Cancers: Radiation-Resistant https://greenmedinfo.com/taxonomy/term/72131/all en "Stem cells: their role in breast cancer development and resistance to treatment." https://greenmedinfo.com/article/stem-cells-their-role-breast-cancer-development-and-resistance-treatment PMID:  Curr Pharm Biotechnol. 2011 Feb 1 ;12(2):196-205. PMID: 21044007 Abstract Title:  Stem cells: their role in breast cancer development and resistance to treatment. Abstract:  About 20% of the total cells from primary breast tumors could generate palpable tumors in non-obese diabetic severe combined immunodeficient (NOD/SCID) immunocompromised mice. All the tumorigenic cells originate from a normal mammary stem cell. Human mammary stem cells are sensitive to oncogenic mutations and in mouse models they share similarities with breast cancer stem cells (BrCSCs). Tumorigenicity, invasion, progression and metastasization are further BrCSCs properties likely depending on their CD44+/CD24- phenotype. Local invasion and tumor metastasization seem to be facilitated by the epithelial to mesenchymal transition (EMT) program. This program may be reactivated from stable genetic alterations or through exposure of cancer cells to factors present in the surrounding micro-environment, or by an up-regulation of EMT-inducing transcription factors. One main explanation for resistance to treatment by cancer cells is that a rare subpopulation of cells in residual tumors with tumorigenic potential is intrinsically resistant to therapy. Consistent with this hypothesis, in human breast tumors, the subpopulation of tumor-initiating cancer cells with CD44(high)/CD24(low) cell surface-marker profile was found more resistant to cancer therapies (chemo, hormone and radiotherapy) than is the major population of more differentiated breast cancer cells. The reasons for CSC resistance to chemotherapy, hormone therapy and radiotherapy also have been examined and they opened new scenarios for cancer therapy. https://greenmedinfo.com/article/stem-cells-their-role-breast-cancer-development-and-resistance-treatment#comments Breast Cancer Breast Cancer Stem Cells Cancers: Drug Resistant Cancers: Radiation-Resistant Review Tue, 17 Jul 2012 17:41:03 +0000 greenmedinfo 78643 at https://greenmedinfo.com 2-Methoxyestradiol, an endogenous estrogen metabolite, sensitizes radioresistant breast cancer cells through multiple mechanisms. https://greenmedinfo.com/article/2-methoxyestradiol-endogenous-estrogen-metabolite-sensitizes-radioresistant-br PMID:  Int J Radiat Oncol Biol Phys. 2011 May 1 ;80(1):231-9. Epub 2011 Mar 9. PMID: 21392897 Abstract Title:  2-Methoxyestradiol, an endogenous estrogen metabolite, sensitizes radioresistant MCF-7/FIR breast cancer cells through multiple mechanisms. Abstract:  PURPOSE: The requirement for a well-tolerated and highly effective radiosensitizer that preferentially sensitizes tumor cells at multiple levels of radioresistance remains largely unmet. 2-Methoxyestradiol (2ME) has polypharmacological profiles that target multiple signaling pathways involved in the development of radioresistance. In the current study, we investigated the radiosensitizing effect of 2ME on the radioresistant breast cancer MCF-7/FIR cell line and explored the underlying mechanisms. METHODS AND MATERIALS: The radiosensitizing effect of 2ME was evaluated on the basis of cell death and clonogenic survival. Formation of reactive oxygen species (ROS), apoptosis, and cell cycle progression were assessed by flow cytometry. Radiation-induced DNA damage was evaluated on the basis of histoneγ-H2AX phosphorylation and foci formation. Immunoblotting was used to assess the effects of γ radiation and/or 2ME on radioresistance pathways. RESULTS: Our data demonstrate that MCF-7/FIR cells expressed higher levels of Bcl-2 and HIF-1α and displayed a lower ROS phenotype than the parental MCF-7 cells. Treatment of parental MCF-7 cells with 2ME (0.5 μM) had minimal effect on γ radiation-induced cell proliferation and surviving fractions. On the contrary, in MCF-7/FIR cells, treatment with 2ME significantly enhanced γ radiation-induced reduction in cell proliferation and surviving fraction. This combination was effective in activating apoptosis, arresting the cell cycle at the G(2)/M phase, and increasing the level of γ radiation-induced ROS and the number of γ-H2AX foci. In addition, 2ME significantly ameliorated γ radiation-induced expression of the HIF-1α transcription factor and its downstream targets AKT/mTOR. CONCLUSION: 2ME preferentially sensitizes radioresistant MCF-7/FIR cells toγ radiation by targeting multiple signaling pathways involved in the development of radioresistance. This polypharmacological profile qualifies 2ME as a promising radiosensitizer in the treatment of radioresistant breast cancer cells and warrants systematic preclinical and clinical studies. https://greenmedinfo.com/article/2-methoxyestradiol-endogenous-estrogen-metabolite-sensitizes-radioresistant-br#comments 2-Methoxyestradiol Breast Cancer Breast Cancer: Conventional Treatment Cancers: Radiation-Resistant DNA damage Radiation Induced Illness Antiproliferative Apoptotic Bcl-2 protein down-regulation Cell cycle arrest Radiosensitizer In Vitro Study Tue, 17 Jul 2012 17:55:35 +0000 greenmedinfo 78647 at https://greenmedinfo.com An antioxidant-rich extract of seaweed polyphenols combined with current PC treatment modalities may inhibit tumor relapse by targeting therapy-orchestrated autophagy in residual cells. https://greenmedinfo.com/article/antioxidant-rich-extract-seaweed-polyphenols-combined-current-pc-treatment-mod PMID:  J Biomed Sci. 2015 ;22(1):28. Epub 2015 Apr 17. PMID: 25898131 Abstract Title:  Novel adjuvants from seaweed impede autophagy signaling in therapy-resistant residual pancreatic cancer. Abstract:  BACKGROUND: Identifying the drug-deliverables that target autophagy is crucial to finding a cure for pancreatic cancer (PC), as activated autophagy is associated with poor patient outcomes. Our recent studies recognized the anti-PC potential of an antioxidant-rich collection of seaweed polyphenols and identified potential compounds for the treatment of PC. Accordingly, we investigated whether such compounds could regulate autophagy in therapy-resistant PC cells in vitro and in residual PC in vivo.RESULTS: Human Panc-3.27 and MiaPaCa-2 cells were exposed to fractionated irradiation (FIR) with/without ethyl acetate (EA) polyphenol from Spatoglossum asperum (SA-EA), Padina tetrastromatica (PT-EA), or Hormophysa triquerta (HT-EA). The cells were subjected to QPCR to examine transcriptional alterations in the following autophagy functional regulators: ATG3, ATG5, ATG7, ATG12, LC3A, LC3B, Beclin, Myd88, HMGB1, Rage, and TLRs 1-9. Using a clinically relevant mouse model of residual PC, we use tissue microarray (TMA) and immunohistochemistry (IHC) procedures to investigate the potential of polyphenol(s) to target ATG3, ATG5, ATG12, LC3A, LC3B, BECN1, and SURIVIN after clinical radiotherapy. Radiation significantly increased the transcription of autophagy functional regulators in both cell lines. Seaweed polyphenols completely suppressed the transcription of all investigated autophagy regulators in both cell-lines. Gene silencing approach defined the role of LC3B in radiation-induced cell survival in this setting. TMA-IHC analysis revealed the complete regulation of ATG3, ATG5, ATG12, LC3A, LC3B, BECN1, and SURVIVIN in residual PC following SA-EA, PT-EA, and HT-EA treatment.CONCLUSIONS: These data demonstrate the autophagy blue print in therapy-resistant PC cells for the first time. Moreover, the data strongly suggest that the selected polyphenols could serve as effective adjuvants for current PC treatment modalities and may inhibit tumor relapse by comprehensively targeting therapy-orchestrated autophagy in residual cells. https://greenmedinfo.com/article/antioxidant-rich-extract-seaweed-polyphenols-combined-current-pc-treatment-mod#comments Cancers: Drug Resistant Cancers: Radiation-Resistant Pancreatic Cancer Polyphenols Seaweed Antiproliferative Autophagy Inhibitors Chemotherapeutic Chemotherapeutic Synergy: Gemcitabine Gene Expression Regulation Significant Treatment Outcome Animal Study In Vitro Study Sun, 03 May 2015 16:07:25 +0000 greenmedinfo 117095 at https://greenmedinfo.com Fractionated radiotherapy might induce epithelial-mesenchymal transition and radioresistance in a cellular context manner. https://greenmedinfo.com/article/fractionated-radiotherapy-might-induce-epithelial-mesenchymal-transition-and-r PMID:  J Cell Biochem. 2018 Nov 28. Epub 2018 Nov 28. PMID: 30485518 Abstract Title:  Fractionated radiotherapy might induce epithelial-mesenchymal transition and radioresistance in a cellular context manner. Abstract:  Despite the fact that radiotherapy is a main therapeutic modality in cancer treatment, recent evidence suggests that fractionated radiotherapy (FR) might confer radioresistance through epithelial-mesenchymal transition (EMT). Nevertheless, the effects of FR on EMT phenotype and the potential link between EMT induction and radioresistance development yet to be clarified. The aim of this study was to assess whether FR could promote EMT, and to elucidate if induction of EMT contributes to the acquisition of radioresistance. To this end, two human cancer cell lines (A549 and HT-29) were irradiated (2 Gy/day) and analyzed using wound healing, transwell migration and invasion assays, real-time polymerase chain reaction (for E-cadherin, N-cadherin, Vimentin, CD44, CD133, Snail, and Twist), clonogenic assay, Annexin V/PI, and 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay. Irradiation of A549 (for 5 or 10 consecutive days) resulted in morphological changes including elongation of cytoplasm and nuclei and pleomorphic nuclei. Also, irradiation-enhanced migratory and invasive potential of A549. These phenotypic changes were in agreement with decreased expression of the epithelial marker (E-cadherin), enhanced expression of mesenchymal markers (N-cadherin, Vimentin, Snail, and Twist) and increased stemness factors (CD44 and CD133). Moreover, induction of EMT phenotype was accompanied with enhanced radioresistance and proliferation of irradiated A549. However, FR(for 5 consecutive days) did not increase HT-29 motility. Furthermore, molecular alterations did not resemble EMT phenotype (downregulation of E-cadherin, Vimentin, ALDH, CD44, CD133, and Snail). Eventually, FR led to enhanced radiosensitivity and decreased proliferation of HT-29. Altogether, our findings suggest that FR might induce EMT and confer radioresistance in a cell context-dependent manner. <p><a href="https://greenmedinfo.com/article/fractionated-radiotherapy-might-induce-epithelial-mesenchymal-transition-and-r" target="_blank">read more</a></p> https://greenmedinfo.com/article/fractionated-radiotherapy-might-induce-epithelial-mesenchymal-transition-and-r#comments Cancer Metastasis Cancers: Radiation-Resistant Radiotherapy Risk Factors In Vitro Study Sun, 21 Apr 2019 17:11:53 +0000 greenmedinfo 185666 at https://greenmedinfo.com Intravenous vitamin C application seems to reduce pain in patients in comparison to other patients who did not receive it https://greenmedinfo.com/article/intravenous-vitamin-c-application-seems-reduce-pain-patients-comparison-other- PMID:  Nutr Cancer. 2015 Jul 13:1-5. Epub 2015 Jul 13. PMID: 26168394 Abstract Title:  Palliative Vitamin C Application in Patients with Radiotherapy-Resistant Bone Metastases: A Retrospective Study. Abstract:  The aim of this study was to observe effects of ascorbic acid application on pain, performance status, and survival time in cancer patients. A retrospective cohort of 39 patients with bone metastases treated with radiotherapy was identified. All patients were radiotherapy-resistant. Fifteen patients who received chemotherapy, and 15 patients who received an infusion of 2.5 g ascorbic acid were included in the study. Nine control patients were treated with neither chemotherapy nor vitamin C. Eastern Cooperative Oncology Group Performance Status Scale and Visual Analog Scale were used to determine performance status and pain assessments. Survival time and rate in patients were defined. Statistical analyses were performed to compare the results of groups. Performance status was increased in 4 patients of vitamin C group and 1 patient of chemotherapy group, whereas performance status in control group was decreased. A median reduction of 50% in pain was observed among the patients in the vitamin C group. Median survival time was 10 mo in patients receiving ascorbic acid, whereas the chemotherapy and control groups had a median survival of 2 mo. Intravenous vitamin C application seems to reduce pain in patients in comparison to other patients who did not receive it. Patient performance status and survival rate were increased using vitamin C. https://greenmedinfo.com/article/intravenous-vitamin-c-application-seems-reduce-pain-patients-comparison-other-#comments Cancer Metastasis Cancers: Radiation-Resistant Vitamin C: Intravenous Analgesics Median Survival Time Human Study Thu, 16 Jul 2015 21:45:21 +0000 greenmedinfo 119069 at https://greenmedinfo.com Piperlongumine conquers temozolomide chemoradiotherapy resistance to achieve immune cure in refractory glioblastoma. https://greenmedinfo.com/article/piperlongumine-conquers-temozolomide-chemoradiotherapy-resistance-achieve-immu PMID:  J Exp Clin Cancer Res. 2023 May 10 ;42(1):118. Epub 2023 May 10. PMID: 37161450 Abstract Title:  Piperlongumine conquers temozolomide chemoradiotherapy resistance to achieve immune cure in refractory glioblastoma via boosting oxidative stress-inflamation-CD8-T cell immunity. Abstract:  BACKGROUND: The failure of novel therapies effective in preclinical animal models largely reflects the fact that current models do not really mimic the pathological/therapeutic features of glioblastoma (GBM), in which the most effective temozolomide chemoradiotherapy (RT/TMZ) regimen can only slightly extend survival. How to improve RT/TMZ efficacy remains a major challenge in clinic.METHODS: Syngeneic G422-GBM model mice were subject to RT/TMZ, surgery, piperlongumine (PL),αPD1, glutathione. Metabolomics or transcriptomics data from G422-GBM and human GBM were used for gene enrichment analysis and estimation of ROS generation/scavenging balance, oxidative stress damage, inflammation and immune cell infiltration. Overall survival, bioluminescent imaging, immunohistochemistry, and immunofluorescence staining were used to examine therapeutic efficacy and mechanisms of action.RESULTS: Here we identified that glutathione metabolism was most significantly altered in metabolomics analysis upon RT/TMZ therapies in a truly refractory and reliable mouse triple-negative GBM (G422) preclinical model. Consistently, ROS generators/scavengers were highly dysregulated in both G422-tumor and human GBM. The ROS-inducer PL synergized surgery/TMZ, surgery/RT/TMZ or RT/TMZ to achieve long-term survival (LTS) in G422-mice, but only one LTS-mouse from RT/TMZ/PL therapy passed the rechallenging phase (immune cure). Furthermore, the immunotherapy of RT/TMZ/PL plus anti-PD-1 antibody (αPD1) doubled LTS (50%) and immune-cured (25%) mice. Glutathione completely abolished PL-synergistic effects. Mechanistically, ROS reduction was associated with RT/TMZ-resistance. PL restored ROS level (mainly via reversing Duox2/Gpx2), activated oxidative stress/inflammation/immune responses signature genes, reduced cancer cell proliferation/invasion, increased apoptosis and CD3/CD4/CD8T-lymphocytes in G422-tumor on the basis of RT/TMZ regimen.CONCLUSION: Our findings demonstrate that PL reverses RT/TMZ-reduced ROS and synergistically resets tumor microenvironment to cure GBM. RT/TMZ/PL or RT/TMZ/PL/αPD1 exacts effective immune cure in refractory GBM, deserving a priority for clinical trials. <p><a href="https://greenmedinfo.com/article/piperlongumine-conquers-temozolomide-chemoradiotherapy-resistance-achieve-immu" target="_blank">read more</a></p> https://greenmedinfo.com/article/piperlongumine-conquers-temozolomide-chemoradiotherapy-resistance-achieve-immu#comments Cancers: Drug Resistant Cancers: Radiation-Resistant Glioblastoma Oxidative Stress Piperlongumine Chemosensitizer Immunomodulatory Radiosensitizer Tumor Microenvironment Animal Study Wed, 02 Aug 2023 17:00:16 +0000 greenmedinfo 277392 at https://greenmedinfo.com Pterostilbene treatment suppressed glioma stem cell development via negatively modulating GRP78 signaling. https://greenmedinfo.com/article/pterostilbene-treatment-suppressed-glioma-stem-cell-development-negatively-mod PMID:  J Nutr Biochem. 2015 May ;26(5):466-75. Epub 2015 Jan 19. PMID: 25736407 Abstract Title:  Pterostilbene suppressed irradiation-resistant glioma stem cells by modulating GRP78/miR-205 axis. Abstract:  Glioblastoma multiforme (GBM) is the most aggressive type characterized by relapse and resistance even with the combination of radio- and chemotherapy. The presence of glioma stem cells (GSCs) has been shown to contribute to tumorigenesis, recurrence and treatment resistance. Particularly, CD133-positive glioma cells have been shown to represent the subpopulation that confers glioma radioresistance and suggested to be the source of tumor recurrence after radiation. Thus, a better understanding and the development of agents which target GSCs could potentially lead to a significant improvement in treating GBM patients. Here, we demonstrated that GRP78 (an antistress protein) was highly expressed in GBM cells along withβ-catenin and Notch and correlated to the development of GSCs. CD133+ GSCs exhibited enhanced migration/invasion and self-renewal abilities. When GRP78 was silenced, GSC properties were suppressed and the sensitivity towards irradiation increased. In addition, the level of microRNA 205 appeared tobe negatively associated with GRP78 expression. Our previous study indicated that pterostilbene (PT) possessed anticancer stem cell properties in hepatocellular carcinoma. Thus, we examined whether PT is also effective against GSCs. We found that PT-treated GSCs exhibited suppressed self-renewal andirradiation-resistant abilities. PT-mediated effects were associated with an increase of miR-205. Finally, we showed that PT treatment suppressed tumorigenesis in GSC xenograft mice. In conclusion, we provided evidence that GRP78/miR-205 axis played an important role in GSC maintenance and irradiation resistance. PT treatment suppressed GSC development via negatively modulating GRP78 signaling. PT may be considered for combined therapeutic agent to enhance irradiation efficacy in GBM patients. https://greenmedinfo.com/article/pterostilbene-treatment-suppressed-glioma-stem-cell-development-negatively-mod#comments Cancers: Radiation-Resistant Glioblastoma Multiforme Pterostilbene Chemotherapeutic MicroRNA modulator Cancer Stem Cells Animal Study In Vitro Study Wed, 08 Jul 2015 03:01:30 +0000 greenmedinfo 118799 at https://greenmedinfo.com Radiotherapy may confer greater aggressiveness to breast cancer stem cells, resulting in recurrence. https://greenmedinfo.com/article/radiotherapy-may-confer-greater-aggressiveness-breast-cancer-stem-cells-result PMID:  Oncogene. 2012 Feb 13. Epub 2012 Feb 13. PMID: 22330142 Abstract Title:  CD24(-/low) stem-like breast cancer marker defines the radiation-resistant cells involved in memorization and transmission of radiation-induced genomic instability. Abstract:  A growing body of evidence attributes properties of chemo- and/or radiation-resistance to cancer stem cells (CSCs). Moreover, non-targeted delayed effects such as genomic instability, transmitted through many generations, can be observed in the progeny of surviving irradiated cells. As a consequence, we propose that radiation-resistance properties associated to CSCs could confer a key role to this subpopulation in the transmission of genomic instability. To test this hypothesis, we searched the CSC markers associated to radiation-resistance in breast cancer cell lines and studied the role of the resistant cells in the transmission of genomic instability. First, we show that irradiation induces a 2-4 weeks period of intense cell death leading to the emergence of chromosomal unstable cells during more than 35 population doublings. Then, among seven breast CSC markers, we identify CD24(-/low) labelling as a marker of radiation-resistance. We demonstrate that CD24(+) progeny of irradiated cells exclusively descends from CD24(-/low) cells. Finally, we show that delayed chromosomal instability is only expressed by CD24(+) cells, but is transmitted by stable surviving CD24(-/low) cells. So, for the first time a CSC marker, CD24, is associated with the transmission of genomic instability. This work may assign a new deleterious role to breast CSCs in aggressive recurrence after radiotherapy, as the transmitted genomic instability potentially leads tumour cells to acquire more aggressive characteristics.Oncogene advance online publication, 13 February 2012; doi:10.1038/onc.2012.31. https://greenmedinfo.com/article/radiotherapy-may-confer-greater-aggressiveness-breast-cancer-stem-cells-result#comments Breast Cancer Stem Cells Cancer Stem Cells Cancers: Radiation-Induced Cancers: Radiation-Resistant Radiotherapy Tumorigenic In Vitro Study Tue, 17 Jul 2012 16:51:41 +0000 greenmedinfo 78632 at https://greenmedinfo.com Radiotherapy may result in the enrichment of highly malingant cancer stem cells in breast cancer patients. https://greenmedinfo.com/article/radiotherapy-may-result-enrichment-highly-malingant-cancer-stem-cells-breast-c PMID:  Transl Oncol. 2011 Aug ;4(4):227-33. Epub 2011 Aug 1. PMID: 21804918 Abstract Title:  Ablation of breast cancer stem cells with radiation. Abstract:  Tumor radioresistance leads to recurrence after radiation therapy. The radioresistant phenotype has been hypothesized to reside in the cancer stem cell (CSC) component of breast and other tumors and is considered to be an inherent property of CSC. In this study, we assessed the radiation resistance of breast CSCs using early passaged, patient-derived xenografts from two separate patients. We found a patient-derived tumor in which the CSC population was rapidly depleted 2 weeks after treatment with radiation, based on CD44(+) CD24(-) lin(-) phenotype and aldehyde dehydrogenase 1 immunofluorescence, suggesting sensitivity to radiotherapy. The reduction in CSCs according to phenotypic markers was accompanied by a decrease in functional CSC activity measured by tumor sphere frequency and the ability to form tumors in mice. In contrast, another patient tumor sample displayed enrichment of CSC after irradiation, signifying radioresistance, in agreement with others. CSC response to radiation did not correlate with the level of reactive oxygen species in CSC versus non-CSC. These findings demonstrate that not all breast tumor CSCs are radioresistant and suggest a mechanism for the observed variability in breast cancer local recurrence. https://greenmedinfo.com/article/radiotherapy-may-result-enrichment-highly-malingant-cancer-stem-cells-breast-c#comments Breast Cancer Stem Cells Cancer Stem Cells Cancers: Radiation-Induced Cancers: Radiation-Resistant Radiotherapy Tumorigenic Review Tue, 17 Jul 2012 17:05:33 +0000 greenmedinfo 78636 at https://greenmedinfo.com Recurrence at secondary locations, often years after removal of the primary tumor, accounts for most of the mortality associated with solid tumors; most current anticancer regimens select for cells with mesenchymal and CSC properties. https://greenmedinfo.com/article/recurrence-secondary-locations-often-years-after-removal-primary-tumor-account PMID:  Front Biosci (Elite Ed). 2012 ;4:1528-41. Epub 2012 Jan 1. PMID: 22201973 Abstract Title:  The role of cancer stem cells in relapse of solid tumors. Abstract:  Recurrence at secondary locations, often years after removal of the primary tumor, accounts for most of the mortality associated with solid tumors. Metastasis, resistance to chemo- and radiotherapy, and eventual relapse have been attributed to a distinct tumor subpopulation known as cancer stem cells (CSCs). In this review, we consider the properties of CSCs that lead to these outcomes, in particular the relation between epithelial-to-mesenchymal transition, stemness, and tumor initiation. We compare recent clinical and laboratory studies of breast cancer, glioblastoma, and melanoma that illustrate how most current anticancer regimens select for cells with mesenchymal and CSC properties and therefore sow the seeds of relapse. Finally, we discuss the emerging paradigm of combined therapy that targets both CSC and non-CSC tumor components. https://greenmedinfo.com/article/recurrence-secondary-locations-often-years-after-removal-primary-tumor-account#comments Cancer Stem Cells Cancers: Drug Resistant Cancers: Multi-Drug Resistant Cancers: Radiation-Resistant Chemotherapy Radiotherapy Surgical Procedures Review Tue, 17 Jul 2012 16:56:55 +0000 greenmedinfo 78633 at https://greenmedinfo.com Resveratrol and piperine enhance radiosensitivity of tumor cells. https://greenmedinfo.com/article/resveratrol-and-piperine-enhance-radiosensitivity-tumor-cells PMID:  BMB Rep. 2012 Apr ;45(4):242-6. PMID: 22531135 Abstract Title:  Resveratrol and piperine enhance radiosensitivity of tumor cells. Abstract:  The use of ionizing radiation (IR) is essential for treating many human cancers. However, radioresistance markedly impairs the efficacy of tumor radiotherapy. IR enhances the production of reactive oxygen species (ROS) in a variety of cells which are determinant components in the induction of apoptosis. Much interest has developed to augment the effect of radiation in tumors by combining it with radiosensitizers to improve the therapeutic ratio. In the current study, the radiosensitizing effects of resveratrol and piperine on cancer cells were evaluated. Cancer cell lines treated with these natural products exhibited significantly augmented IR-induced apoptosis and loss of mitochondrial membrane potential, presumably through enhanced ROS generation. Applying natural products as sensitizers for IR-induced apoptotic cell death offers a promising therapeutic approach to treat cancer. https://greenmedinfo.com/article/resveratrol-and-piperine-enhance-radiosensitivity-tumor-cells#comments Cancers: Radiation-Resistant Colon Cancer Piperidines Piperine Resveratrol Stilbenes Anticarcinogenic Agents Apoptotic Radiosensitizer In Vitro Study Mon, 17 Jun 2013 15:05:25 +0000 greenmedinfo 101176 at https://greenmedinfo.com Review: Radiation resistance in breast cancer. https://greenmedinfo.com/article/review-radiation-resistance-breast-cancer PMID:  Breast Cancer Res. 2010 ;12(2):105. Epub 2010 Apr 7. PMID: 20377923 Abstract Title:  Radiation resistance in breast cancer: are CD44+/CD24-/proteosome low/PKH26+ cells to blame? Abstract:  Identification and characterization of cancer-initiating cells (CICs) enriched for stem cell-like functions and the establishment of a link between CICs and tumor recurrence, chemotherapy resistance and radiation resistance, and metastasis have been the focus of cancer research for the last eight years. Although this field has its share of controversies, it is becoming apparent that cells isolated from recurrent or residual tumors or both are enriched for cancer cells that have a specific phenotype compared with heterogeneous cells in the primary tumor. Enrichment of CICs in tumors subjected to radiation therapy could be due in part to the delivery of sublethal doses of treatment and the efficient radical scavenging system within CICs. Sublethal doses of radiation are sufficient to induce senescence of non-CICs while forcing CICs to gain several new properties related to cell cycle progression in addition to maintaining or enhancing stem cell characteristics of pre-treatment CICs. Characterizing pathways responsible for the increase in CICs after therapy and exploiting the unique characteristics of therapy-resistant CICs for developing targeted therapies are becoming a central focus of research in the rapidly evolving field of CICs. https://greenmedinfo.com/article/review-radiation-resistance-breast-cancer#comments Breast Cancer Breast Cancer Stem Cells Cancer Stem Cells Cancers: Radiation-Resistant Antiproliferative Cell cycle arrest Proteasome Inhibitors Radiotherapy Cancer Stem Cells Review Tue, 17 Jul 2012 17:58:30 +0000 greenmedinfo 78648 at https://greenmedinfo.com Turmeric's 'Smart Kill' Properties Put Chemo & Radiation To Shame https://greenmedinfo.com/blog/turmerics-smart-kill-properties-put-chemo-radiation-shame1 <div class="copyright">This article is copyrighted by GreenMedInfo LLC, 2023<br/><strong><a href="/greenmedinfocom-re-post-guidelines">Visit our Re-post guidelines</a></strong></div><p class="rtecenter"><img alt="" src="//cdn.greenmedinfo.com/sites/default/files/ckeditor/Sayer Ji/images/turmeric_smart_kill_greenmedinfo.jpg" style="width: 600px; height: 400px;" /></p> <p><span style="font-size:24px;"><em><strong>The ancient Indian spice turmeric strikes again! Research finds turmeric extract selectively and safely killing cancer stem cells in a way that chemo and radiation can not.</strong></em></span></p><p><a href="https://greenmedinfo.com/blog/turmerics-smart-kill-properties-put-chemo-radiation-shame1" target="_blank">read more</a></p> https://greenmedinfo.com/blog/turmerics-smart-kill-properties-put-chemo-radiation-shame1#comments Brain Cancer Stem Cells Breast Cancer Stem Cells Cancer Stem Cells Cancers: All Cancers: Radiation-Resistant Chemotherapy Curcumin Digestive System Cancer Melanoma Stem Cell Turmeric Turmeric: Fermented Cancer Chemotherapy Health Guide: Turmeric Health Guides: Healing Foods Radiotherapy Radiotherapy: Stereotactic Surgical Procedures Cancer Stem Cells Selective Cytotoxicity Wed, 02 Jan 2019 13:04:47 +0000 Sayer Ji 116477 at https://greenmedinfo.com Vitamin K2-derived compounds inhibit growth in radioresistant cancer cells. https://greenmedinfo.com/article/vitamin-k2-derived-compounds-inhibit-growth-radioresistant-cancer-cells PMID:  Kobe J Med Sci. 2010 ;56(2):E38-49. Epub 2010 Sep 28. PMID: 21063145 Abstract Title:  Vitamin K2-derived compounds induce growth inhibition in radioresistant cancer cells. Abstract:  A strategy to overcome radioresistance in cancer treatment has been expected. To evaluate the strategy, appropriate experimental models are needed. Radioresistant tumour models were originally established from human colon cancer cells, and we evaluated their molecular basis. Next, the growth inhibitory effects of newly synthesized vitamin K2 (VK2)-related compounds were tested. Here, we showed that these novel compounds have growth inhibitory effects not only on cancer cells of various origins, but also on radioresistant cells, through the generation of reactive oxygen species (ROS). Human colon, lung, and breast cancer cell lines were used for testing the growth inhibitory activities of several chemical compounds. Radioresistant tumour models were established by fractionated radiation exposure. Irradiated cells were selected by a single cell cloning method, and their sensitivity to ionizing radiation was evaluated by a colony-forming assay. The VK2 derivatives (named MQ-1, MQ-2, and MQ-3) were chemically synthesized. To evaluate the generation of ROS, flow cytometer analyses were performed. A radioresistant tumour model was established from the HCT116 human colon cancer cell line. The radioresistant cells from HCT116 also showed resistance to cisplatin. In the radioresistant cells, NF-κB was highly activated. MQ-1, MQ-2, and MQ-3 showed greater growth inhibitory activities than VK2 not only in various cancer cells but also in radioresistant cells through the generation of ROS. In conclusion, a radioresistant tumour model was originally established from colon cancer cell lines through NF-κB activation, and it could be a useful tool for evaluating anti-tumour agents. Newly synthesized VK2 derivatives (MQ-1, MQ-2 and MQ-3) seemed to be potential anti-tumour agents in various cancers and radioresistant cancers. The efficacy of those compounds was related to the generation ofROS. These findings together might pave the way for the treatment of radioresistant or recurrent cancers. https://greenmedinfo.com/article/vitamin-k2-derived-compounds-inhibit-growth-radioresistant-cancer-cells#comments Cancers: Radiation-Resistant Vitamin K2 Antiproliferative NF-kappaB Inhibitor Radiosensitizer In Vitro Study Tue, 17 Jul 2012 17:37:33 +0000 greenmedinfo 78642 at https://greenmedinfo.com