Relevant bibliographies by topics / Chemotherapy biomarker

Academic literature on the topic 'Chemotherapy biomarker'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Chemotherapy biomarker"

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Bukhari, Ali A., and Ranjit K. Goudar. "Thymidylate Synthase as a Predictive Biomarker for Pemetrexed Response in NSCLC." Lung Cancer International 2013 (December 25, 2013): 1–7. http://dx.doi.org/10.1155/2013/436409.

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In recent years, major strides in cancer research have made it possible to select personalized chemotherapy recommendations based on an individual patient’s tumor biology. The prognostic and/or predictive ability of biomarkers seeks to tailor the use of targeted chemotherapy and can result in improved clinical outcomes with reduced toxicity. A proliferation of new technology and pharmacotherapeutics in the setting of current FDA Clinical Laboratory Improvement Amendment (CLIA) standards has resulted in a recent surge in direct-to-physician biomarker tests. However, in the absence of clinical validation, there is the concern that the biomarkers may be utilized prematurely, resulting in improper chemotherapy selection and patient harm. Thymidylate synthase (TS) has been marketed as a predictive biomarker for the use of pemetrexed in NSCLC. We will examine the evidence behind the use of TS as a predictive biomarker to predict response to pemetrexed in NSCLC. At this time, the evidence does not currently support using TS assays to guide chemotherapy selection outside of a clinical research protocol.
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Cho, William CS, Timothy TC Yip, Roger KC Ngan, Tai-Tung Yip, Vladimir N. Podust, Christine Yip, Harry HY Yiu, et al. "ProteinChip Array Profiling for Identification of Disease- and Chemotherapy-Associated Biomarkers of Nasopharyngeal Carcinoma." Clinical Chemistry 53, no. 2 (February 1, 2007): 241–50. http://dx.doi.org/10.1373/clinchem.2005.065805.

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Abstract Background: We previously used ProteinChip array profiling analysis to discover a serum biomarker associated with nasopharyngeal carcinoma (NPC). In this study, we used the same method to examine other biomarkers associated with NPC and response to chemotherapy (CT) in NPC patients. Methods: We performed ProteinChip array analysis in 209 serum samples from 66 relapsed patients before and after salvage CT with gemcitabine and cisplatin or etoposide and cisplatin combinations, 11 patients in remission, and 35 healthy individuals. Intensities of the biomarker peaks were correlated with CT response of the patients and other clinical parameters. Results: We discovered 13 candidate biomarkers associated with different clinical parameters. Two biomarkers (2803 and 3953 Da) were significantly increased in patients compared with controls at all stages of disease. Analysis of pre- and post-CT paired serum samples revealed 7 biomarkers correlated with impact of CT. Of these 7 biomarkers, 2 (2509 and 2756 Da) were significantly increased and 5 (7588, 7659, 7765, 7843, and 8372 Da) were significantly decreased post-CT in either 1 or both CT cohorts. Four biomarkers from pre-CT sera were correlated with CT response, with 3 (2950, 13 510, and 14 855 Da) being significantly decreased and 1 (6701 Da) significantly increased in patients who did not respond to CT. Tandem mass spectrometric sequencing and/or immunoaffinity capture assay identified the 3953 Da biomarker as a fragment of interα-trypsin inhibitor precursor and 7765 Da biomarker as platelet factor-4. Conclusions: Treatment-associated serum biomarkers found might serve to triage NPC patients for appropriate CT treatment.
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Ruddy, Kathryn Jean, Anne M. O'Neill, Kathy Miller, Bryan P. Schneider, Emily Baker, Joseph A. Sparano, Chau T. Dang, Donald W. Northfelt, and George W. Sledge. "Biomarker prediction of chemotherapy-related amenorrhea." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 9508. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.9508.

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9508 Background: Chemotherapy-related amenorrhea (CRA) is associated with infertility and may impact treatment decision-making. We investigated whether anti-mullerian hormone (AMH) levels before chemotherapy predict likelihood of CRA. Methods: 591 patients enrolled on the quality of life substudy of ECOG5103, which randomized breast cancer patients to doxorubicin-cyclophosphamide followed by paclitaxel: 1) alone; 2) with concurrent bevacizumab; or 3) with prolonged bevacizumab. 144 of the 195 women who reported a period <12 months before enrollment consented to serum collection prior to chemotherapy. AMH was measured in 143 with available serum. Participants self-reported menstrual frequency at 12 and 18 months after enrollment. 12-month CRA was defined as no menses for 6 months before the 12-month survey, and 18-month CRA as no menses for 6 months before the 18-month survey. Fisher’s exact test was used to identify associations with CRA. Results: Of the 143, 16 were excluded due to bilateral oophorectomy or initiation of ovarian function suppression within 12 months, and 2 due to missing data at 12 months. In the remaining 125, median age at enrollment was 45 (range 25-55). 103 (82%) had CRA at 12 months, including 68% of patients </= 45 (43/63) and 97% of patients >45 (60/62). Median pre-chemotherapy AMH was 0.11 (range 0.01-8.63). 12-month CRA was more likely in women who received bevacizumab (p<0.01), were >45 (p<0.01), and had AMH </=0.11 (p<0.01) pre-treatment. Hormonal tx was not associated with 12-month CRA (p=0.63). 100 patients were eligible for 18-month CRA analysis: 81 (81%) had CRA, including 63% of patients </= 45 (33/52) and 100% (48/48) of patients >45. 18-month CRA was more likely in women >45 (p<0.01) and with AMH </=0.11 (p<0.01) pre-treatment. Bevacizumab (p=0.15) and hormonal tx (p=0.07) were not statistically significant predictors of 18-month CRA. Conclusions: Pre-chemotherapy AMH predicts risk of CRA at 12 and 18 months, and is a promising biomarker of ovarian reserve in young breast cancer survivors. Longer studies will be needed to ascertain whether lower pre-treatment AMH is associated with increased risk of later infertility. Clinical trial information: NCT00433511.
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Christensen, Ib Jarle, Gunilla Høyer-Hansen, Tine Thurison, Barry Dowell, Julia S. Johansen, Rikke Henriksen, Kristoffer Staal Rohrberg, Nils Brunner, and Hans J. Nielsen. "The prognostic value of seven soluble proteins measured in plasma or serum from patients with colorectal cancer in TNM stages I-III." Journal of Clinical Oncology 30, no. 30_suppl (October 20, 2012): 35. http://dx.doi.org/10.1200/jco.2012.30.30_suppl.35.

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35 Background: In colorectal cancer (CRC) several independent blood-borne biomarkers have been proposed as prognostic and/or predictive markers. However only CEA is at present recommended as a serological CRC biomarker. We have identified 6 other biomarkers and the aim of this study is to see if a combination of markers improves the prognostic and/or predictive value. Methods: Two-hundred and twenty-eight patients with CRC have been included in this study, all with TNM stages I-III. Overall survival (OS) was chosen as the primary endpoint with 93 events and the minimum follow-up was 47 months. Seven biomarkers measured in plasma or serum were analysed: CEA, TIMP-1, the 3 soluble uPAR forms suPAR(I-III), suPAR(I-III)+(II-III) and uPAR(I), PAI-1 and YKL-40. Multivariable analyses of OS were done using regression analysis and results presented by 3 and 5 year OS rates with area under the receiver operating characteristic curve (AUC). All biomarker levels were analysed on the log scale (base 2). Results: High levels of each of the included biomarker were significantly associated in a multivariable analysis (adjusted for age, gender, TNM stage, tumor localization, adjuvant chemotherapy,interaction between adjuvant therapy and biomarker) to poor prognosis in patients not receiving adjuvant chemotherapy. The results are shown for those patients (see Table). The uPAR forms were the only biomarkers significantly associated to OS in patients receiving adjuvant chemotherapy. Combining the markers resulted in an enhanced prediction of 3 and 5 year OS. For TNM stage II patients not receiving adjuvant therapy, the AUC was 0.765 for 3 year OS and 0.745 for 5 year OS. The corresponding AUC’s for TNM stage III were 0.859 and 0.861. Conclusions: The presented combination of blood biomarkers are shown to predict OS with higher precision than any single marker for patients not receiving adjuvant chemotherapy and may provide useful information for use in the management of patients with CRC. [Table: see text]
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Moik, Florian, Sabine Zöchbauer-Müller, Florian Posch, Ingrid Pabinger, and Cihan Ay. "Systemic Inflammation and Activation of Haemostasis Predict Poor Prognosis and Response to Chemotherapy in Patients with Advanced Lung Cancer." Cancers 12, no. 6 (June 18, 2020): 1619. http://dx.doi.org/10.3390/cancers12061619.

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Systemic inflammation and activation of haemostasis are common in patients with lung cancer. Both conditions support tumour growth and metastasis. Therefore, inflammatory and haemostatic biomarkers might be useful for prediction of survival and therapy response. Patients with unresectable/metastatic lung cancer initiating 1st-line chemotherapy (n = 277, 83% non-small cell lung cancer) were followed in a prospective observational cohort study. A comprehensive panel of haemostatic biomarkers (D-dimer, prothrombin fragment 1+2, soluble P-selectin, fibrinogen, coagulation factor VIII, peak thrombin generation), blood count parameters (haemoglobin, leucocytes, thrombocytes) and inflammatory markers (neutrophil-lymphocyte ratio, lymphocyte-monocyte ratio, platelet-lymphocyte ratio, C-reactive protein) were measured at baseline. We assessed the association of biomarkers with mortality, progression-free-survival (PFS) and disease-control-rate (DCR). A biomarker-based prognostic model was derived. Selected inflammatory and haemostatic biomarkers were strong and independent predictors of mortality and therapy response. The strongest predictors (D-dimer, LMR, CRP) were incorporated in a unified biomarker-based prognostic model (1-year overall-survival (OS) by risk-quartiles: 79%, 69%, 51%, 24%; 2-year-OS: 53%, 36%, 23%, 8%; log-rank p < 0.001). The biomarker-based model further predicted shorter PFS and lower DCR. In conclusion, inflammatory and haemostatic biomarkers predict poor prognosis and treatment-response in patients with advanced lung cancer. A biomarker-based prognostic score efficiently predicts mortality and disease progression beyond clinical characteristics.
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Parks, R. M., L. H. Alfarsi, A. R. Green, and K. L. Cheung. "Biology of primary breast cancer in older women beyond routine biomarkers." Breast Cancer 28, no. 5 (June 24, 2021): 991–1001. http://dx.doi.org/10.1007/s12282-021-01266-5.

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Abstract Purpose There are numerous biomarkers which may have potential predictive and prognostic significance in breast cancer. This is extremely important in older adults, who may opt for less aggressive therapy. This work outlines the literature on biological assessment outside of standard biomarkers (defined as ER, PgR, HER2, Ki67) in women ≥ 65 years with primary operable invasive breast cancer, to determine which additional biomarkers are relevant to outcome in older women. Methods Medline and Embase databases were searched. Studies were eligible if included ≥ 50 patients aged ≥ 65 years; stratified results by age; measured a biomarker outside of standard assay and reported patient data. Results A total of 12 studies were appraised involving 5000 patients, measuring 28 biomarkers. The studies were extremely varied in methodology and outcome but three themes emerged: 1. Differences in biomarker expression between younger and older women, indicating that breast cancer in older women is generally less aggressive compared to younger women; 2. Relationship of biomarker expression with survival, suggesting biomarkers which may exclusively predict response to primary treatment in older women; 3. Association of biomarker with chemotherapy, suggesting that older patients should not be declined chemotherapy based on age alone. Conclusion There is evidence to support further investigation of B-cell lymphoma (BCL2), liver kinase (LK)B1, epidermal growth factor receptor (EGFR), cytoplasmic cyclin-E, mucin (MUC)1 and cytokeratins (CKs) as potential predictive or prognostic markers in older women with breast cancer undergoing surgery. Studies exploring these biomarkers in larger cohorts and in women undergoing non-operative therapies are required.
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Adashek, Jacob, Alexey Goloubev, Shumei Kato, and Razelle Kurzrock. "179 Immunotherapy trials lack a biomarker for inclusion: implications for drug development." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (November 2020): A192. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0179.

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BackgroundNext-generation sequencing and other biomarkers have demonstrated the capability to identify potentially pathogenic molecular aberrancies. Immune checkpoint inhibitors (ICI) have benefited patients in almost every oncologic histology. Combining these innovations has transformed how oncologists treat previously untreatable diseases.MethodsThe 413 trials from clinicaltrials.gov website were reviewed using the terms ‘nivolumab’ or ‘pembrolizumab’ between January 1, 2019 and December 31, 2019. Additionally, all 33 interventional therapeutic trials for ‘glioblastoma multiforme’ and 79 for ‘pancreatic cancer’ that were either recruiting, not yet recruiting, or active not recruiting trials between January 1, 2019 and December 31, 2019 were analyzed.ResultsIn total of 413 trials, 57,853 were planned for enrollment with 37 (8.96%) trials requiring a biomarker for entry (n = 5,602 [9.7%]). Overall, there were 41 trials with single-agent immunotherapy planned to enroll 6222 patients and of those trials 7 (17.1%) required a biomarker for enrollment (n = 285 [4.6%]). There were 193 trials with >2 immunotherapies combined planned to enroll 21,360 patients and of those trials 17 (8.8%) required a biomarker for enrollment (n = 1254 [5.9%]). There were 69 trials with immunotherapy and chemotherapy combined planned to enroll 12,354 patients and of those trials 3 (4.3%) required a biomarker for enrollment (n = 83 [0.67%]). There were 58 trials with immunotherapy and targeted therapy combined planned to enroll 11,967 patients and of those trials 6 (10.3%) required a biomarker for enrollment (n = 3244 [27.1%]). There were 52 trials with other immunotherapy combinations (e.g. vaccine) planned to enroll 5950 patients and of those trials 4 (7.7%) required a biomarker for enrollment (736 [12.4%]). Within pancreatic cancer, 31 trials were planned to use immunotherapy (monotherapy, combination, with chemotherapy, with targeted therapy) including 4493 patients total; 5 (16%) of those trials required biomarkers enrolling 309 (7%) patients. Within glioblastoma multiforme, 13 trials were planned to use immunotherapy (monotherapy, combination, with chemotherapy, with targeted therapy) including 730 patients total; 1(8%) of those trials required biomarkers enrolling 10 (1%) patients.ConclusionsFor immunotherapy-based trials in 2019, <10% of patients expected to be enrolled would be selected by a biomarker for inclusion. Precision oncology continues to struggle in the era of ICI with an all-comers approach to patient selection and trial initiation. Selecting patients for trials based on biomarkers may help better identify responders to ICI.
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Chen, Yong-Zi, Youngchul Kim, Hatem H. Soliman, GuoGuang Ying, and Jae K. Lee. "Single drug biomarker prediction for ER− breast cancer outcome from chemotherapy." Endocrine-Related Cancer 25, no. 6 (June 2018): 595–605. http://dx.doi.org/10.1530/erc-17-0495.

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ER-negative breast cancer includes most aggressive subtypes of breast cancer such as triple negative (TN) breast cancer. Excluded from hormonal and targeted therapies effectively used for other subtypes of breast cancer, standard chemotherapy is one of the primary treatment options for these patients. However, as ER− patients have shown highly heterogeneous responses to different chemotherapies, it has been difficult to select most beneficial chemotherapy treatments for them. In this study, we have simultaneously developed single drug biomarker models for four standard chemotherapy agents: paclitaxel (T), 5-fluorouracil (F), doxorubicin (A) and cyclophosphamide (C) to predict responses and survival of ER− breast cancer patients treated with combination chemotherapies. We then flexibly combined these individual drug biomarkers for predicting patient outcomes of two independent cohorts of ER− breast cancer patients who were treated with different drug combinations of neoadjuvant chemotherapy. These individual and combined drug biomarker models significantly predicted chemotherapy response for 197 ER− patients in the Hatzis cohort (AUC = 0.637, P = 0.002) and 69 ER− patients in the Hess cohort (AUC = 0.635, P = 0.056). The prediction was also significant for the TN subgroup of both cohorts (AUC = 0.60, 0.72, P = 0.043, 0.009). In survival analysis, our predicted responder patients showed significantly improved survival with a >17 months longer median PFS than the predicted non-responder patients for both ER− and TN subgroups (log-rank test P-value = 0.018 and 0.044). This flexible prediction capability based on single drug biomarkers may allow us to even select new drug combinations most beneficial to individual patients with ER− breast cancer.
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Demir, Muzaffer, A. Ciftci, Debra Hoppensteadt, G. Altiay, Mahemut Tobu, Omer Iqbal, Dan Fareed, Cafer Adiquzel, Michelle Kujawski, and Jawed Fareed. "ProteinChip Array Profiling and Markers of Inflammation and Thrombin Generation in Plasma Samples from Lung Cancer Patients and Their Modulation by Chemotherapy with or without Warfarin Anticoagulation." Blood 110, no. 11 (November 16, 2007): 3978. http://dx.doi.org/10.1182/blood.v110.11.3978.3978.

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Abstract While the increased prevalence of venous thromboembolic events (VTE) is fully recognized in lung cancer, its pathogenesis is not fully understood. Profiling of surrogate markers of thrombosis and inflammation provides an opportunity to understand the pathogenesis of VTE. More recently, ProteinChip Array technology has provided a novel approach to profile unique biomarkers in cancer patients. Protease activation in these patients results in the generation of unique biomarkers, which can be identified and monitored during the course of patient management. In a prospective, randomized, controlled study patients with inoperable lung cancer (n=100) were randomized to receive A) chemotherapy, radiation and warfarin (INR 1.5–2.5) or B) chemotherapy, radiation without warfarin (n=50). Blood samples were drawn prior to and after the second treatment cycle in both groups A and B. All samples were also analyzed for such inflammation markers as the tumor necrosis factor alpha (TNFa), CD 40 ligand (CD 40L), C-reactive protein (CRP), interleukin 1 beta (IL-1B), asymmetric dimethylarginine (ADMA) and nitric oxide (NO). In addition, prothrombin fragment F1.2 (F1.2), thrombin antithrombin complex (TAT) and functional microparticles were also measured. Proteomic profiling is widely used to identify unique biomarkers in various hemotologic disorders. Albumin was used as control proteins throughout the study. The baseline blood levels of the inflammatory markers and coagulation activation marker were increased in both the warfarin treated and control group. After the second treatment cycle, the warfarin treated group exhibited varying levels of decrease in all of the surrogate markers of coagulation activation and inflammation (13 – 15%). On the other hand, none of the warfarin treated group showed a marked increase in the TNFα, CD40L, NO, F1.2 and TAT (18–30%). No change in the IL-1B was noted in this group. However, CRP levels were markedly reduced (46%). Most of the baseline samples in both groups showed a unique biomarker peak at 11.9 kDa. The prevalence of this unique biomarker peak was decreased after the second cycle of chemotherapy and after the final course of chemotherapy, it was totally diminished. No significant differences in the down regulation of this unique biomarker were obvious in both groups. Since inflammatory markers showed a decrease (13–50%) in the warfarin treated group, whereas the non-warfarin treated group exhibited an increase (18–30%) in all markers except IL-1B, CRP and ADMA, anticoagulation down regulates these mediators. Markers of thrombin generation were also down regulated in the warfarin treated group. The identification of the unique biomarker at 11.9 kDa in both groups and its gradual down regulation eventually leading to diminution in both groups, suggests that chemotherapy and radiation treatment appear to regulate this biomarker. The levels of various inflammatory markers are upregulated in lung cancer suggesting a pathogenic role of this process in lung cancer. Warfarin down regulated the inflammatory process in contrast to the non-warfarin treated group. However, the unique biomarker at 11.9 kDa appears to be regulated by chemotherapy and radiation. The clinical relevance of these observations requires additional investigations.
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Carcò, Daniela, Paolo Castorina, Paola Guardo, Valeria Iachelli, Tecla Pace, Paola Scirè, Rosaria Stanco, et al. "Combination of Interleukin-6, C-Reactive Protein and Procalcitonin Values as Predictive Index of Sepsis in Course of Fever Episode in Adult Haematological Patients: Observational and Statistical Study." Journal of Clinical Medicine 11, no. 22 (November 17, 2022): 6800. http://dx.doi.org/10.3390/jcm11226800.

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Haematological patients represent a vulnerable population to opportunistic infections, mainly due to the disease itself and chemotherapy-induced neutropenia. The level of immune suppression strongly increases the importance of timely antibiotic treatment in order to prevent sepsis-related mortality. During the initial fever episode, serum biomarkers are usually used to estimate the probability of blood stream infection prior to the results of microbial diagnosis. A new serum biomarker combination study on a febrile haematological population, including C-reactive protein (CRP), interleukin-6 (IL−6) and procalcitonin (PCT), is proposed in order to improve their predictive accuracy. In our prospective study, CRP, IL−6 and PCT were evaluated in 34 immunosuppressed haematological patients immediately after the onset of 51 fever episodes, either during the course of standard chemotherapy or high-dose chemotherapy and autologous stem cell transplant. The fever episodes were divided into documented infections and fever alone. Receiver operating characteristic analysis (ROC) was performed for each biomarker and a combination of all three biomarkers (multiROC) to define a new predictive index. Significant differences were evidenced between the two groups (documented infection and no infection) for both PCT and IL−6 (p = 0.03 and p = 0.035, respectively), but none for CRP (p = 0.1). The composite parameter is more reliable than any single biomarker alone, with an area under the curve (AUC) of 79% and with high sensitivity and specificity. IL−6 gave the closest response compared to the composite index. Composite parameters of serum biomarkers could be used for an early diagnosis of infection at fever onset in haematological patients.
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Dissertations / Theses on the topic "Chemotherapy biomarker"

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Muhammad, Aun. "Microbubble ultrasound as surrogate imaging biomarker for response to systemic and regional chemotherapy." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/44958.

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New treatments such as anti-angiogenic therapy, chemoembolisation, radio-embolisation cause tumour stabilisation which may render conventional size based imaging invalid for monitoring early response to therapy. The aim of this thesis was to develop an alternative index which can predict response for patients with liver tumours earlier, at 2 weeks, than the contemporary gold standard response evaluation criteria at 3 months. This technique was based on the use of microbubble ultrasound as an alternative method for detection of hepatic arterialisation. In this thesis, I evaluated the microbubble ultrasound derived liver blood flow parameters to reflect global liver blood flow in phantom as well as in patients. I also evaluated the impact of several variable factors affecting the liver blood flow and studied the potential role of the blood flow parameters and proposed an alternative index -the contrast enhanced hepatic perfusion index (CE-HPI) - in prediction of early response to treatment for liver tumours. We showed the ability of this technique to reflect global liver blood flow parameters in vitro as well as in patients. Subsequently the index was applied to determine the response assessment in patients receiving treatments. The results from these experiments present the first demonstration in humans that microbubble ultrasound derived liver blood flow parameters including CE-HPI can be helpful in early identification of non-responders. I propose that the microbubble ultrasound technique developed in this thesis can be used to further probe and investigate response assessment in randomized and multicentre studies.
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Bunting, David Mark. "The performance of circulating biomarkers in the prediction of response to neoadjuvant therapy in patients with oesophago-gastric cancer." Thesis, University of Plymouth, 2016. http://hdl.handle.net/10026.1/6565.

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Introduction The prognosis in oesophago-gastric cancer is poor with less than 15% patients surviving beyond 5 years after diagnosis. The addition of neoadjuvant therapy has been shown to increase survival in patients suitable for curative surgery. However, the additional gains are modest and the majority of patients do not respond sufficiently from therapy to gain any benefit. There is an urgent need to identify markers that can predict response to neoadjuvant therapy in order provide safer, more effective, individualised treatment regimes. Methods A prospective, multi-centre, collaborative study was undertaken in patients with oesophago-gastric cancer undergoing neoadjuvant therapy and potentially curative surgery. Levels of circulating biomarkers M2-Pyruvate kinase, alkaline phosphatase, CA19-9, CEA and CA 72-4 were measured in patients before and after administering the first cycle of chemotherapy. Binary logistic regression analysis was performed to assess the ability of biomarkers to predict histological response to therapy. Results 165 patients were recruited to the main study. 105 patients had complete histopathological data for analysis. There were 27 responders and 78 non-responders to neoadjuvant therapy. There were no differences in pre-therapy demographic, pathological or treatment factors between the two groups. Responders had less post-operative lymphovascular invasion (P= 0.004) and higher R0 resection rates (P=0.03). Pre-therapy M2-Pyruvate kinase levels were lower in responders compared to non-responders (P=0.037) and levels were able to predict response with each unit increase in the biomarker level being associated with a 4.1% decrease in the likelihood of response (P=0.027). M2-PK levels were not associated with any pre-operative demographic, clinical or pathological factors. Conclusions Pre-therapy dimeric M2-PK levels can predict response to neoadjuvant therapy in patients with oesophago-gastric cancer. The test could be of clinical value for 1 in every 8 patients undergoing the test.
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Thornton, Michael. "The 78 kDa glucose regulated protein (GRP78) as a potential treatment predictive biomarker and therapeutic target in colorectal cancer adjuvant chemotherapy." Thesis, University of Liverpool, 2014. http://livrepository.liverpool.ac.uk/17993/.

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Introduction: Glucose-regulated protein 78-kDa (GRP78) is an endoplasmic reticulum (ER)-resident molecular chaperone that is essential for correct protein folding and assembly in the ER lumen. Micro-environmental stress and a requirement for increased protein synthesis, typical of solid tumours, leads to a disruption of ER homeostasis, and accumulation of misfolded proteins. The ability of GRP78 to dissociate from several important ER-resident transmembrane proteins under conditions of ER stress leads to a cascade of signal transduction pathways, known as the unfolded protein response (UPR), that modulate cell survival or, if the stress is significantly severe, apoptosis. GRP78 has been found to be overexpressed in a variety of cancers compared with benign tissue and has been associated with poor outcome. In-vitro data indicate that GRP78 expression is often associated with aggressive phenotype and drug resistance. Thus, GRP78 has potential as a biomarker for tumour behaviour and treatment response. For stage III colorectal cancer, there is overwhelming evidence to recommend the use of fluoropyrimidine-based adjuvant chemotherapy. Unfortunately, a large proportion of patients do not benefit from adjuvant chemotherapy, and biomarkers that can determine the likelihood of response to chemotherapy remain elusive. The benefit of chemotherapy in stage II disease is less certain and markers that could reliably predict benefit would be particularly useful in this population. This study explores a potential mechanistic relationship between GRP78 and 5-FU sensitivity using both siRNA transfection and treatment with an engineered fusion protein, epidermal growth factor (EGF)-SubA, which has been demonstrated to cause highly selective cleavage of GRP78 at a single amino acid point. It was then examined whether GRP78 may have prognostic or predictive value in the context of colorectal cancer patients treated with fluoropyrimidine-based chemotherapy. The potential therapeutic value of targeting GRP78 in vitro using EGF-SubA is also examined. Methods: Colon cancer cell lines were used to examine response to 5-FU upon modulation of endogenous GRP78 using siRNA technology and EGF-SubA. Apoptosis and cell cycle progression were assessed using flow cytometry. Immunohistochemistry was used to characterise GRP78 expression in a large cohort of colorectal cancers on tissue microarrays and the results were correlated with clinicopathological parameters and with 5-year survival for the whole cohort and those treated with fluoropyrimidine-based (5-FU) adjuvant chemotherapy. The action of EGF-SubA upon colon cancer cells was examined using western blotting, MTT assay and flow cytometry. Results: GRP78 promotes apoptosis in response to 5-FU. Better overall 5-year survival was associated with high GRP78 expression (P=0.036). Stage III patients with high GRP78 showed significant benefit from adjuvant chemotherapy (P=0.026), whereas patients with low GRP78 failed to benefit (P=0.805). Low GRP78 was an independent poor prognostic indicator of overall 5-year survival (P=0.005; HR=1.536; 95%CI 1.139-2.122). Colon cancer cells expressing EGFR were highly sensitive to EGF-SubA, demonstrating reduced proliferation and cell cycle arrest. However, EGF-SubA did not induce significant apoptosis and reduced the effectiveness of 5-FU in vitro. Conclusion: This study demonstrates a mechanistic relationship between GRP78 expression and response to 5-FU. GRP78 expression may provide a useful additional risk stratification to inform the adjuvant treatment of colorectal cancer. EGF-SubA does not have therapeutic value in colorectal cancer but is a useful tool for studying GRP78 and the UPR.
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Zanjirband, Maryam. "The genomic and functional status of TP53 in ovarian cancer : biomarker for chemotherapy outcome and determinant of response to MDM2 inhibitors." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3831.

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Background: Mutation and loss of TP53 function is one of the most frequent genetic abnormalities in ovarian cancer. TP53 genomic and functional status have been shown to provide potentially prognostic and predictive value in ovarian cancer; however, the results are controversial and evaluation in the context of a controlled clinical trial with single agent treatment have been lacking. Reactivation of p53 using MDM2-p53 antagonists is a promising therapeutic target for most patients with type I epithelial ovarian cancer and those left from type II harbouring wild-type TP53. BRCA1/2 mutations are present in 70-85% of germline mutations in patients with inherited ovarian cancer, and deficiencies in homologous recombination repair (HRR) account for up to 50% of epithelial ovarian cancer, indicating the possible sensitivity of ovarian cancer patients to PARP inhibitors. MDM2-p53 antagonists and PARP inhibitors are now undergoing clinical trials as targeted therapy for different types of cancer. The effect of RG7388 on its own and in combination with cisplatin, and combined treatment between MDM2-p53 antagonists and PARP inhibitors have not been investigated in ovarian cancer. Hypotheses: 1) Different genomic and functional status of p53 and some of its downstream targets such as p21WAF1, MDM2 and WIP1 can be used as prognostic and predictive biomarkers for the outcome of chemotherapy and overall survival in ovarian cancer. 2) Reactivation of p53 by inhibition of its negative regulator MDM2, using the MDM2-p53 antagonists Nutlin-3 and RG7388, will result in p53-mediated growth arrest and apoptosis in wild-type TP53 ovarian cancer cells, and combination of them with current therapeutic agents or rucaparib increases growth inhibition and/or apoptosis in ovarian cancer cell lines compared to either agent alone. Methods: TP53 was sequenced in 260 ovarian cancer samples from the ICON3 trial using Sanger sequencing and Next Generation Sequencing (NGS) methods. The prognostic value of the expression levels of p53, p21WAF1, MDM2 and WIP1 was investigated using immunohistochemistry (IHC). The effect of MDM2-p53 antagonists, Nutlin-3/RG7112/RG7388, and PARP inhibitor, rucaparib, as single agents and in combination with cisplatin or together were investigated on a panel of ovarian cancer cell lines. Sensitivity was measured by growth inhibition, clonogenic cell survival assay, apoptosis assays including caspase 3/7 activity and flow cytometry. The effect on the p53 molecular pathway and p53-regulated candidate gene expression were investigated by western blotting and Quantitative Reverse-Transcription Polymerase Chain Reaction (qRT-PCR) respectively. Results: Patients from the ICON3 clinical trial treated with carboplatin whose tumours harbour wild-type TP53 had a significantly better overall survival based on both univariate and multivariate analysis compared to those with mutant TP53 regardless of sequencing method. Adding paclitaxel to the platinum-based treatment showed a trend in favour of greater benefit for those with mutant TP53, although this failed to reach statistical significance (p > 0.05). Overexpression of p53 has potential prognostic value for overall survival of ovarian cancer patients. Ovarian cancer cell lines with wild-type TP53 were sensitive to MDM2-p53 antagonists, Nutlin-3/RG7112/RG7388, while those with mutant TP53 were resistant to MDM2 inhibitors. Among the individual cell lines, A2780 and MDAH-2774 were sensitive and other cell lines (IGROV-1, OAW42, CP70, MLH1-corrected CP70+ and SKOV-3) were resistant to rucaparib regardless of BRCA1/BRCA2 status or deficiencies in HRR reported for these cell lines. Combination of Nutlin-3/RG7388 with cisplatin or rucaparib has synergistic and/or dose reduction potential dependent on cell genotype and the type of MDM2-p53 antagonist. Combined treatments using Nutlin-3/RG7388 and cisplatin led to greater levels of p53 stabilisation and upregulation of p21WAF1 and MDM2, and higher expression of p21WAF1 was associated with a greater synergistic effect for growth inhibition. In combination treatment with rucaparib and Nutlin-3/RG7388, rucaparib showed no increase in the effect of MDM2 inhibitors on the p53 pathway, indicating that the mechanism of observed synergy does not involve enhancement of p53 pathway activation by MDM2 inhibitors. Nutlin-3/RG7388 in combination with cisplatin or rucaparib resulted in changes in cell cycle distribution, SubG1 events and caspase 3/7 activity in a cell type, time and compound-dependent manner. The fold changes in expression of candidate genes in response to MDM2 inhibitors were less in A2780 cells than IGROV-1 and OAW42. The balance of activity between growth inhibitory/pro-survival and pro-apoptotic genes dominates a small increase in the expression of several DNA repair genes as an explanation for the synergy observed for treatment with cisplatin and MDM2 inhibitors. Conclusions: The genomic and functional status of TP53 have potentially important prognostic and predictive values in ovarian cancer. Targeting the interaction between MDM2 and p53 using MDM2-p53 antagonists is a promising therapeutic strategy for ovarian cancer patients with wild-type TP53 tumours, and combination treatment with them and cisplatin or rucaparib.
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5

Ait-Belkacem, Rima. "Caractérisation du glioblastome multiforme et suivi de ses chimiothérapies par imagerie MALDI couplée à l'approche top-down." Thesis, Aix-Marseille, 2014. http://www.theses.fr/2014AIXM5503.

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Le glioblastome est la forme la plus agressive des tumeurs du système nerveux central. Le traitement de référence consiste en l'exérèse chirurgicale, suivie d'une radiothérapie associée à une chimiothérapie concomitante et adjuvante par le témozolomide. Son bénéfice est démontré par une médiane de survie entre 12 et 14 mois. Le glioblastome est caractérisé par une population cellulaire hétérogène hautement infiltrante, angiogénique et résistante à la chimiothérapie. Dans le but d'optimiser l'effet des molécules thérapeutiques, un suivi de leur pharmacocinétique ainsi qu'une bonne caractérisation tumorale sont nécessaires. L'imagerie par désorption laser assistée par matrice en spectrométrie de masse (IMS MALDI) a été utilisée pour l'identification de marqueurs diagnostiques, pronostiques et prédictifs de réponse aux traitements. Elle a aussi permis de suivre la pharmacocinétique in situ des chimiothérapies.L'identification de protéines directement sur tissu par fragmentation en source a permis la mise en évidence de différents isotypes de tubuline, une des cibles majeures en thérapie anticancéreuse. Le couplage de cette stratégie d'identification à l'imagerie MALDI a permis d'identifier et de localiser dans des zones tumorales, des protéines impliquées dans la tumorigenèse. La distribution intra-tissulaire du bévacizumab et du témozolomide a été étudiée pour la première fois.Des marqueurs de réponse aux traitements ont ensuite été identifiés par comparaison des profils d'expression protéique de tumeurs avec et sans traitement. Ces résultats montrent l'intérêt de l'imagerie MALDI pour l'étude des chimiothérapies et permettent d'envisager son utilisation clinique future
Glioblastoma is the most aggressive of the gliomas, a collection of tumors arising from glia or their precursors within the central nervous system. The current standard of care, comprised of surgical resection followed by radiation and the chemotherapeutic agent temozolomide, only provides patients with a 12-14 months survival period post-diagnosis. The glioblastoma is characterized by a heterogeneous population of cells that are highly infiltrative, angiogenic and resistant to chemotherapy. In order to optimize the therapy effect, a pharmacokinetic monitoring and a better understanding and characterization of tumor biology are needed. For this purpose, matrix assisted laser desorption/ionization imaging mass spectrometry imaging mass spectrometry (MALDI IMS) technology was applied to identify diagnostic, prognostic and predictive markers of therapy response; and to understand/follow the pharmacokinetic of chemotherapies. The top-down in-source decay strategy was used for protein identification directly on tissue. This strategy allowed tubulin protein isoforms distinction and identification, which is one of the main targets in cancer therapy. MALDI imaging coupled to ISD identified tumorigenesis proteins within tumor structures. Bevacizumab and temozolmide distribution was followed within brain tissue sections. For the first time a monoclonal antibody was deciphered on tissue. Finally, markers that predict therapy response were demonstrated by a comparison between protein expression profiles from tumors with and without chemotherapy treatment. These results highlight the interest of MALDI imaging for chemotherapy improvement and open the way for its use in the clinics
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6

Hendlisz, Alain. "Multimodality imaging for treatment response prediction in colorectal cancer." Doctoral thesis, Universite Libre de Bruxelles, 2015. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209109.

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L’hypothèse prédominante de cette thèse est que les changements métaboliques tumoraux mesurés par FDG-PET/CT sous l’influence des traitements anticancéreux, apparaissent plus précocement et parfois exclusivement par rapport aux modalités d’imagerie morphologique classique. L’imagerie multimodale, en combinant les avantages de chacune des techniques, dépasse leur limitations et pourrait permettre (i) une évaluation du bénéfice du traitement plus rapide et plus adéquate ;(ii) de modifier les algorithmes thérapeutiques à différents stades de cancer colorectal et (iii) d’améliorer la compréhension des mécanismes d’échappement aux traitements anticancéreux. Pour évaluer l’apport de l’imagerie multimodale dans l’évaluation de la réponse au traitement des cancers colorectaux (CCR), nous avons poursuivi 3 séries d’expérimentation cliniques.

1) Le premier projet explore l’imagerie multimodale comme un outil d’individualisation pour la radio-embolisation (microsphères chargées en 90Yttrium) chez des patients porteurs d’un CCR métastatique au niveau du foie, pour laquelle l’imagerie morphologique classique est incapable de mesurer l’effet thérapeutique. Nous montrons que l’usage non sélectif de la radio-embolisation améliore l’histoire clinique de ces patients, bien que certains d’entre eux ne semblent pas en bénéficier. Ensuite, par une analyse multimodale lésion par lésion intégrant angiographie-CT Scan, FDG-PET/CT et scintigraphie aux macro-agrégats d’albumine marqués au 99mTechnetium, nous démontrons que la distribution pré-thérapeutique des macro-agrégats d’albumine est hétérogène entre les différentes lésions des patients et prédictive de la réponse métabolique au sein de ces lésions, permettant le développement d’un outil de prédiction et de planification pour la radio-embolisation.

2) Le deuxième projet explore le domaine du CCR métastatique traité par chimiothérapie palliative. (i) Nous démontrons d’abord que la réponse métabolique (RM) tumorale après une cure de chimiothérapie cytolytique prédit plus vite et plus adéquatement que l’imagerie morphologique basée sur les critères RECIST les bénéfices cliniques du traitement. La RM précoce a une excellente valeur prédictive négative sur l’absence de réponse morphologique et met en évidence une variabilité de réponse inter-lésionnelle chez une proportion importante des patients. (ii) L’étude SoMore explore ensuite des patients présentant un CCR avancé et réfractaire, traités par capecitabine et sorafenib, et confirme l’importance pronostique des RM mixtes, suggérant une méthodologie de classification clinique basée sur la consistance de la RM. (iii) Cette classification cherche confirmation dans l’étude RegARd-C, encore en cours, évaluant les effets du regorafenib, et explorant également la signification génomique et épigénétique de la variabilité de RM.

3) Le troisième projet cherche à utiliser les propriétés de l’imagerie métabolique pour modifier l’algorithme de traitement adjuvant des patients porteurs d’un cancer du côlon de stade III. Ce projet, encore en cours, fait l’hypothèse que l’absence de RM de la lésion primitive après une cure de chimiothérapie prédit l’absence de bénéfice du traitement adjuvant complet. Une analyse intérimaire en démontre la faisabilité et confirme la présence de 40% de tumeurs présentant des caractéristiques métaboliques de chimio-résistance.

En conclusion, pour des patients porteurs d’un CCR, l’imagerie multimodale comprenant une évaluation du métabolisme tumoral permet une évaluation plus précoce et plus adéquate du bénéfice au traitement anticancéreux pour différentes modalités thérapeutiques comme la radio-embolisation, la chimiothérapie cytotoxique et les agents biologiques. L’imagerie multimodale permet de prédire et planifier les radio-embolisations et se révèle très prometteuse pour les traitements chimiothérapiques cytotoxiques ou combinés à des biologiques en situation adjuvante ou métastatique. Elle démontre par ailleurs une importante variabilité de réponse métabolique inter-lésionnelle qui représente un axe de recherche majeur sur les mécanismes moléculaires d’hétérogénéité génomique tumorale et de résistance aux traitements anti-cancéreux.


Doctorat en Sciences médicales
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7

Ferraioli, Domenico. "Assessment and relevance of the putative DNA/RNA helicase Schlafen-11 in ovarian and breast cancer." Thesis, Lyon, 2019. http://www.theses.fr/2019LYSE1324/document.

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Schlafen 11 (SLFN11) est une ADN/ARN hélicase décrite pour la première fois pour son rôle dans le développement et la différenciation des thymocytes chez la souris. Elle fait partie d'une famille de protéines présentant divers degrés d'homologie entre les espèces, mais qu’est présente de façon constante chez les mammifères. Le rôle de cette ADN/ARN hélicase, SLFN11, a été associé de façon causale à la sensibilité de réponse aux différents agents alkylants (agents endommageant l'ADN, les inhibiteurs de topo-isomérase I et II) dans le NCI-60. Dans la première étude, nous avons développé un protocole d’immunohistochimie (IHC) sur des biopsies paraffinées de carcinome séreux de l'ovaire de haut grade (HGSOC), afin de valider un anticorps (Ab) anti-SLFN11 et d’en déterminer l'expression. En IHC, nous avons testé et validé un Ab anti-SLFN11, en choisissant entre deux anti-SLFN11 Ab utilisés normalement pour le Western Blot. Premièrement, il a été développé dans une culture cellulaire (CCB) de HGSOC et, successivement, dans une série indépendante de micro-array (TMA) de HGSOC. Pour chaque cas, nous avons évalué soit le score d'intensité (IS) que le score de distribution (DS) en évaluant au moins 300 cellules. Un score histologique (HS) a été obtenu comme suit : HS=IS x DS. Successivement, nous avons appliqué notre protocole à une plus large série d'échantillons de HGSOC pour confirmer nos résultats préliminaires. Nous avons trouvé un anticorps fiable dans les séries CCB et TMA permettant de déterminer l'expression IHC de SLFN11. Ces résultats ont été confirmés dans notre plus large série de HGSOC. Brièvement, comme pour les séries indépendantes de TMA, nous avons constaté que la HS de l'expression de SLFN11 est présente dans environ 60%. En parallèle, le SLFN11 n'a pas été exprimé dans 40 % des cas qui, cliniquement, correspondent, dans environ 60 % de ces cas (16/27), aux patients résistant aux sels de platine. Une faible expression de SLFN11 en IHC pourrait être corrélée à la réponse à la chimiothérapie(CT) à base de platine. Dans la deuxième étude, nous étudions l’état transcriptionnel du SLFN11 dans le cancer du sein en effectuant une méta-analyse de plus de 7000 cas à partir de 35 étudies publiquement disponibles. Par l’analyse de corrélation, nous avons identifié 537 transcrits qui corrèle, au-delà du 95e percentile selon le coefficient de Pearson, avec l’expression de SLFN11. En particulier, voie l’analyse par “Gene Ontology” SLFN11 est lié au transcrits impliqués dans le système immunitaire : "réponse immunitaire", "l’activation lymphocytaire" et "l’activation des lymphocytes T". En outre, voie le “likehood lasso regression ”, nous avons signalé une très forte association entre le SLFN11 et les signatures immunitaires dans le cancer du sein. Enfin, grâce à la “multiple corresponded analysis ”, nous avons découvert un sous-groupe de patients, défini "SLFN11-Hot cluster", caractérisé par une expression élevé de SLFN11, récepteurs d'œstrogènes(ER) négatives, un phénotype basal, un jeune âge, une signature élevée de CD3D et de STAT1. En utilisant la "Cox proportional hazard regression", l’expression élevé de SLFN11, l’indice de prolifération élevé et le ER négative sont des paramètres indépendants lié à la survie sans maladie chez les patients soumises à la CT. Notre deuxième travail decrit un rôle spécifique pour le SLFN11 dans le cancer du sein probablement en relation avec la modulation du système immunitaire et une forte corrélation entre l’expression de SFLN11 et un sous-type moléculaire spécifique de cancer du sein (récepteurs négatifs aux œstrogènes, phénotype de type basal). Autres études devront être réalisées afin de: 1) mieux comprendre la fonction du SLFN11 dans les cellules cancéreuses, 2) valider un protocole IHC fiable et standardisé pour évaluer l’expression de SLFN11, 3) utiliser SFLN11 comme biomarqueur prédictif de réponse aux DDA et PARP inhibiteurs et 4) établir sa relation avec le système immunitaire
Schlafen 11 (SLFN11) is a putative DNA/RNA helicase, first described for its role in thymocyte development and differentiation in mouse models. SLFN11 is part of a family of proteins with various degree of homology across species, but intriguingly being consistently present only in vertebrates and especially in mammals. Recently, the role of this putative DNA/RNA helicase, SLFN11, was causally associated with sensitivity to DNA damaging agents, such as platinum salts, topoisomerase I and II inhibitors, and other alkylators in the NCI-60 panel of cancer cell lines. In the first study, we validate an anti-SLFN11 antibody in formalin-fixed paraffin-embedded (FFPE) high-grade serous ovarian carcinoma (HGSOC) samples, developing an immunohistochemistry (IHC) protocol in order to determinate the expression of SLFN11 in our series of HGSOC. Indeed, we tested and validated a reliable SLFN 11 antibody (Ab) in IHC choosing between two anti-SLFN11 Ab used normally for Western Blot (WB) in culture cell block (CCB) of ovarian carcinoma and in an independent series of HGSOCs tissue micro-array (TMA). For each case, we evaluated both the Intensity Score (IS) and the Distribution Score (DS) evaluating at least 300 cells. A Histological Score (HS)was obtained as follow: HS=IS x DS. Successively, we applied our protocol to a large case series of HGSOC samples to confirm our preliminary results. We found one antibody to be reliable in CCB and TMA series allowing to determinate clearly IHC expression of SLFN11. These results were confirmed in our large case series of FFPE HGSOC samples. Briefly, as for TMA independent series, we found that the HS for SLFN11 expression presents a normal distribution with a prevalent (≈ 60%) intermediate expression. Parallel SLFN11 was not expressed in practically 40% of cases that clinically corresponded to the platinum resistant patients in about 60% of cases (16/27). So, we believe that low IHC expression of SLFN 11 should be correlated to response to the platinum-based chemotherapy. In the second study, we investigate the transcriptional landscape of SLFN11 in breast cancer performing a gene expression microarray meta-analysis of more than 7000 cases from 35 publicly available data sets. By correlation analysis, we identified 537 transcripts in the top 95th percentile of Pearson’s coefficients with SLFN11 identifying “immune response”, “lymphocyte activation” and “T cell activation” as top Gene Ontology enriched processes. Furthermore, we reported very strong association of SLFN11 with immune signatures in breast cancer through penalized maximum likelihood lasso regression. Finally, through multiple corresponded analysis we discovered a subgroup of patients, defined “SLF11-hot cluster”, characterized by high SLFN11 levels, estrogen receptor(ER) negativity, basal-like phenotype, elevated CD3D, STAT1 signature, and young age. Using Cox proportional hazard regression, we characterized that SLFN11 high levels, high proliferation index, and ER negativity are independent parameters for longer disease-free interval in patients undergoing chemotherapy. We believe that our second work supports proof of concept that: i) A clear and specific role for SLFN11 in breast cancer, in likely connection with the immune system modulation in such disease entity, ii) a strong correlation between high SFLN 11 and specific molecular subtype of breast cancer (estrogen receptor negativity, basal-like phenotype). Further studies will be performed to confirm our hypothesis in order to: 1) better understand the function of SLFN 11 in cancer cell, 2) validate an easy, reliable and standardized IHC protocol to assessment SLFN11, 3) use SFLN11expression as a predictive biomarker of response to DDA and PARP inhibitors and 4) determinate the relationship with immune system
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Nelmes, David-John. "Genetic biomarkers of chemotherapy response and resistance in lung cancer patients." Thesis, Cardiff University, 2018. http://orca.cf.ac.uk/109686/.

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In advanced lung cancer, careful selection of systemic anticancer therapy (SACT) is of vital importance. Companion biomarkers can optimise treatment selection, such as with the use of EGFR tyrosine kinase inhibitors (EGFR TKi) in patients with EGFRmut+ve adenocarcinoma of the lung. There is increasing interest in mutation detection and monitoring, in circulating cell free tumour DNA (ctDNA). This thesis reports that Next Generation Sequencing (NGS) with software VarScan with Annovar, can detect mutations at a 10-fold lower alternate allele frequency compared to alternative software available through Ion Torrent, but with a greater number of low level ‘false positive’ genetic variants. Droplet digital PCR (ddPCR) is more sensitive than NGS, successfully detecting mutations as low as 0.1% alternate allele frequency. Lung cancer mutations were successfully detected in small, formalin-fixed, paraffin embedded (FFPE) tumour tissue samples, and ctDNA, from lung cancer patients, using the same NGS technique, with a commercially available, targeted 50 gene cancer hotspot panel. Results are compared to a custom 22-gene panel. The kinetics of mutation levels in serial ctDNA samples is reported in a case series. In EGFRmut+ve lung adenocarcinoma patients treated with EGFR TKi, decreases in levels of mutant EGFR in ctDNA were observed. Levels remained undetectable during periods of disease control/stability, and increases in mutant EGFR in ctDNA were seen several weeks before the diagnosis of clinical or radiological disease progression. NGS of ctDNA during disease progression revealed novel genetic mutations that were not detected in the original tumour biopsy, and may inform subsequent treatment options. Similar ctDNA kinetics was seen in advanced SCLC patients treated with SACT. The levelof mutated ctDNA, at diagnosis may be an independent prognostic biomarker, using a cut-off of 44.3% alternate allele frequency. SCLC patients who experienced a greater absolute decrease in mutant ctDNA had a poorer prognosis.
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Bolze, Pierre-Adrien. "Recherche de biomarqueurs prédictifs de l’évolution et de la réponse au traitement dans les maladies trophoblastiques gestationnelles." Thesis, Lyon, 2019. http://www.theses.fr/2019LYSEN016.

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Les môles hydatiformes sont une prolifération placentaire prétumorale pouvant évolueren tumeur alors traitée par chimiothérapie. Afin de réduire la mortalité et d’optimiser laprise en charge thérapeutique, l’objectif de cette thèse est d’identifier les gènespermettant de prédire la transformation en tumeur post môlaire et la chimiorésistance.Concernant la prédiction de la transformation, l’analyse de l’expression de gènescandidatssur tissu molaire décrit la relocalisation apicale de la Syncytine-1 en cas detransformation maligne, sans modification de transcription de ses récepteurs ni de deuxautres enveloppes rétrovirales placentaires. L’analyse sans à priori du transcriptome par3 méthodes différentes n’a pas permis d’identifier de gène différentiellement expriméselon la transformation. Cela suggère que la variabilité interindividuelle et les diverscritères utilisés pour le diagnostic de tumeur nuisent à l’identification de biomarqueursrobustes.Concernant la prédiction de la chimiorésistance, une approche transcriptomique largespectre sur tissu tumoral de choriocarcinome identifie une réduction de transcriptiond’HLA-G en cas de monochimiorésistance, confirmée au niveau protéique par immunohistochimie. L’analyse en réseaux de l’ensemble des gènes différentiellementexprimés suggère que la monochimiorésistance est associée à une altération de ladifférenciation des lymphocytes T alors que la polychimiorésistance est associée à unealtération de la prolifération des cellules sanguines.In fine, l’objectivation de l’expression trophoblastique du point de contrôle PD-L1 aconduit à évaluer l’efficacité d’un anti PD-L1 chez les patientes chimiorésistantes. Lesrésultats encourageants de cet essai et la possibilité de stratifier les patientes à l’aidedes marqueurs HLA-G et Syncytine-1 incitent à évaluer la place de l’anti PD-L1 associéà une monochimiothérapie en première ligne de traitement des tumeurstrophoblastiques
Hydatidiform moles are a pretumoral placental proliferation which can turn into a tumorrequiring chemotherapy. In order to reduce mortality and propose an optimal therapeuticmanagement, the aim of this thesis is to identify genes which are predictive of postmolartumor transformation and chemoresistance.Concerning the prediction of transformation, the expression analysis of candidate-geneson molar tissue shows a relocalization of Syncytin-1 at the syncytiotrophoblast apicalborder in moles followed by malignant transformation, without modification oftranscription of its receptors and two other retroviral placental envelopes. A wholetranscriptomeapproach using 3 different microarrays-based methods did not identify anydifferentially expressed gene according to the post molar evolution. This may reflect thatinter-individual variability and the different criteria used for tumor diagnosis impede theidentification of robust biomarkers.Concerning the prediction of chemoresistance, a broad-spectrum transcriptomicapproach on choriocarcinoma tumor tissue identifies a down regulation of HLA-G in case of monochemoresistance, confirmed at the protein level by immunohistochemistry.Pathway analysis of the differentially expressed genes suggests thatmonochemoresistance is associated with impaired T-cell differentiation, whereaspolychemoresistance is associated with impaired proliferation of blood cells.Ultimately, the evidence of trophoblastic ubiquitous expression of the PD-L1 immunecheckpoint led us to the evaluation of the efficacy of PD-L1 blockade in chemoresistantpatients. The encouraging results of this trial and the possibility of stratifying patientswith HLA-G and Syncytin-1 markers encourages the assessment of PD-L1 blockadecombined with monochemotherapy as a first line treatment for trophoblastic tumors
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Hodgkinson, Victoria C. "The identification of biomarkers of chemotherapy resistance in breast cancer using comparative proteomics." Thesis, University of Hull, 2011. http://hydra.hull.ac.uk/resources/hull:5275.

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Background:Chemotherapy resistance is a major obstacle in effective neoadjuvant treatment for locally advanced breast cancer. The ability to predict tumour response would allow chemotherapy administration to be directed towards only those patients who would benefit, thus maximising treatment efficiency. This project aimed to identify predictive protein biomarkers associated with chemotherapy resistance, using proteomic analysis of fresh breast cancer tissue samples. Materials and Methods:Chemotherapy-sensitive (CS) and chemotherapy-resistant (CR) tumour samples were collected from breast cancer patients who received neoadjuvant therapy consisting of epirubicin with cyclophosphamide followed by docetaxel. Comparative proteomic analysis was performed, to identify differentially expressed proteins (DEPs) between CS and CR invasive ductal carcinoma samples, using 2-dimensional polyacrylamide gel electrophoresis (2D-PAGE) with MALDI-TOF/TOF mass spectrometry and antibody microarray analysis. DEPs were submitted to Ingenuity Pathway Analysis (IPA) to identify any canonical pathway links, confirmed using western blotting and clinically validated in a pilot series of archival breast cancer samples, from patients treated with neoadjuvant chemotherapy. Results:Five datasets were generated by antibody microarray analysis, revealing 38 targets. Of these, 7 DEPs were identified in at least 2 datasets and these included 14-3-3 theta/tau, BID and Bcl-xL. Three datasets were generated using 2D-PAGE with MALDI-TOF/TOF MS, containing 132 unique DEPs. These included several isoforms of 14-3-3 proteins. The differential expression of 14-3-3, BID and Bcl-xL was confirmed by immunoblotting in samples used for the discovery phase. Clinical validation using immunohistochemical analysis of archival breast cancers revealed 14-3-3 theta/tau and tBID to be significantly associated with chemotherapy resistance. Discussion:The use of comparative proteomic techniques using fresh clinical tumour samples, for the search for putative biomarkers of chemotherapy resistance has been successful. Two DEPs; 14-3-3 theta/tau and tBID have passed through all stages of the biomarker discovery pipeline, and present themselves as putative predictive biomarkers of neoadjuvant chemotherapy resistance in breast cancer.
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Books on the topic "Chemotherapy biomarker"

1

Kim, Kŏn-hong. Yubangam ŭi taje yangmul naesŏng saengchʻe chipʻyo palgul mit kŭ yuyongsŏng kŏmjŭng =: Identification of biomarkers for multidrug resistance and validation of markers in breast cancer tissue. [Seoul]: Sikpʻum Ŭiyakpʻum Anjŏnchʻŏng, 2007.

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Galderisi, Maurizio, Juan Carlos Plana, Thor Edvardsen, Vitantonio Di Bello, and Patrizio Lancellotti. Cardiac oncology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0064.

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Cancer therapeutics may induce cardiac damage in the left and the right ventricle. Radiotherapy most frequently induces valvular damage, carotid stenosis, and coronary artery disease. Pericardial disease may be due to both chemo- and radiotherapy. The manifestations of both chemo- and radiotherapy can develop acutely but also become overt years after their performance, in particular after radiotherapy. The main cardiac damage of cancer therapeutics-related cardiac dysfunction (CTRCD) corresponds to the reduction of left ventricular (LV) systolic function. The Expert Consensus document from ASE and EACVI has defined CTRCD as a decrease in LV ejection fraction (LVEF) of greater than 10 percentage points, to a value less than 53%. The accurate calculation of LVEF at baseline and during follow-up is extremely important. The assessment of LV longitudinal function, in particular of speckle tracking-derived global longitudinal strain (GLS), can provide additional information, allowing early, subclinical detection of CTRCD. The ideal strategy could be to compare the measurements of GLS obtained during chemotherapy, with the one obtained at baseline. An integrated approach with the use of echocardiography at standardized, clinical preselected intervals with biomarker (ultrasensitive troponin) assessment prior to each chemotherapy cycle could be suggested in patients at high risk of CTRCD. Follow-up after therapy should depend on the type of chemotherapy/radiotherapy and the presence/absence of on-therapy CTRCD. Long-term follow-up should be planned after radiotherapy.
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Prati, Raquel, and Olga Olevsky. Breast Cancer Staging and Treatment. Edited by Christoph I. Lee, Constance D. Lehman, and Lawrence W. Bassett. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190270261.003.0012.

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Breast carcinomas are a heterogeneous group of diseases that can be further characterized based on their histology, biomarkers, and molecular profiles. These characteristics, gathered during disease staging, provide crucial information with regard to treatment decisions. Staging has evolved from informing the operability of breast tumors to providing prognostic information, and consequently helping establish local and systemic treatment guidelines. This chapter provides a succinct overview of breast cancer staging and treatment. Topics covered include the histological classification of breast cancers, as well as classification by tumor size and location, lymph node involvement, and metastatic involvement. The topic of molecular assays for prognostic information is reviewed. Finally, current treatment paradigms, including surgery, radiation, and chemotherapy regimens for different types of breast cancer, are discussed.
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Book chapters on the topic "Chemotherapy biomarker"

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Ecke, Thorsten H. "Biomarker in Cisplatin-Based Chemotherapy for Urinary Bladder Cancer." In Advances in Cancer Biomarkers, 293–316. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-7215-0_18.

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Marti, Francisca E., and Mark P. Saunders. "Chemotherapy and Biomarkers." In Contemporary Coloproctology, 187–200. London: Springer London, 2011. http://dx.doi.org/10.1007/978-0-85729-889-8_14.

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Laurent-Puig, Pierre, Thierry Lecomte, Marie-Anne Loriot, Valerie Boige, and Helene Blons. "Prediction of Chemotherapy Toxicities." In Biomarkers in Oncology, 249–73. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-9755-5_10.

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Chotai, Niketa, and Supriya Kulkarni. "Neoadjuvant Chemotherapy and Biomarkers." In Breast Imaging Essentials, 111–23. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-1412-8_15.

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Stanisz, Hedwig, Thomas Vogt, and Knuth Rass. "Chemotherapy for Melanoma." In Diagnostic and Prognostic Biomarkers and Therapeutic Targets in Melanoma, 247–63. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-60761-433-3_19.

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Beyaert, Simon, and Jean-Pascal Machiels. "Is there a Role for Neoadjuvant Targeted Therapy and Immunotherapy?" In Critical Issues in Head and Neck Oncology, 193–203. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_13.

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AbstractNeoadjuvant chemotherapy in head and neck cancer is the subject of much debate. Multiple trials have shown that the concomitant addition of targeted therapies, such as cetuximab to neoadjuvant chemotherapy (docetaxel, cisplatin, 5-fluorouracil), results in increased toxicity. Furthermore, no apparent significant benefit has been demonstrated in small randomized studies. Additional trials are currently being conducted to investigate the role of neoadjuvant immunotherapy, such as anti-PD-(L)1 inhibitors.On the other hand, window of opportunity studies are trials in which patients receive one investigational compound in the period between their cancer diagnosis and the start of standard therapy. The evaluation of new compounds using this approach enables translational research and provides information on molecular and clinical activity as well as predictive biomarkers.
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Stearns, Vered. "Predictive Value of c--erb-B2 for Endocrine Therapy and Chemotherapy in Breast Cancer." In Biomarkers in Breast Cancer, 129–57. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1385/1-59259-915-x:129.

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Castaneda, Carlos A. "Molecular and Cellular Analyses of Breast Cancers in Real Life." In Improving Oncology Worldwide, 75–82. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-96053-7_10.

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AbstractBreast cancer is the most common women’s malignancy. Incorporation of biomarkers of prognosis and prediction of response are needed to improve treatment management. Lectures for immunohistochemistry of estrogen, progesterone, and HER2 receptors as well as Ki67 staining in cancer cells have been incorporated, and their positive cutoffs have periodically been reviewed. Gene expression platforms in tumor lesions as well as germline and somatic mutations have also been included in the practice for treatment selection. Liquid biopsy evaluating circulating tumor cells (CTCs) and circulating DNA can also predict survival and has reached the clinical practice, although it needs better standardization. On the other side, biomarkers can also evaluate stroma cells in the tumor microenvironment, and they can predict survival and response to chemotherapy and targeted treatment. They have been incorporated in the daily practice, and new methodologies for obtaining more information are currently being developed.
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Rischin, Danny. "Biomarkers for Immune Modulatory Treatment in Head and Neck Squamous Cell Carcinoma (HNSCC)." In Critical Issues in Head and Neck Oncology, 83–91. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_6.

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AbstractImmune checkpoint inhibitors have changed the standard of care for recurrent/metastatic head and neck squamous cell carcinoma (R/M HNSCC). However, only a minority of patients respond, hence the search for predictive biomarkers. Potential predictive biomarkers for immune checkpoint inhibitors discussed in this chapter include (1) Immune checkpoint ligand expression e.g., PD-L1, (2) biomarkers of a T-cell inflamed tumour microenvironment (TME) such as gene expression profiles of activated T cells, (3) biomarkers of tumour neoepitope burden such as tumour mutation burden (TMB) and (4) multidimensional quantitative techniques. At present only PD-L1 expression has been shown to have clinical utility in head and neck cancer. It enriches for populations more likely to respond, but the false positive predictive value remains high. In the pivotal Keynote−048 trial that established a role for pembrolizumab (anti-PD1) monotherapy and pembrolizumab + chemotherapy as treatment options in first-line R/M HNSCC, primary endpoints included overall survival in defined subgroups based on PD-L1 expression. In this trial the combined positive score (CPS) was used which takes into account PD-L1 expression in tumour and immune cells. Based on this trial regulatory approvals for first-line pembrolizumab in R/M HNSCC require assessment of PD-L1 expression using the CPS. Finally we discuss emerging evidence that locoregionally advanced HPV-associated oropharyngeal cancers that have high expression of CD103 positive CD8 T cells have an excellent prognosis and features that suggest increased probability of responding to anti-PD1/PD-L1, raising the possibility of incorporating these immune therapies as part of a de-escalation trial strategy.
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Issing, Wolfgang J. "Micronutrients as Intermediate Biomarkers in Chemotherapy and Enhancement for Cancer Treatments." In Primary and Secondary Preventive Nutrition, 55–72. Totowa, NJ: Humana Press, 2001. http://dx.doi.org/10.1007/978-1-59259-039-1_4.

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Conference papers on the topic "Chemotherapy biomarker"

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Takeoka, Tomohira, Kumiko Goto, Mitsunobu Matsumoto, Yasuhiro Miyazaki, Tomoki Makino, Tsuyoshi Takahashi, Yukinori Kurokawa, et al. "Abstract B135: Chemotherapy for esophageal cancer: Off-target effect and biomarker." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-b135.

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Gao, ChongFeng, Luke Wisniewski, Ying Liu, Ben Staal, Ian Beddows, Dennis Plenker, Mohammed Aldakkak, et al. "Abstract PO-002: Detection of chemotherapy-resistant pancreatic cancer using a glycan Biomarker." In Abstracts: AACR Virtual Special Conference on Pancreatic Cancer; September 29-30, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.panca20-po-002.

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Vodicka, Pavel E., Ludmila Vodickova, Miroslav Svoboda, Jana Slyskova, Barbara Pardini, Alessio Naccarati, and Kari Hemminki. "Abstract 4578: Excision DNA repair: a biomarker of colorectal cancer onset and its chemotherapy." 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.am2015-4578.

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Kiechle, Marion, Gabriele Schricker, Rudolf Napieralski, Michaela Aubele, Gert Auer, Kurt Ulm, Jonathan Perkins, Stefan Paepke, Moritz Hamann, and Olaf G. Wilhelm. "Abstract P3-08-65: PITX2 DNA methylation: A prognostic/predictive biomarker for anthracycline-based chemotherapy." In Abstracts: 2019 San Antonio Breast Cancer Symposium; December 10-14, 2019; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-p3-08-65.

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Kwon, Chae Hwa, Sun Jin Lee, Yuri Choi, and Do Youn Park. "Abstract 3365:MAP3K10mutation as a biomarker for predicting response to chemotherapy in gastric cancer patients." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3365.

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Sohn, Joohyuk, Shuyling Liu, Huiqin Chen, Xiaolong Meng, Kim-Anh Do, Gordon B. Mills, Gabriel N. Hortobagyi, Funda Meric-Bernstam, and Ana M. Gonzalez-Angulo. "Abstract 162: Biomarker identification of residual triple negative breast cancer (TNBC) after standard neoadjuvant chemotherapy (NCT)." 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.am2012-162.

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Pataer, Apar, Ruping Shao, Arlene M. Correa, Ignacio I. Wistuba, and Stephen G. Swisher. "Abstract 4527: Major pathologic response and biomarker predict survival in lung cancer patients receiving neoadjuvant chemotherapy." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4527.

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Gowrikumar, Saiprasad, Kristina Pravoverov, Caroline Selisteda, Kiran D. Bastola, Steven Chen, Joshua J. Smith, Mary K. Washington, Amar B. Singh, and Punita Dhawan. "Abstract 3126: A novel biomarker signature in predicting chemoresistance in colorectal cancer: Potential application in chemotherapy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3126.

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Gowrikumar, Saiprasad, Kristina Pravoverov, Caroline Selisteda, Kiran D. Bastola, Steven Chen, Joshua J. Smith, Mary K. Washington, Amar B. Singh, and Punita Dhawan. "Abstract 3126: A novel biomarker signature in predicting chemoresistance in colorectal cancer: Potential application in chemotherapy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3126.

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van Rossum, AGJ, PC Schouten, KE Weber, V. Nekljudova, C. Denkert, G. von Minckwitz, T. Karn, et al. "Abstract P3-07-28: BRCA1-like profile as predictive biomarker in non myeloablative chemotherapy (GAIN study)." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p3-07-28.

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Reports on the topic "Chemotherapy biomarker"

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Wang, He, Jun Chen, Xiaoling Wang, and Jun Dang. Neoadjuvant immune checkpoint inhibitor in combination with chemotherapy or chemoradiotherapy in resectable esophageal cancer: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0052.

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Review question / Objective: It remains unclear whether addition of immune checkpoint inhibitor (ICI) to neoadjuvant chemoradiotherapy (nCRT) or neoadjuvant chemotherapy (nCT) can increase antitumor efficacy in resectable esophageal cancer (EC). we performed the systematic review and meta-analysis to assess antitumor efficacy and safety of nICRT and nICT, and made a comparison with nCRT and nICT. We used pathological complete response (pCR) as the primary outcomes of interest. Condition being studied: Initial findings from a number of phase 1 or 2 trials have supported the tolerability and/or antitumor efficacy of ICI plus nICRT (nICRT) and nICT (nICT). However, the superiority of this combination strategy remains uncertain due to lack of randomized control trials (RCTs) with long-term outcomes. Moreover, there are still outstanding questions such as the selection of nICRT or nICT, the ideal predictive biomarkers, and timing of surgical resection.
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