledged yet still challenging aspect of cancer management. The latest research results show clear evidence towards the existence of cancer stem cells (CSCs) that are responsible for tumour repopulation, dissemination, and distant metastases in most solid cancers. Cancer stem cell quiescence and the loss of asymmetrical division are two powerful mechanisms behind repopulation. Another important aspect in the context of cancer stem cells is cell plasticity, which was shown to be triggered during fractionated radiotherapy, leading to cell dedifferentiation and thus reactivation of stem-like properties. Repopulation during treatment is not limited to radiotherapy, as there is clinical proof for repopulation mechanisms to be activated through other conventional treatment techniques, such as chemotherapy. The dynamic nature of stem-like cancer cells often elicits resistance to treatment by escaping drug-induced cell death. The aims of this scoping review are (1) to describe the main mechanisms used by cancer stem cells to initiate tumour repopulation during therapy; (2) to present clinical evidence for tumour repopulation during radio- and chemotherapy; (3) to illustrate current trends in the identification of CSCs using specific imaging techniques; and (4) to highlight novel technologies that show potential in the eradication of CSCs.

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Harriss-Phillips, W. M., E. Bezak, and E. Yeoh. "The HYP-RT Hypoxic Tumour Radiotherapy Algorithm and Accelerated Repopulation Dose per Fraction Study." Computational and Mathematical Methods in Medicine 2012 (2012): 1–13. http://dx.doi.org/10.1155/2012/363564.

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The HYP-RT model simulates hypoxic tumour growth for head and neck cancer as well as radiotherapy and the effects of accelerated repopulation and reoxygenation. This report outlines algorithm design, parameterisation and the impact of accelerated repopulation on the increase in dose/fraction needed to control the extra cell propagation during accelerated repopulation. Cell kill probabilities are based on Linear Quadratic theory, with oxygenation levels and proliferative capacity influencing cell death. Hypoxia is modelled through oxygen level allocation based on pO2histograms. Accelerated repopulation is modelled by increasing the stem cell symmetrical division probability, while the process of reoxygenation utilises randomised pO2increments to the cell population after each treatment fraction. Propagation of 108tumour cells requires 5–30 minutes. Controlling the extra cell growth induced by accelerated repopulation requires a dose/fraction increase of 0.5–1.0 Gy, in agreement with published reports. The average reoxygenation pO2increment of 3 mmHg per fraction results in full tumour reoxygenation after shrinkage to approximately 1 mm. HYP-RT is a computationally efficient model simulating tumour growth and radiotherapy, incorporating accelerated repopulation and reoxygenation. It may be used to explore cell kill outcomes during radiotherapy while varying key radiobiological and tumour specific parameters, such as the degree of hypoxia.

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Marcu, Loredana, and Eva Bezak. "Modelling of tumour repopulation after chemotherapy." Australasian Physical & Engineering Sciences in Medicine 33, no. 3 (2010): 265–70. http://dx.doi.org/10.1007/s13246-010-0026-4.

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Huang, Huei-Tyng, Michael G. Nix, Douglas H. Brand, et al. "Dose-Response Analysis Describes Particularly Rapid Repopulation of Non-Small Cell Lung Cancer during Concurrent Chemoradiotherapy." Cancers 14, no. 19 (2022): 4869. http://dx.doi.org/10.3390/cancers14194869.

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(1) Purpose: We analysed overall survival (OS) rates following radiotherapy (RT) and chemo-RT of locally-advanced non-small cell lung cancer (LA-NSCLC) to investigate whether tumour repopulation varies with treatment-type, and to further characterise the low α/β ratio found in a previous study. (2) Materials and methods: Our dataset comprised 2-year OS rates for 4866 NSCLC patients (90.5% stage IIIA/B) belonging to 51 cohorts treated with definitive RT, sequential chemo-RT (sCRT) or concurrent chemo-RT (cCRT) given in doses-per-fraction ≤3 Gy over 16–60 days. Progressively more detailed dose-response models were fitted, beginning with a probit model, adding chemotherapy effects and survival-limiting toxicity, and allowing tumour repopulation and α/β to vary with treatment-type and stage. Models were fitted using the maximum-likelihood technique, then assessed via the Akaike information criterion and cross-validation. (3) Results: The most detailed model performed best, with repopulation offsetting 1.47 Gy/day (95% confidence interval, CI: 0.36, 2.57 Gy/day) for cCRT but only 0.30 Gy/day (95% CI: 0.18, 0.47 Gy/day) for RT/sCRT. The overall fitted tumour α/β ratio was 3.0 Gy (95% CI: 1.6, 5.6 Gy). (4) Conclusion: The fitted repopulation rates indicate that cCRT schedule durations should be shortened to the minimum in which prescribed doses can be tolerated. The low α/β ratio suggests hypofractionation should be efficacious.

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Hami, Rihab, Sena Apeke, Pascal Redou, et al. "Predicting the Tumour Response to Radiation by Modelling the Five Rs of Radiotherapy Using PET Images." Journal of Imaging 9, no. 6 (2023): 124. http://dx.doi.org/10.3390/jimaging9060124.

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Despite the intensive use of radiotherapy in clinical practice, its effectiveness depends on several factors. Several studies showed that the tumour response to radiation differs from one patient to another. The non-uniform response of the tumour is mainly caused by multiple interactions between the tumour microenvironment and healthy cells. To understand these interactions, five major biologic concepts called the “5 Rs” have emerged. These concepts include reoxygenation, DNA damage repair, cell cycle redistribution, cellular radiosensitivity and cellular repopulation. In this study, we used a multi-scale model, which included the five Rs of radiotherapy, to predict the effects of radiation on tumour growth. In this model, the oxygen level was varied in both time and space. When radiotherapy was given, the sensitivity of cells depending on their location in the cell cycle was taken in account. This model also considered the repair of cells by giving a different probability of survival after radiation for tumour and normal cells. Here, we developed four fractionation protocol schemes. We used simulated and positron emission tomography (PET) imaging with the hypoxia tracer 18F-flortanidazole (18F-HX4) images as input data of our model. In addition, tumour control probability curves were simulated. The result showed the evolution of tumours and normal cells. The increase in the cell number after radiation was seen in both normal and malignant cells, which proves that repopulation was included in this model. The proposed model predicts the tumour response to radiation and forms the basis for a more patient-specific clinical tool where related biological data will be included.

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Kuznetsov, Maxim, and Andrey Kolobov. "Mathematical modelling for spatial optimization of irradiation during proton radiotherapy with nanosensitizers." Russian Journal of Numerical Analysis and Mathematical Modelling 38, no. 5 (2023): 303–21. http://dx.doi.org/10.1515/rnam-2023-0023.

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Abstract A spatially distributed mathematical model is presented that simulates the growth of a non-invasive tumour undergoing treatment by fractionated proton therapy with the use of non-radioactive tumour-specific nanosensitizers. Nanosensitizers are injected intravenously before each irradiation to increase the locally deposited dose via a chain of reactions with therapeutic protons. Modelling simulations show that the use of nanosensitizers allows increasing treatment efficacy. However, their effect is restricted by the necessity of decreasing the energy deposited in tumour in order to comply to the normal damage restrictions. Normalization of tumour microvasculature that accompanies the treatment, also compromises nanosensitizers effect as it impairs their inflow in tumour. It is shown that spatial optimization of irradiation, with conservation of total dose deposited in tumour, can increase tumour cell damage for each single irradiation. However, eventually it may not lead to the overall increase of treatment efficacy, in terms of minimization of the number of remaining viable tumour cells, due to the influence of tumour cell repopulation between irradiations. It is suggested that an efficient way towards minimization of tumour cell repopulation may be the faster suppression of angiogenesis by eradication of metabolically deprived tumour cells. This method can be efficient even despite the fact that it would also cause the decrease of supply of nanosensitizers into the tumour.

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Kurtova, Antonina V., Jing Xiao, Qianxing Mo, et al. "Blocking PGE2-induced tumour repopulation abrogates bladder cancer chemoresistance." Nature 517, no. 7533 (2014): 209–13. http://dx.doi.org/10.1038/nature14034.

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Tarnawski, Rafal, Krzysztof Skladowski, Andrzej Swienrniak, Andrzej Wygoda, and Anna Mucha. "Repopulation of Tumour Cells during Radiotherapy Is Doubled during Treatment Gaps." Journal of Theoretical Medicine 2, no. 4 (2000): 297–305. http://dx.doi.org/10.1080/10273660008833056.

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The aim of this work is to analyse the proliferation of tumour cells in the treatment gapduring the radiotherapy for head neck cancer.Material and Methods: The clinical material is based on records of head and neck patients treated by radiotherapyalone in our institution. The effect of radiotherapy was assumed to be described by a linearquadratic model. The patient data were fitted directly to the radiobiological model and theparameters were estimated using maximum-likelihood procedures.Results: According to our model results of treatment were significantly correlated with Normalised Total Dose of radiation, the tumour progression (according to TNM), the overall treatment time and the gap duration. The laryngeal cancers had better prognosis then cancers of oroand nasopharynx. When the treatment time is prolonged without treatment interruptions 0.36 Gylday is lost due to the repopulation of tumour cells. During the treatment gap proliferation is faster and 0.67 Gylday is lost.Conclusion: Proliferation of tumour cells is faster during the treatment gap then during the days with irradiation.

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Maciejewski, Boguslaw, and Stanislaw Majewski. "Dose fractionation and tumour repopulation in radiotherapy for bladder cancer." Radiotherapy and Oncology 21, no. 3 (1991): 163–70. http://dx.doi.org/10.1016/0167-8140(91)90033-d.

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Dissertations / Theses on the topic "Tumour repopulation"

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Shirazi, Hosseini Dokht Alireza. "Kinetics, mechanism and modulation of accelerated repopulation in mouse epidermis during daily irradiation." Thesis, Queen Mary, University of London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243323.

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Fung, Andrea. "The Effect of Molecular Targeted Agents used in Combination with Chemotherapy to Inhibit the Repopulation of Tumour Cells and Xenografts." Thesis, 2010. http://hdl.handle.net/1807/26174.

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Chemotherapy is often administered once every three weeks to allow repopulation of essential normal tissues such as the bone marrow. Repopulation of surviving tumour cells can also occur between courses of chemotherapy and can decrease the efficacy of anticancer treatment. This thesis aims to characterize repopulation, to study the effect of targeted cytostatic agents to inhibit repopulation, and to determine the optimal scheduling of chemotherapy and molecular targeted treatment. The distribution of proliferating and apoptotic cells in human squamous cell carcinoma (A431) xenografts was studied following chemotherapy using fluorescence immunohistochemistry. There was an initial decrease in cell proliferation and in the total functional blood vessels, and an increase in apoptosis observed following treatment with paclitaxel chemotherapy. A rebound in cell proliferation occurred approximately 12 days following treatment, which corresponded with a rebound in vascular perfusion. The effect of gefitinib, an epidermal growth factor receptor (EGFR) inhibitor, to inhibit repopulation between courses of chemotherapy was determined using EGFR-overexpressing A431 cells and xenografts. Furthermore, concurrent and sequential schedules of combined chemotherapy and molecular targeted treatment were compared. Gefitinib inhibited the repopulation of A431 cells in culture when administered sequentially between chemotherapy; sequential treatment was more efficacious than concurrent treatment probably because concomitant scheduling rendered quiescent cells less responsive to chemotherapy. However, in vivo studies using chemotherapy in combination with gefitinib or temsirolimus, a mammalian target of rapamycin (mTOR) inhibitor, showed that concurrent scheduling of combined treatment was more effective at delaying regrowth of xenografts than sequential treatment; this was likely due to dominant effects on the tumour microenvironment. The work completed in this thesis has shown that repopulation occurs in A431 xenografts following paclitaxel treatment, and these changes are associated with changes in the tumour vasculature. Repopulation of A431 cells was inhibited by gefitinib administered sequentially with paclitaxel. However, studies in mice showed better inhibitory effects when chemotherapy was given concomitantly with cytostatic agents such as gefitinib or temsirolimus. Our in vivo data highlight the importance of characterizing changes in the tumour microenvironment when determining optimal scheduling of chemotherapy and molecular targeted treatment.

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Vassileva, Vessela. "The effects of sustained and intermittent intraperitoneal paclitaxel chemotherapy on tumour repopulation and response in ovarian cancer /." 2008. http://proquest.umi.com/pqdlink?did=1659961731&sid=7&Fmt=2&clientId=12520&RQT=309&VName=PQD.

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Liu, Hsin-Yi, and 劉欣怡. "Nuclear pyruvate kinase M2 induces tumor repopulation to strive against glucose depletion stress." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/84908354611254268179.

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碩士<br>國立臺灣大學<br>生化科學研究所<br>103<br>The reprogramming of cancer metabolism is recognized as the Warburg effect, which demonstrates that cancer cells rely on aerobic glycolysis for energy generation. However, cancer cells are generally glucose deprived due to rapid proliferation and poor vascularization, hence cancer cells are forced to cope with glucose depletion stress and survive. Previous studies revealed that cancer cells manipulate the Warburg effect, gluconeogenesis pathway, migration ability, ER stress and cancer stem cell phenotypes in response to glucose depletion. Focus on the correlation between cancer stem cells and glucose depletion, it has been reported that the brain tumor initiation cell (BTIC) phenotypes are enhanced during glucose depletion, and BTICs preferentially survive under glucose depletion through enhancing glucose uptake. Nevertheless, some reports have opposite suggestions that glucose starvation causes a rapid depletion of side population (SP) cells, which are stem-like cells within cancer cells. Hence, the role of glucose depletion in affecting cancer stem cells largely remains unclear. Herein, we observed that glucose depletion enhanced the sphere formation ability and up-regulated the expression of cancer stem cell markers like CD133, CD44, EPCAM, NANOG, NOTCH1, OCT4 and SOX2. We confirmed that PKM2 (pyruvate kinase M2), the glycolytic key enzyme, plays an important role in this response. By knockdown PKM2, cancer stemness gene expression and sphere formation ability which were enhanced by glucose depletion were abolished. Recent evidences reveal that PKM2 not only plays a role in glycolysis, but also acts as a protein kinase or transcriptional coactivator in the nucleus. Thus we analyzed the distribution of PKM2 during glucose depletion. By immunofluorescence staining and cell fractionation, we confirmed that glucose depletion induced PKM2 nuclear translocation. Besides, AMPK is a key regulator of energy homeostasis. We dissect that AMPK, which is activated by glucose depletion, interacted with PKM2 and regulated its Tyr105 phosphorylation, resulting in the nuclear translocation of PKM2. In fact, we observed that only a small fraction of cancer cells was nuclear PKM2 accumulated. Thus we proposed that glucose depletion induced PKM2 nuclear translocation and cancer stem cell properties in a small population of cancer cells, which could preferentially survive and lead to cancer repopulation. We certainly found that the sorted CD133 positive subpopulations within cancer cells were nuclear PKM2 enriched, whereas CD133 negative cells were not. Collectively, we demonstrated a new role of nuclear PKM2 on glucose depletion-induced cancer stem cell properties and cancer repopulation, which helps cancer cells to thrive against this metabolic stress.

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Χαλίμου, Ιωάννα. "Symptom documentation and tumor repopulation factors as a basis for treatment modifications in non-small cell lung cancer radiotherapy." Thesis, 2009. http://nemertes.lis.upatras.gr/jspui/handle/10889/2487.

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Recent studies have suggested significant variation in radiotherapy schedules used to treat advanced NSCLC, both between different centres as well as between countries. In this study, treatment methodologies have been explored using management plans proposed by radiation oncologists when given general questions and theoretical case histories for patients with advanced NSCLC. Methods and Materials The survey was conducted by sending a questionnaire to twenty four radiotherapy centres in Europe. The questionnaire was composed of two sections. The first section concerned reasons for starting radiotherapy, parameters that influence the choice of total dose and fractionation for radiotherapy and the kind of equipment that is used. The second section examines five case histories and asked the responders about the management of these five theoretical patients also regarding the radiotherapy techniques proposed and the aim of treatment (radical or palliative). Furthermore, trials comparing different regimens of palliative radiotherapy in patients with NSCLC were compared. Nineteen trials were reviewed. There were important differences in the doses of radiotherapy investigated, the patient characteristics and the outcome measures. Results In the first part responders (70% of the centres) suggested as the most important factors that influence the choice of total dose and fractionation for radiotherapy, distant metastases, performance status of the patient, lung function and size of the primary tumour. The most common reasons for starting the treatment is not only symptom relief, but also cure and prolongation of life. In the second part, more than 95% of the responders replied that they would give radiotherapy in each of these cases. The median total doses proposed where 20Gy/5fractions/1week or 30Gy/10fractions/2weeks for cases A and D (equivalent dose for fractionation 2Gy per fraction=23 and 33Gy) and 60-68Gy/30fractions/6weeks or 68Gy/34fractions/7weeks for cases B, C and E. For case E, 20% of the responders suggested Stereotactic Body Radiotherapy with 63Gy in 3 Fractions. The total dose and number of fractions of radiotherapy could be related to the perceived aims and expectations of treatment e.g. those aiming to extent life would give significantly higher total doses in a larger number of fractions, whereas those aiming to relieve symptoms would give significantly lower total doses. For the review to the literature there is no strong evidence that any regimen gives greater palliation. Higher dose regimens give more acute toxicity, especially oesophagitis. There is evidence for a modest increase in survival (5% at 1 year and 3% at 2 years) in patients with better performance status (PS) given higher dose radiotherapy. Some regimens are associated with an increased risk of radiation myelitis. Conclusions This survey demonstrates a range of treatment strategies for advanced and inoperable NSCLC within Europe. There are a number of factors that influence the perceived aims of treatment and treatment planning. These factors should be taken into account when evaluating the effectiveness of different irradiation techniques, especially in the determination of radiobiological parameters and dose-response relations. The majority of patients should be treated with short courses of palliative radiotherapy, of 1 or 2 fractions. Care should be taken with the dose to the spinal cord. The use of high dose palliative regimens should be considered for and discussed with selected patients with good performance status. More research is needed into reducing the acute toxicity of large fraction regimens and into the role of radical compared to high dose palliative radiotherapy. In the future, large trials comparing different RT regimens may be difficult to set up because of the increasing use of systemic chemotherapy. Trials looking at how best to integrate these two modalities, particularly in good PS patients need to be carried out.<br>Πρόσφατες μελέτες έχουν αναδείξει σημαντική ποικιλία στα ακτινοθεραπευτικά σχήματα που χρησιμοποιούνται στην ακτινοθεραπεία του μη μικροκυτταρικού καρκίνου του πνεύμονα προχωρημένου σταδίου. Στη συγκεκριμένη μελέτη θεραπευτικές μεθοδολογίες έχουν διερευνηθεί χρησιμοποιώντας τεχνικές που προτείνονται από ογκολόγους ακτινοθεραπευτές . Υλικά και Μέθοδοι: Η μελέτη αποτελείται από δυο μέρη. Στο πρώτο ένα ερωτηματολόγιο εστάλη σε είκοσι τέσσερα ακτινοθεραπευτικά κέντρα στην Ευρώπη .Το ερωτηματολόγιο αποτελούνταν από δυο τμήματα. Στο πρώτο ζητούνταν οι λόγοι για τους οποίους γίνεται έναρξη της ακτινοθεραπείας, οι παράμετροι που επηρεάζουν την επιλογή για τη συνολική δόση και τις συνεδρίες για την θεραπεία και τον εξοπλισμό που χρησιμοποιούν. Στο δεύτερο τμήμα παρουσιαστήκαν πέντε θεωρητικά κλινικά περιστατικά και ζητήθηκε η αντιμετώπιση αυτών των θεωρητικών ασθενών. Στο δεύτερο μέρος της μελέτης πραγματοποιήθηκε ανασκόπηση στη βιβλιογραφία και σύγκριση των αποτελεσμάτων κλινικών δοκιμών που έχουν πραγματοποιηθεί στο παρελθόν. Αποτελέσματα: Στο ερωτηματολόγιο απάντησαν το εβδομήντα τοις εκατό των κέντρων στα όποια εστάλη. Στο πρώτο μέρος ως οι πιο σημαντικοί παρόντες που επηρεάζουν την επιλογή της τελικής δόσης και τις συνεδρίες οριστήκαν οι παρουσία απομακρυσμένων μεταστάσεων, η κλινική εικόνα του ασθενούς, η πνευμονική λειτουργία και το μέγεθος του πρωτογενούς όγκου. Οι σημαντικότεροι λόγοι για έναρξη θεραπείας είναι ανακούφιση από τα συμπτώματα καθώς και επιμήκυνση της ζωής. Στο δεύτερο μέρος ενενήντα πέντε τοις εκατό των κέντρων απάντησαν ότι θα πραγματοποιούσαν ακτινοθεραπεία και στους πέντε αυτούς ασθενείς. Η επιλογή της συνολικής δόσης και συνεδρίων επηρεάζεται από την θεώρηση της θεραπείας ως παρηγορική ή θεραπευτική. Τα κέντρα που είχαν στόχο την επιμήκυνση της ζωής έδιναν μεγαλύτερες δόσεις και περισσότερες συνεδρίες εν αντιθέσει με τα κέντρα που είχαν στόχο την υποχώρηση των συμπτωμάτων που έδιναν μικρότερης δόσεις σε λιγότερες συνεδρίες. Στο δεύτερο μέρος υπολογιστήκαν οι σχετικές βιολογικές δραστικότητες από τα δεδομένα της βιβλιογραφίας καθώς και ο παράγοντας πολλαπλασιασμού του όγκου και κατασκευάστηκαν καμπύλες δόσης απόκρισης. Συμπεράσματα: Η μελέτη αποδεικνύει την ύπαρξη ποικιλίας στις τεχνικές που χρησιμοποιούνται στη θεραπεία προχωρημένου και ανεγχείρητου μη μικροκυτταρικού καρκίνου του πνεύμονα. Αυτοί οι παράγοντες πρέπει να συνυπολογίζονται όταν εκτιμάται η αποτελεσματικότητα διαφορετικών ακτινοθεραπευτικών τεχνικών, κυρίως στο προσδιορισμό ακτινολογικών παραμέτρων και σχέσεων δόσης –απόκρισης.

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Books on the topic "Tumour repopulation"

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Speke, Anna Katherine. Repopulation in murine tumours during fractionated irradiation. National Library of Canada = Bibliothèque nationale du Canada, 1993.

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Book chapters on the topic "Tumour repopulation"

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Marcu, Loredana G., Iuliana Toma-Dasu, Alexandru Dasu, and Claes Mercke. "The Mechanisms Behind Tumour Repopulation." In Radiotherapy and Clinical Radiobiology of Head and Neck Cancer. CRC Press, 2018. http://dx.doi.org/10.1201/9781351002004-5.

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Sminia, Peter, Olivier Guipaud, Kristina Viktorsson, et al. "Clinical Radiobiology for Radiation Oncology." In Radiobiology Textbook. Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-18810-7_5.

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AbstractThis chapter is focused on radiobiological aspects at the molecular, cellular, and tissue level which are relevant for the clinical use of ionizing radiation (IR) in cancer therapy. For radiation oncology, it is critical to find a balance, i.e., the therapeutic window, between the probability of tumor control and the probability of side effects caused by radiation injury to the healthy tissues and organs. An overview is given about modern precision radiotherapy (RT) techniques, which allow optimal sparing of healthy tissues. Biological factors determining the width of the therapeutic window are explained. The role of the six typical radiobiological phenomena determining the response of both malignant and normal tissues in the clinic, the 6R’s, which are Reoxygenation, Redistribution, Repopulation, Repair, Radiosensitivity, and Reactivation of the immune system, is discussed. Information is provided on tumor characteristics, for example, tumor type, growth kinetics, hypoxia, aberrant molecular signaling pathways, cancer stem cells and their impact on the response to RT. The role of the tumor microenvironment and microbiota is described and the effects of radiation on the immune system including the abscopal effect phenomenon are outlined. A summary is given on tumor diagnosis, response prediction via biomarkers, genetics, and radiomics, and ways to selectively enhance the RT response in tumors. Furthermore, we describe acute and late normal tissue reactions following exposure to radiation: cellular aspects, tissue kinetics, latency periods, permanent or transient injury, and histopathology. Details are also given on the differential effect on tumor and late responding healthy tissues following fractionated and low dose rate irradiation as well as the effect of whole-body exposure.

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Zips, Daniel. "Influence of Time Factor and Repopulation on Treatment Resistance." In The Impact of Tumor Biology on Cancer Treatment and Multidisciplinary Strategies. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-74386-6_16.

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Davis, Alison J., and Ian F. Tannock. "Tumor Physiology and Resistance to Chemotherapy: Repopulation and Drug Penetration." In Cancer Treatment and Research. Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1173-1_1.

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Dubrovska, Anna, Mechthild Krause, and Michael Baumann. "Biological effect of radiotherapy on cancer cells." In Oxford Textbook of Cancer Biology, edited by Francesco Pezzella, Mahvash Tavassoli, and David J. Kerr. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779452.003.0030.

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Radiation therapy is a mainstay for curative treatment of many types of tumours. The cure rate of radiation therapy depends on its ability to induce non-repairable DNA damage leading to cellular death or loss of proliferative capacity. In addition to clinical factors, efficacy of radiation therapy has been explained by the radiobiological concept of 4R parameters summarized by Rodney Withers in 1975, which include Repair of DNA damage, Repopulation, Redistribution of tumour cells in the cell cycle, and Reoxygenation. This chapter reviews the direct and indirect effects of irradiation on cancer cells, mechanisms of DNA repair and radiation-induced cell death, and also discusses implementation of the cancer stem cell model for the radiobiological concept of tumour radioresistance.

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Ajithkumar, Thankamma. "Principles of radiotherapy." In Radiotherapy Planning. Oxford University PressOxford, 2023. http://dx.doi.org/10.1093/med/9780198722694.003.0001.

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Abstract This chapter discusses the evolution of cancer and the basic principles of treatment. While DNA damage predominates the radiation-induced cell kill, there are other mechanisms which might influence radiation damage. This chapter also discusses types of radiations and their interaction with tissues, and the fundamental principles of radiotherapy. Radiotherapy cannot distinguish between multiplying cancer and normal cells and therefore results in damage of both cells. However, fractionation of radiotherapy governed by the 5Rs (redistribution of cells, reoxygenation, repair of sublethal damage, repopulation and radiosensitivity) is helpful to maximise tumour kill with acceptable normal tissue toxicities. The concepts of tumour control and normal tissue complication probabilities and clinical application of altered fractionations are also included.

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G., Loredana, and Eric Yeoh. "Tumour Repopulation During Treatment for Head and Neck Cancer: Clinical Evidence, Mechanisms and Minimizing Strategies." In Head and Neck Cancer. InTech, 2012. http://dx.doi.org/10.5772/31184.

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"Tumor-Repopulating Cells." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_102375.

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"Tumor-Repopulating Cells." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_6050.

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Hinkenjann, B., O. Heidinger, W. Wagner, R. Pötter, and A. Härle. "Repopulation of Different Xenograft Tumor Lines During Conventional and Accelerated Irradiation." In Immunodeficient Mice in Oncology. S. Karger AG, 1992. http://dx.doi.org/10.1159/000421326.

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Conference papers on the topic "Tumour repopulation"

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Chen, Li, peter Choyke, Robert Clarke, Zaver Bhujwalla, and Yue Wang. "Abstract A10: Unsupervised deconvolution of dynamic imaging reveals intratumor vascular heterogeneity and repopulation dynamics." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-a10.

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Kurtova, Antonina V., Jing Xiao, Qianxing Mo, et al. "Abstract 5470: Blocking wound-induced tumor repopulation between chemotherapy cycles as a novel approach to abrogate chemoresistance." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5470.

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Saggar, Jasdeep K., and Ian F. Tannock. "Abstract 3801A: Reoxygenation and repopulation of hypoxic cells in a solid tumor after chemotherapy: a cause of treatment failure." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3801a.

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Han, Bumsoo, Matthew D. Egberg, Pung-Pung Haung, David J. Swanlund, and John C. Bischof. "Cryoinjury Enhancement of Breast Cancer Cells by Use of a Molecular Adjuvant (TNF-alpha)." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61593.

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Cryoinjury of human breast cancer cells (MCF7) in engineered tissue equivalents and the enhancement of the cryoinjury by use of a molecular adjuvant (tumor necrosis factor alpha, TNF-α) was studied. Tissue equivalents (TEs) were constructed by seeding MCF7 cells in collagen solutions at the concentration of 100,000 cells/ml. After cultured in vitro for 2 days, the TEs were exposed with 100ng/ml TNF-α and cultured for 24 hours, and then underwent a single freeze-thaw cycle by a cryosurgery simulator. With the concentration and duration of TNF-α treatment studied, no apoptotic or necrotic cell death was observed by the administration of TNF-α only. After a freeze/thaw, MCF7 cells within the frozen region of the TEs were significantly injured immediately (i.e. ≤ 20% survival), but gradually repopulated and reached approximately 80% survival in Day3 without TNF-α pre-treatment. MCF7 with TNF-α pre-treatment showed the slight enhancement of immediate injury in the frozen region (i.e. ≤ 10% survival), and the repopulation was significantly inhibited so the viability remained below 40% even in Day 3. These results imply that TNF-α can be a potent adjuvant for cryosurgery.

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Saggar, Jasdeep K., and Ian F. Tannock. "Abstract A51: Chemotherapy rescues hypoxic tumor cells and induces reoxygenation and repopulation - an effect that is inhibited by the hypoxia-activated pro-drug TH-302." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-a51.

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Saggar, Jasdeep K., and Ian F. Tannock. "Abstract 5247: Use of two markers of hypoxia to study migration, re-oxygenation and repopulation of originally hypoxic cells in MCF-7 tumor xenografts following chemotherapy." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5247.

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