Статті в журналах: "Minimal Residual Disease Detection"

1

MORITA, KIMIO. "Detection of Minimal Residual Disease." KITAKANTO Medical Journal 48, no. 3 (1998): 229–31. http://dx.doi.org/10.2974/kmj.48.229.

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2

Hangenbeek, A. "Detection of minimal residual disease." Current Diagnostic Pathology 1, no. 4 (December 1994): 240. http://dx.doi.org/10.1016/0968-6053(94)90021-3.

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3

Carlo-Stella, Carmelo, Lina Mangoni, Gian Pietro Dotti, and Vittorio Rizzoli. "Techniques for Detection of Minimal Residual Disease." Leukemia & Lymphoma 18, sup1 (January 1995): 75–80. http://dx.doi.org/10.3109/10428199509075308.

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4

Katz, F. E. "Detection of minimal residual disease in leukaemia." Archives of Disease in Childhood 67, no. 6 (June 1, 1992): 671–73. http://dx.doi.org/10.1136/adc.67.6.671.

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5

Weitz, J�rgen, and Christian Herfarth. "Surgical strategies and minimal residual disease detection." Seminars in Surgical Oncology 20, no. 4 (2001): 329–33. http://dx.doi.org/10.1002/ssu.1051.

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6

Eldessouki, Ihab A., Ola Khorshid, Eman Kandeel, and Nasr Lahloubi. "Minimal Residual Disease In Adult AML." Blood 122, no. 21 (November 15, 2013): 4969. http://dx.doi.org/10.1182/blood.v122.21.4969.4969.

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Abstract Background The achievement of complete hematologic remission (CR) is used as predictor for treatment response in patients with myeloid leukemia (AML).However <5% blasts in the bone marrow does not reflect the presence of tumor burden precisely. Minimal residual disease (MRD) in the first complete remission (CR1) may play a critical rule in assessment of treatment response and prediction of subsequent relapse. Patients and Methods Leukemia associated immunophenotyping (LAIP) for 73 patients with denovo AML monitored at diagnosis , day 14 and day28 post-induction by multiparametric flow cytometry (MFC). Results CR achieved in 60(82%) patients and 13(18%) patients did not. Among the 60(80%) patients who achieved CR 9 (15%) were MRD negative and 51(85%) were MRD positive at day14. Significant association between MRD detection and disease free survival (DFS) using 0.01% cut off value (P=.015). Day 28 post induction show highly significant association between MRD and DFS using 0.01% cut off value (P=0.001) as 38(63%) patients were MRD negative and (27%) were positive. Significant association between MRD detection and overall survival (50 month) at day 14 and day 28 (P=0.02, P=0.001) respectively using cut off value 0.01%. MRD was positive in 63(86%) at day 14 and (37%) at day 28. Conclusion MRD detection at day28 and d14 at the end of induction in patients in CR may have a prognostic significance on clinical outcome and may thus be a useful marker for risk stratification. Disclosures: No relevant conflicts of interest to declare.

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7

Chudacek, Josef, Tomas Bohanes, Jiri Klein, Andrea Benedikova, Josef Srovnal, Marek Szkorupa, Pavel Skalicky, Jozef Skarda, Marian Hajduch, and Cestmir Neoral. "Detection of minimal residual disease in lung cancer." Biomedical Papers 158, no. 2 (June 23, 2014): 189–93. http://dx.doi.org/10.5507/bp.2013.019.

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8

Andreani, Giacomo, and Daniela Cilloni. "Strategies for minimal residual disease detection: current perspectives." Blood and Lymphatic Cancer: Targets and Therapy Volume 9 (February 2019): 1–8. http://dx.doi.org/10.2147/blctt.s172693.

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9

Sausville, Justin E., Rita G. Salloum, Lynn Sorbara, Douglas W. Kingma, Mark Raffeld, Robert J. Kreitman, Paula D. Imus, David Venzon, and Maryalice Stetler-Stevenson. "Minimal Residual Disease Detection in Hairy Cell Leukemia." American Journal of Clinical Pathology 119, no. 2 (February 2003): 213–17. http://dx.doi.org/10.1309/g6299513nglcub1k.

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10

Paietta, Elisabeth. "Leukemia and Lymphoma: Detection of Minimal Residual Disease." Medical Oncology 20, no. 3 (2003): 307–10. http://dx.doi.org/10.1385/mo:20:3:307.

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11

Rothberg, Paul G. "Leukemia and Lymphoma: Detection of Minimal Residual Disease." Leukemia Research 27, no. 11 (November 2003): 1068. http://dx.doi.org/10.1016/s0145-2126(03)00064-x.

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12

Kruse, Abdel-Azim, Kim, Ruan, Phan, Ogana, Wang, et al. "Minimal Residual Disease Detection in Acute Lymphoblastic Leukemia." International Journal of Molecular Sciences 21, no. 3 (February 5, 2020): 1054. http://dx.doi.org/10.3390/ijms21031054.

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Minimal residual disease (MRD) refers to a chemotherapy/radiotherapy-surviving leukemia cell population that gives rise to relapse of the disease. The detection of MRD is critical for predicting the outcome and for selecting the intensity of further treatment strategies. The development of various new diagnostic platforms, including next-generation sequencing (NGS), has introduced significant advances in the sensitivity of MRD diagnostics. Here, we review current methods to diagnose MRD through phenotypic marker patterns or differential gene patterns through analysis by flow cytometry (FCM), polymerase chain reaction (PCR), real-time quantitative polymerase chain reaction (RQ-PCR), reverse transcription polymerase chain reaction (RT-PCR) or NGS. Future advances in clinical procedures will be molded by practical feasibility and patient needs regarding greater diagnostic sensitivity.

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13

Radich, Jerry, and Blythe Thomson. "Advances in the detection of minimal residual disease." Current Opinion in Hematology 4, no. 4 (1997): 242–47. http://dx.doi.org/10.1097/00062752-199704040-00004.

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14

Sievers, Eric L., and Jerald P. Radich. "Detection of minimal residual disease in acute leukemia." Current Opinion in Hematology 7, no. 4 (July 2000): 212–16. http://dx.doi.org/10.1097/00062752-200007000-00003.

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15

SHARP, J. G., M. BISHOP, W. C. CHAN, T. GREINER, S. S. JOSHI, A. KESSINGER, E. REED, et al. "Detection of Minimal Residual Disease in Hematopoietic Tissues." Annals of the New York Academy of Sciences 770, no. 1 Bone Marrow T (December 1995): 242–61. http://dx.doi.org/10.1111/j.1749-6632.1995.tb31060.x.

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16

Moss, Thomas J. "Detection of Minimal Residual Disease in Autologous Grafts." ImmunoMethods 5, no. 3 (December 1994): 226–31. http://dx.doi.org/10.1006/immu.1994.1060.

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17

Druley, Todd E. "Novel Technologies to Detect Minimal Residual Disease." Blood 128, no. 22 (December 2, 2016): SCI—31—SCI—31. http://dx.doi.org/10.1182/blood.v128.22.sci-31.sci-31.

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Abstract The widespread use of ribonucleic acid (RNA) analysis as a measure of minimal residual disease (MRD) in leukemia has primarily been performed via real-time quantitative polymerase chain reaction (PCR) (RQ-PCR) for common translocations, insertions/deletions and duplications (e.g. FLT3-ITD, MLL-PTD). While RQ-PCR for known rearrangements can offer a limit of detection as low as 1:106, these make up a minority of the total leukemia cases. MLL-rearrangements are generally not amenable to RQ-PCR due to the many fusion partners and breakpoints in these translocations. The ability to use quantitative RNA sequencing (RNA-seq) for MRD assessment would enable detection of allele-specific gene expression, alternative splicing and cryptic splice forms in addition to common rearrangements. While a few institutions are performing reflexive genome, transcription and methylome sequencing for cancer patients, standard RNA-seq library preparation is relatively low efficiency, which causes loss of rare transcripts1 required for meaningful MRD assessment. Three methods currently employed to overcome this inherent bias in RNA-seq are targeted RNA sequencing of cancer-related genes to reduce off target, non-specific sequencing which improves read depth and mutation detection2; single cell transcriptomes to obtain a digital readout of gene expression in single cells rather than a population-based average; and the addition of unique molecular indexes (UMI) to normalize amplification bias and obtain digital quantitation of transcripts in populations of cells. None of these methods have been carefully studied for their applicability to diagnostic testing, but single cell transcriptome profiling has been applied to solid tumor biology3,4. In this presentation, we explore whether digital RNA-seq can serve as a viable modality for MRD either as a stand-alone method or in conjunction with other methods of genomic profiling or immunophenotyping. While single-cell RNA profiling allows for co-localization of mutations within the same cell and is now capable of surveying hundreds to thousands of cells in a single experiment for reasonable costs, this scale remains far below the throughput necessary for MRD detection of cells present at 1:105. One would need to process tens of thousands of cells and analyze the resulting data to confidently identify any residual leukemia cells, which is not currently feasible in timescales amenable to clinical decision making. We present data from the combination of targeted RNA sequencing of a pan-cancer gene expression array with the addition of UMIs to normalize amplification bias and computationally eliminate errors introduced by the sequencing platform while specifically sequencing cancer-associated genes to high read depths. This enables high-throughput detection of allele and isoform-specific transcripts at frequencies below 1:5,000. This method can be coupled with an equivalent DNA sequencing analysis from the same sample to ascertain the relative expression of leukemia-associated mutant alleles. However, one significant drawback to the addition of UMIs compared to single-cell RNA-seq is that the ability to co-localize mutations is lost. As epigenetic modifiers and targeted agents continue to permeate cancer therapy, these evolving technologies should offer more than direct quantification of residual leukemia cells, but a rich series of data on expression differences in healthy and cancer cells before, during and after therapy. References:Fu GK, Xu W, Wilhemly J, et al. Molecular indexing enables quantitative targeted RNA sequencing and reveals poor efficiencies in standard library preparations. PNAS. 2014;111(5):1891-1896.Lin L, Abo R, Dolcen D, et al. Targeted RNA sequencing improves transcript analysis in cancer samples. Cancer Res. 2015;75:1115 (abstract).Kim KT, Lee HW, Lee HO, et al. Application of single-cell RNA sequencing in optimizing a combinatorial therapeutic strategy in metastatic renal carcinoma. Genome Biol. 2016;17:80.Tirosh I, Izar B, Prakadan SM, et al. Dissecting the multicellular ecosystem of metastatic melanoma by single-cell RNA-seq. Science. 2016;352:189-196. Disclosures No relevant conflicts of interest to declare.

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18

Faderl, Stefan, Razelle Kurzrock, and Zeev Estrov. "Minimal Residual Disease in Hematologic Disorders." Archives of Pathology & Laboratory Medicine 123, no. 11 (November 1, 1999): 1030–34. http://dx.doi.org/10.5858/1999-123-1030-mrdihd.

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Abstract In almost no other area of medical oncology has the introduction of new drugs, combinations of chemotherapeutic agents, and novel biologic treatments caused such dramatic responses as it has in the treatment of malignant hematologic disorders. However, despite some therapeutic success, many patients relapse and die from recurrence of their disease. The implications of minimal residual disease (MRD), a term referring to disease that is undetectable by conventional morphologic methods, have therefore attracted increasing attention in recent years. New and powerful laboratory tools such as polymerase chain reaction assays have extraordinary sensitivity and provide exciting new insights into the detection, nature, quantification, and kinetics of MRD. This article summarizes methods used in the identification of MRD and its importance as exemplified in the case of acute leukemias and chronic myelogenous leukemia.

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19

Valk, Peter. "Molecular Minimal Residual Disease Detection in Acute Myeloid Leukemia." Blood 128, no. 22 (December 2, 2016): SCI—30—SCI—30. http://dx.doi.org/10.1182/blood.v128.22.sci-30.sci-30.

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Abstract Minimal residual disease (MRD) detection based on the standardized molecular monitoring of the t(9;22)-related BCR-ABL1 fusion transcript is well established for patients with chronic myeloid leukemia (CML). The levels of BCR-ABL1 serve as a guide to tailor treatment of the CML patient. In acute myeloid leukemia (AML) MRD detection based on polymerase chain reaction (PCR) approaches targeted towards the acquired molecular abnormalities is less well established. MRD measurement of the CBFB-MYH11 and RUNX1-RUNX1T1 fusion transcripts after induction therapy has been shown to be of some clinical importance. However, these transcripts can persist during long term complete remission, without having an effect on treatment outcome. In contrast, sequential MRD monitoring of the PML-RARA fusion transcript in acute promyelocytic leukemia (APL) is a strong predictor of relapse. Initial molecular MRD studies were limited to these favorable AML subtypes. Due to the discovery of novel recurrent abnormalities in AML the potential of molecular MRD detection has increased substantially. Although, certain acquired mutations, such as those in NPM1, are known for a number of years, only recently the application of these molecular abnormalities for MRD detection has been investigated in larger clinical trials. By NPM1 mutant MRD detection we can now recognize patients with higher risk of relapse. Highly sensitive targeted detection of the hotspot mutations in AML subsets is feasible by means of real-time PCR, but detection of patient specific mutations with this technology is still challenging. Next generation sequencing (NGS) revealed that AML is an extremely heterogeneous disease, as illustrated by the multitude of acquired mutations, but this technology has also opened possibilities for detection of MRD in virtually every patient. With NGS there is no need for patient specific assays since practically all mutations are detected. These molecular abnormalities, as single marker or in combination, will most certainly improve MRD monitoring of AML. However, it remains yet to be determined how MRD levels are assessed and which combination of markers in a MRD detection result in clinically relevant information, requiring extensive validation in large clinical AML trials. Smaller studies already demonstrated the variable dynamics of MRD during treatment and associations between somatic mutations persistence and risk of relapse. However, clonal hematopoiesis of undetermined potential, i.e., preleukemic mutations that may persist after treatment, provides an extra layer of complexity to the applicability of MRD detection. For example, the clinical applicability of MRD detection in the setting of mutant DNMT3A and IDH mutations is likely less effective due to the persistent DNMT3A and IDH mutant preleukemic cells following treatment. However, should all mutations be cleared after treatment or can preleukemic mutations in otherwise normal hematopoiesis persist without resulting in relapse? Taken together, there is need for molecular approaches to understand the dynamics of residual disease in AML during treatment. Disclosures No relevant conflicts of interest to declare.

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20

Vonk, Christian M., Adil S. A. Al Hinai, Diana Hanekamp, and Peter J. M. Valk. "Molecular Minimal Residual Disease Detection in Acute Myeloid Leukemia." Cancers 13, no. 21 (October 29, 2021): 5431. http://dx.doi.org/10.3390/cancers13215431.

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Initial induction chemotherapy to eradicate the bulk of acute myeloid leukemia (AML) cells results in complete remission (CR) in the majority of patients. However, leukemic cells persisting in the bone marrow below the morphologic threshold remain unaffected and have the potential to proliferate and re-emerge as AML relapse. Detection of minimal/measurable residual disease (MRD) is a promising prognostic marker for AML relapse as it can assess an individual patients’ risk profile and evaluate their response to treatment. With the emergence of molecular techniques, such as next generation sequencing (NGS), a more sensitive assessment of molecular MRD markers is available. In recent years, the detection of MRD by molecular assays and its association with AML relapse and survival has been explored and verified in multiple studies. Although most studies show that the presence of MRD leads to a worse clinical outcome, molecular-based methods face several challenges including limited sensitivity/specificity, and a difficult distinction between mutations that are representative of AML rather than clonal hematopoiesis. This review describes the studies that have been performed using molecular-based assays for MRD detection in the context of other MRD detection approaches in AML, and discusses limitations, challenges and opportunities.

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21

Odeny, Beryne. "Cancer Special Issue: Early detection and minimal residual disease." PLOS Medicine 18, no. 10 (October 12, 2021): e1003794. http://dx.doi.org/10.1371/journal.pmed.1003794.

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22

Raanani, P., and I. Ben-Bassat. "Detection of Minimal Residual Disease in Acute Myelogenous Leukemia." Acta Haematologica 112, no. 1-2 (2004): 40–54. http://dx.doi.org/10.1159/000077559.

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23

Levis, Mark J., Jeffrey Edward Miller, Zhiyi Xie, Valerie McClain, Andrew R. Carson, and Tim Stenzel. "Detection of minimal residual disease in FLT3/ITD AML." Journal of Clinical Oncology 34, no. 15_suppl (May 20, 2016): 7015. http://dx.doi.org/10.1200/jco.2016.34.15_suppl.7015.

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24

Sievers, Eric L., and Michael R. Loken. "Detection of Minimal Residual Disease in Acute Myelogenous Leukemia." Journal of Pediatric Hematology/Oncology 17, no. 2 (May 1995): 123–33. http://dx.doi.org/10.1097/00043426-199505000-00005.

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25

Bai, Yinlei, Alberto Orfao, and Chor Sang Chim. "Molecular detection of minimal residual disease in multiple myeloma." British Journal of Haematology 181, no. 1 (December 19, 2017): 11–26. http://dx.doi.org/10.1111/bjh.15075.

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26

DWENGER, ANNE, ALBRECHT LINDEMANN, and ROLAND MERTELSMANN. "Minimal Residual Disease: Detection, Clinical Relevance, and Treatment Strategies." Journal of Hematotherapy 5, no. 5 (October 1996): 537–48. http://dx.doi.org/10.1089/scd.1.1996.5.537.

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27

San Miguel, J. "Immunophenotypical detection of minimal residual disease in acute leukemia." Critical Reviews in Oncology/Hematology 32, no. 3 (December 1999): 175–85. http://dx.doi.org/10.1016/s1040-8428(99)00032-3.

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28

Nunes, P. C., H. R. Caires, M. A. Sobrinho-Simões, and M. H. Vasconcelos. "Circulating EVs for AML minimal residual disease biomarkers detection." Porto Biomedical Journal 2, no. 5 (September 2017): 228. http://dx.doi.org/10.1016/j.pbj.2017.07.121.

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29

Kim, Miyoung, and Chan-Jeoung Park. "Minimal Residual Disease Detection in Pediatric Acute Lymphoblastic Leukemia." Clinical Pediatric Hematology-Oncology 27, no. 2 (October 31, 2020): 87–100. http://dx.doi.org/10.15264/cpho.2020.27.2.87.

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30

Baer, Maria R. "Detection of minimal residual disease in acute myeloid leukemia." Current Oncology Reports 4, no. 5 (October 2002): 398–402. http://dx.doi.org/10.1007/s11912-002-0033-z.

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31

Manachai, Nawin, Sitthichok Lacharoje, Somporn Techangamsuwan, and Anudep Rungsipipat. "Detection of minimal residual disease (MRD) in canine lymphoma." Comparative Clinical Pathology 23, no. 1 (August 23, 2012): 199–204. http://dx.doi.org/10.1007/s00580-012-1597-0.

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32

Plander, Márk, Judit Skrapits, Tünde Bozsó, Tamás Szendrei, and János László Iványi. "Detection and impact of minimal residual disease on outcome of chronic lymphocytic leukemia." Orvosi Hetilap 153, no. 41 (October 2012): 1622–28. http://dx.doi.org/10.1556/oh.2012.29458.

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Introduction: Minimal residual disease is associated with longer overall survival in patients with chronic lymphocytic leukemia. Aim: The aim of the authors was to determine the clinical significance of remission and minimal residual disease on the survival of patients with chronic lymphocytic leukemia. Methods: Data from 42 first-line treated patients with chronic lymphocytic leukemia were analyzed. Minimal residual disease was determined by flow cytometry. Results: Overall response and complete remission was achieved in 91%, 86%, 100% and 87%, 0%, 60% of patients with fludarabine-based combinations, single-agent fludarabine and cyclophosphamide + vincristin + prednisolone regimen, respectively. Minimal residual disease eradication was feasible only with fludarabine-based combinations in 60% of these cases. The ratio of minimal residual disease was 0.5% on average. During a median follow-up period lasting 30 months, the overall survival of patients with fludarabine-resistant disease proved to be significantly shorter (p = 0.04), while complete remission without minimal residual disease was associated with significantly longer progression free survival (p = 0.02). Conclusion: Only fludarabine-based combinations were able to eradicate minimal residual disease in patients with chronic lymphocytic leukemia. Complete remission without minimal residual disease may predict longer progression free survival in these patients. Orv. Hetil., 2012, 153, 1622–1628.

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Herrera, Alex F., and Philippe Armand. "Minimal Residual Disease Assessment in Lymphoma: Methods and Applications." Journal of Clinical Oncology 35, no. 34 (December 1, 2017): 3877–87. http://dx.doi.org/10.1200/jco.2017.74.5281.

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Standard methods for disease response assessment in patients with lymphoma, including positron emission tomography and computed tomography scans, are imperfect. In other hematologic malignancies, particularly leukemias, the ability to detect minimal residual disease (MRD) is increasingly influencing treatment paradigms. However, in many subtypes of lymphoma, the application of MRD assessment techniques, like flow cytometry or polymerase chain reaction–based methods, has been challenging because of the absence of readily detected circulating disease or canonic chromosomal translocations. Newer MRD detection methods that use next-generation sequencing have yielded promising results in a number of lymphoma subtypes, fueling the hope that MRD detection may soon be applicable in clinical practice for most patients with lymphoma. MRD assessment can provide real-time information about tumor burden and response to therapy, noninvasive genomic profiling, and monitoring of clonal dynamics, allowing for many possible applications that could significantly affect the care of patients with lymphoma. Further validation of MRD assessment methods, including the incorporation of MRD assessment into clinical trials in patients with lymphoma, will be critical to determine how best to deploy MRD testing in routine practice and whether MRD assessment can ultimately bring us closer to the goal of personalized lymphoma care. In this review article, we describe the methods available for detecting MRD in patients with lymphoma and their relative advantages and disadvantages. We discuss preliminary results supporting the potential applications for MRD testing in the care of patients with lymphoma and strategies for including MRD assessment in lymphoma clinical trials.

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Morley, Alexander A., Sue Latham, Michael J. Brisco, Pamela J. Sykes, Bryone Kuss, and Keith Waters. "Improved Measurement of Minimal Residual Disease (MRD)." Blood 108, no. 11 (November 1, 2006): 2284. http://dx.doi.org/10.1182/blood.v108.11.2284.2284.

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Abstract A new and improved method for measurement of minimal residual disease (MRD) was developed. Method the total repertoire of leukaemic rearrangements of the immunoglobulin heavy chain (IgH) gene.was determined by performing multiple parallel Q-PCRs in microplates to determine usage of individual V and J segments. This enabled detection and quantification of clones ranging in size from 100% to approximately 0.03% of the leukemic population. MRD measurement involved nested Q-PCR using the specific V and J primers and internal primers based on the sequence of the rearrangement of interest. Following informed parental consent, 25 children with B-ALL were studied at the end of induction therapy. Under general anesthesia, 4 aspirations, 2 from each iliac spine, were performed and on each sample MRD was measured on 2 different days. This enabled definition of the laboratory and sampling factors important in measurement of MRD. Results Repertoire analysis was very effective in identifying rearrangements of the IgH gene suitable for use as molecular markers, being superior to the commonly-used BIOMED-2 protocol for identification of both large and small clones. Two or more rearrangements marking large clones were detected in 20 of the 25 patients. The median MRD level at the end of induction was 2.1 x 10−5. A level of > 10−3 was seen in 4 patients and < 10−7 in 4. Sensitivity of detection in a single sample was approximately 2 x 10−6, which is 1–2 orders of magnitude better than current techniques. Figure Figure The SD of measurement depended on the number of target rearrangements present in the sample, reflecting the Poisson statistical uncertainty inherent in measurement of small numbers of events. For > 50 rearrangements SD was 0.23 log units, but below this level the SD rose steeply. 50 targets in 1 μg of DNA corresponds to an MRD of approximately 3 x 10−4. Figure Figure There was significant sampling error. In 1 patient there was 1000-fold MRD difference between the 2 iliac spines. Conclusions We recommend that, for MRD measurement, -an aspiration should be performed from each iliac spine, with each sample being quantified separately and an average obtained -each measurement should involve at least 10 μg of good-quality DNA The MRD value so obtained should have sufficient accuracy, sensitivity and precision for clinical decisions based upon the value to be made with confidence. The described methods for MRD measurement should also be applicable to monitoring of all B-lymphocyte neoplasms, in addition to ALL.

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35

Seshadri, R. "Detection of minimal residual disease in acute leukemia [letter; comment]." Blood 86, no. 6 (September 15, 1995): 2452. http://dx.doi.org/10.1182/blood.v86.6.2452b.bloodjournal8662452b.

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36

Dworzak, M. N. "Immunological Detection of Minimal Residual Disease in Acute Lymphoblastic Leukemia." Oncology Research and Treatment 24, no. 5 (2001): 442–48. http://dx.doi.org/10.1159/000055124.

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37

Grosveld, G., D. Bootsma, A. de Klein, N. Heisterkamp, K. Stam, and J. Groffen. "Specific breakpoint analysis: Potentials for detection of minimal residual disease." Leukemia Research 10, no. 1 (January 1986): 80. http://dx.doi.org/10.1016/0145-2126(86)90113-x.

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38

Potter, M. N. "The detection of minimal residual disease in acute lymphoblastic leukaemia." Blood Reviews 6, no. 2 (June 1992): 68–82. http://dx.doi.org/10.1016/0268-960x(92)90009-f.

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39

Radich, Jerald. "Detection of minimal residual disease in acute and chronic leukemias." Current Opinion in Hematology 3, no. 4 (1996): 310–14. http://dx.doi.org/10.1097/00062752-199603040-00010.

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40

Gaipa, Giuseppe, Giuseppe Basso, Andrea Biondi, and Dario Campana. "Detection of minimal residual disease in pediatric acute lymphoblastic leukemia." Cytometry Part B: Clinical Cytometry 84, no. 6 (June 26, 2013): 359–69. http://dx.doi.org/10.1002/cyto.b.21101.

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41

Lacroix, Jeannine, and Magnus von Knebel Doeberitz. "Technical aspects of minimal residual disease detection in carcinoma patients." Seminars in Surgical Oncology 20, no. 4 (2001): 252–64. http://dx.doi.org/10.1002/ssu.1042.

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42

Tangri, Shabnam, Annalee Estrellado, Julie Ranuio, Elisa Romeo, Jonathan Lawson, Lana Feng, Mike I. Nerenberg, Jonathan Diver, and Sarah Harris. "Validation of Minimal Residual Disease Flow Cytometry Method for Residual Disease Monitoring in Chronic Lymphocytic Leukemia." Blood 112, no. 11 (November 16, 2008): 4196. http://dx.doi.org/10.1182/blood.v112.11.4196.4196.

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Abstract Monitoring Minimal Residual Disease (MRD) of Chronic Lymphocytic Leukemia (CLL) patients who achieved complete remission has been difficult and challenging using flow cytometry detection methods in peripheral blood Earlier flow cytometry methods described for detection of MRD relied on the assessment of CD20 expression that maybe compromised during rituximab therapy (CD5/19/20/79B and light chain analysis) or were done using the classic CLL staining panel (CD5/19/23 and light chain analysis) that had a low sensitivity. To facilitate the development of methods that would be suitable for rituximab containing regimens and have better sensitivity, a panel of antibody combinations was identified for use in an internationally standardized flow cytometric approach for MRD detection in CLL-treated patients (Rawstron et al., 2007). This panel consists of 5 combinations of antibodies specific for 1-sIgKappa/sIgLambda/CD19/CD5, 2-CD45/CD14/CD19/CD5, 3-CD43/CD79b/CD19/CD5, 4-CD22/CD81/CD19/CD5 and 5-CD20/CD38/CD19/CD5 antigens. The first two combinations are utilized for confirmation of clonality and assessment of Tcell contamination rate within the B cell gate, whereas combinations 3, 4 and 5 are specific for MRD detection. This standardized 5-combination panel was technically validated by Genoptix Medical Laboratory for use in BiogenIdec’s clinical trials in CLL with Lumiliximab. To validate this panel assay, selected CLL samples were mixed with normal donor blood or “disease-free” bone marrow specimens, to achieve 1%, 0.1%, 0.05% and 0.01% of CLL cells in “non-CLL” leukocytes. Our results show that it is possible to identify up to 1 CLL cell in 10,000 normal cells in some but not all cases, and that on a consistent basis our analysis is able to identify 1 CLL cell in 1000 normal cells. In comparison, the classic screening panel commonly used to diagnose CLL has a limit of detection (LOD) of about 1% (1 leukemic cell in 100 normal cells); thus this new method provides a 10 to 100 fold improvement in sensitivity. The enhanced sensitivity and LOD of the new assay is mainly due to the reduction of the non-CLL cell background in peripheral blood and bone marrow Furthermore, to make analysis guidelines consistent among analysts, an internal semi-quantitative clustering scoring analysis system was developed for this assay. The cluster scoring scheme assigns a negative score to scattered events with no clearly visible clone; well grouped events with tight visible clones are assigned positive scores and those gated events are considered for MRD final call. To reliably define the presence of MRD, at least 2 of the 3 MRD specific antibody combinations must have a positive clustering score. Due to the small number of cells to be analyzed, collection of 500,000 events is recommended. Finally, the results of additional studies showed that the anticoagulant employed may impact the stability of the antigens over a period of 7 days, and for accurate MRD determination blood specimens should be drawn into Heparin vacutainer tubes when long shipping times are expected.

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43

Schrappe, Martin. "Detection and management of minimal residual disease in acute lymphoblastic leukemia." Hematology 2014, no. 1 (December 5, 2014): 244–49. http://dx.doi.org/10.1182/asheducation-2014.1.244.

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Abstract The detection of minimal residual disease (MRD) has become part of the state-of-the-art diagnostics to guide treatment both in pediatric and adult acute lymphoblastic leukemia (ALL). This applies to the treatment of de novo and recurrent ALL. In high-risk ALL, MRD detection is considered an important tool to adjust therapy before and after hematopoietic stem cell transplantation. Precise quantification and quality control is instrumental to avoid false treatment assignment. A new methodological approach to analyzing MRD has become available and is based on next-generation sequencing. In principle, this technique will be able to detect a large number of leukemic subclones at a much higher speed than before. Carefully designed prospective studies need to demonstrate concordance or even superiority compared with those techniques in use right now: detection of aberrant expression of leukemia-specific antigens by flow cytometry of blood or bone marrow, or detection of specific rearrangements of the T-cell receptor or immunoglobulin genes by real-time quantitative polymerase chain reaction using DNA of leukemic cells. In some cases with known fusion genes, such as BCR/ABL, reverse transcriptase-polymerase chain reaction has been used as additional method to identify leukemic cells by analyzing RNA in patient samples. MRD detection may be used to modulate treatment intensity once it has been demonstrated at well-defined informative checkpoints that certain levels of MRD can reliably predict the risk of relapse. In addition, MRD is used as end point to determine the activity of a given agent or treatment protocol. If activity translates into antileukemic efficacy, MRD may be considered a surrogate clinical end point.

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Yee, Andrew J., and Noopur Raje. "Minimal residual disease in multiple myeloma: why, when, where." Hematology 2021, no. 1 (December 10, 2021): 37–45. http://dx.doi.org/10.1182/hematology.2021000230.

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Abstract Improvements in multiple myeloma therapy have led to deeper responses that are beyond the limit of detection by historical immunohistochemistry and conventional flow cytometry in bone marrow samples. In parallel, more sensitive techniques for assessing minimal residual disease (MRD) through next-generation flow cytometry and sequencing have been developed and are now routinely available. Deep responses when measured by these assays correspond with improved outcomes and survival. We review the data supporting MRD testing as well as its limitations and how it may fit in with current and future clinical practice.

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45

Gribben, JG, D. Neuberg, AS Freedman, CD Gimmi, KW Pesek, M. Barber, L. Saporito, SD Woo, F. Coral, and N. Spector. "Detection by polymerase chain reaction of residual cells with the bcl-2 translocation is associated with increased risk of relapse after autologous bone marrow transplantation for B-cell lymphoma." Blood 81, no. 12 (June 15, 1993): 3449–57. http://dx.doi.org/10.1182/blood.v81.12.3449.3449.

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Abstract Although molecular biologic techniques can now detect minimal numbers of residual cancer cells in patients in complete clinical remission, the clinical significance of minimal residual disease has never been conclusively established. If the detection of minimal residual disease predicts which patients will relapse, then therapy could be altered based upon the detection of these cells. The t(14;18) can be detected by polymerase chain reaction (PCR) amplification in 50% of patients with B-cell non-Hodgkin's lymphoma and allows detection of one lymphoma cell in up to 1 million normal cells. To determine the clinical significance of the detection of minimal residual lymphoma cells in the bone marrow (BM) PCR amplification was used to detect the presence of residual lymphoma cells after autologous BM transplantation (ABMT) in serial BM samples from 134 patients with B-cell lymphoma in whom a bcl- 2 translocation could be detected. PCR analysis was performed on a total of 542 BM samples obtained while these patients were in complete remission. Disease-free survival was markedly increased in patients with no PCR-detectable lymphoma cells in the marrow compared with those in whom residual lymphoma cells were detected (P < .00001), and the presence of detectable lymphoma cells was associated with a 48-fold increase in the risk of relapse. Of the 77 patients (57%) with no PCR- detectable lymphoma cells in their most recent BM sample, none have relapsed. In contrast, all 33 patients (25%) who have relapsed had PCR- detectable lymphoma cells detected in their BM before clinical relapse occurred. In 19 patients (14%), residual lymphoma cells in the BM were detected early following transplantation and subsequently were no longer detectable, although these patients received no further therapy. In these patients, residual lymphoma cells may already have been irreversibly damaged by the high-dose therapy or an endogenous immune mechanism may be capable of eliminating residual lymphoma cells in some patients. Therefore, although the detection of minimal residual disease by PCR following ABMT in patients with lymphoma identifies those patients at high risk of relapse, the presence of residual minimal disease early after transplantation may not be associated with poor prognosis in a small subset of patients. Confirmatory studies will be required to determine more definitively the role of minimal disease detection to identify which patients require additional therapy.

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46

Gribben, JG, D. Neuberg, AS Freedman, CD Gimmi, KW Pesek, M. Barber, L. Saporito, SD Woo, F. Coral, and N. Spector. "Detection by polymerase chain reaction of residual cells with the bcl-2 translocation is associated with increased risk of relapse after autologous bone marrow transplantation for B-cell lymphoma." Blood 81, no. 12 (June 15, 1993): 3449–57. http://dx.doi.org/10.1182/blood.v81.12.3449.bloodjournal81123449.

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Although molecular biologic techniques can now detect minimal numbers of residual cancer cells in patients in complete clinical remission, the clinical significance of minimal residual disease has never been conclusively established. If the detection of minimal residual disease predicts which patients will relapse, then therapy could be altered based upon the detection of these cells. The t(14;18) can be detected by polymerase chain reaction (PCR) amplification in 50% of patients with B-cell non-Hodgkin's lymphoma and allows detection of one lymphoma cell in up to 1 million normal cells. To determine the clinical significance of the detection of minimal residual lymphoma cells in the bone marrow (BM) PCR amplification was used to detect the presence of residual lymphoma cells after autologous BM transplantation (ABMT) in serial BM samples from 134 patients with B-cell lymphoma in whom a bcl- 2 translocation could be detected. PCR analysis was performed on a total of 542 BM samples obtained while these patients were in complete remission. Disease-free survival was markedly increased in patients with no PCR-detectable lymphoma cells in the marrow compared with those in whom residual lymphoma cells were detected (P < .00001), and the presence of detectable lymphoma cells was associated with a 48-fold increase in the risk of relapse. Of the 77 patients (57%) with no PCR- detectable lymphoma cells in their most recent BM sample, none have relapsed. In contrast, all 33 patients (25%) who have relapsed had PCR- detectable lymphoma cells detected in their BM before clinical relapse occurred. In 19 patients (14%), residual lymphoma cells in the BM were detected early following transplantation and subsequently were no longer detectable, although these patients received no further therapy. In these patients, residual lymphoma cells may already have been irreversibly damaged by the high-dose therapy or an endogenous immune mechanism may be capable of eliminating residual lymphoma cells in some patients. Therefore, although the detection of minimal residual disease by PCR following ABMT in patients with lymphoma identifies those patients at high risk of relapse, the presence of residual minimal disease early after transplantation may not be associated with poor prognosis in a small subset of patients. Confirmatory studies will be required to determine more definitively the role of minimal disease detection to identify which patients require additional therapy.

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47

Galtseva, I. V., S. Y. Smirnova, and E. N. Parovichnikova. "Methodological aspects of the detection of minimal residual disease in patients with acute leukemia." Russian journal of hematology and transfusiology 67, no. 1 (April 11, 2022): 108–20. http://dx.doi.org/10.35754/0234-5730-2022-67-1-108-120.

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Introduction. The study of minimal residual disease (MRD) has become an integral part of various treatment protocols for acute leukemia. Methods of polymerase chain reaction (PCR) and multicolor fl ow cytometry (MFC) are most widely used to assess MRD.Aim — to characterize the main technologies for the detection of residual tumor cells in acute leukemiaMain findings. Various approaches for detecting MRD are described: PCR with patient-specifi c primers for rearranged genes of immunoglobulin and/or T-cell receptors, reverse transcription PCR for detecting chimeric transcripts and assessing the expression of overexpressed genes, as well as the basics of detecting MRD by MFC. Each of these approaches has its own advantages, disadvantages, and limitations of use.

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48

Coustan-Smith, Elaine, Guangchun Song, Christopher Clark, Laura Key, Peixin Liu, Mohammad Mehrpooya, Patricia Stow, et al. "New markers for minimal residual disease detection in acute lymphoblastic leukemia." Blood 117, no. 23 (June 9, 2011): 6267–76. http://dx.doi.org/10.1182/blood-2010-12-324004.

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Abstract To identify new markers for minimal residual disease (MRD) detection in acute lymphoblastic leukemia (ALL), we compared genome-wide gene expression of lymphoblasts from 270 patients with newly diagnosed childhood ALL to that of normal CD19+CD10+ B-cell progenitors (n = 4). Expression of 30 genes differentially expressed by ≥ 3-fold in at least 25% of cases of ALL (or 40% of ALL subtypes) was tested by flow cytometry in 200 B-lineage ALL and 61 nonleukemic BM samples, including samples containing hematogones. Of the 30 markers, 22 (CD44, BCL2, HSPB1, CD73, CD24, CD123, CD72, CD86, CD200, CD79b, CD164, CD304, CD97, CD102, CD99, CD300a, CD130, PBX1, CTNNA1, ITGB7, CD69, CD49f) were differentially expressed in up to 81.4% of ALL cases; expression of some markers was associated with the presence of genetic abnormalities. Results of MRD detection by flow cytometry with these markers correlated well with those of molecular testing (52 follow-up samples from 18 patients); sequential studies during treatment and diagnosis-relapse comparisons documented their stability. When incorporated in 6-marker combinations, the new markers afforded the detection of 1 leukemic cell among 105 BM cells. These new markers should allow MRD studies in all B-lineage ALL patients, and substantially improve their sensitivity.

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49

Dworzak, Michael N., and Eva R. Panzer-Grümayer. "Flow Cytometric Detection of Minimal Residual Disease in Acute Lymphoblastic Leukemia." Leukemia & Lymphoma 44, no. 9 (January 2003): 1445–55. http://dx.doi.org/10.3109/10428190309178763.

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50

Chen, Kevin, Misty D. Shields, Pradeep S. Chauhan, Ricardo J. Ramirez, Peter K. Harris, Melissa A. Reimers, Jose P. Zevallos, Andrew A. Davis, Bruna Pellini, and Aadel A. Chaudhuri. "Commercial ctDNA Assays for Minimal Residual Disease Detection of Solid Tumors." Molecular Diagnosis & Therapy 25, no. 6 (November 2021): 757–74. http://dx.doi.org/10.1007/s40291-021-00559-x.

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