Готові списки джерел за темами / Cytogenetics

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Добірка наукової літератури з теми "Cytogenetics"

Автор: Grafiati
Опубліковано: 4 червня 2021
Оновлено: 1 серпня 2024

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Статті в журналах з теми "Cytogenetics"

1

Vance, Gail H., Haesook Kim, Gary Hicks, Athena Cherry, Rodney Higgins, Martin S. Tallman, Hugo F. Fernandez, and Gordon Dewald. "Utility of Interphase FISH To Stratify Patients into Cytogenetic Risk Categories at Diagnosis of AML in an ECOG Clinical Trial (E1900)." Blood 106, no. 11 (November 16, 2005): 2377. http://dx.doi.org/10.1182/blood.v106.11.2377.2377.

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Abstract Background: Cytogenetic risk categories based on conventional chromosome studies are widely used in clinical practice to make treatment decisions for AML. We evaluated the efficacy of interphase FISH to detect chromosome anomalies in the workup of young (<60 years) patients with AML. Methods: Study subjects were enrolled in E1900, a front-line Eastern Cooperative Oncology Group (ECOG) clinical trial for AML. This is an on-going Phase III clinical trial with Daunorubicin dose-intensification ± Gemtuzumab-Ozogamicin consolidation therapy prior to stem cell transplant. This trial opened December 2002; as of February 2005, 223 patients were enrolled. The protocol was designed to collect bone marrow for both cytogenetic and FISH studies at study entry (diagnosis). Cytogenetic studies were done by local laboratories with results reviewed centrally by the ECOG Cytogenetics Committee. Each case was classified as acceptable or unacceptable based on predefined ECOG cytogenetic criteria. FISH for each patient was performed in the ECOG FISH laboratory at Mayo Clinic and utilized eight probe sets to detect t(8;21), t(9;22), t(11;var), t(15;17), inv(16), +8, −5/5q, and −7/7q (Vysis, Downer Grove, IL). Results: 64 (29%) of 223 specimens had incomplete cytogenetic and/or FISH results. We analyzed the remaining 159 (71%) specimens with complete cytogenetic and FISH results. Results for each specimen were classified by probe set into one of the following categories: Normal cytogenetics and normal FISH; Abnormal cytogenetics and abnormal FISH for the anomaly the probe was designed to detect; Abnormal cytogenetics and abnormal FISH for an anomaly the probe was not primarily designed to detect; Normal cytogenetics and abnormal FISH; Abnormal cytogenetics and normal FISH; or Abnormal cytogenetics and abnormal FISH that further defined the karyotype. Figure 1: Results for 159 patients by category and FISH probe set: *t(8;21); t(9;22); t(11;var); t(15;17); inv(16); cen(8); del(5/5q); de(7/7q). Figure 1:. Results for 159 patients by category and FISH probe set: *t(8;21); t(9;22); t(11;var); t(15;17); inv(16); cen(8); del(5/5q); de(7/7q). The concordance rate between cytogenetic and FISH results ranged from 97 to 100% for all probe sets and kappa analysis for concordance had a p value of <0.0001. Of the total 159 cases, discrepancies between FISH and cytogenetic results occurred in only 4 cases; two with normal cytogenetics and abnormal FISH and two with abnormal cytogenetics and normal FISH results. Conclusions: The high level of agreement between cytogenetics and FISH demonstrates the accuracy of a panel of 8 FISH probe sets for the detection of significant abnormalities in AML. The data from this investigation support the use of FISH as an adjunct in cases of failed cytogenetic analyses to increase the yield of useful cytogenetic results in large cooperative trials. Furthermore, because of the strong correlation between cytogenetics and FISH, our results demonstrate the potential of FISH as a follow-up study of minimal residual disease in ECOG trials.
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2

Chennamaneni, Rachana, Sadashivudu Gundeti, Meher Lakshmi Konatam, Stalin Bala, Ashok Kumar, and Lakshmi Srinivas. "Impact of cytogenetics on outcomes in pediatric acute lymphoblastic leukemia." South Asian Journal of Cancer 07, no. 04 (October 2018): 263–66. http://dx.doi.org/10.4103/sajc.sajc_13_18.

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Abstract Context: In acute lymphoblastic leukemia (ALL), the most important prognostic factors are age, leukocyte count at presentation, immunophenotype, and cytogenetic abnormalities. The cytogenetic abnormalities are associated with distinct immunologic phenotypes of ALL and characteristic outcomes. Aims: The present study was primarily aimed at analyzing the impact of cytogenetics on postinduction responses and event-free survival (EFS) in pediatric patients with ALL. The secondary objective was to study the overall survival (OS). Subjects and Methods: A total of 240 patients with age <18 years and diagnosed with ALL between January 2011 and June 2016 were retrospectively analyzed. Cytogenetics was evaluated with conventional karyotyping or reverse transcriptase polymerase chain reaction. Based on cytogenetic abnormalities, the patients were grouped into five categories, and the outcomes were analyzed. Results: Of the 240 patients, 125 (52%) patients had evaluable cytogenetics. Of these, 77 (61.6%) patients had normal cytogenetics, 19 (15.2%) had t(9;22) translocation, 10 (8%) had unfavorable cytogenetics which included t(9;11), hypodiploidy, and complex karyotype, 10 (8%) had favorable cytogenetics which included t(12;21), t(1;19), and high hyperdiploidy, 9 (7.2%) had miscellaneous cytogenetics. Seventy-one percent of patients were treated with MCP 841 protocol, while 29% of patients received BFM-ALL 95 protocol. The 3-year EFS and OS of the entire group were 52% and 58%, respectively. On univariate analysis, EFS and OS were significantly lower in t(9;22) compared to normal cytogenetics (P = 0.033 and P = 0.0253, respectively) and were not significant for other subgroups compared to normal cytogenetics. On multivariate analysis, EFS was significantly lower for t(9;22) and unfavorable subgroups. Conclusions: Cytogenetics plays an important role in the molecular characterization of ALL defining the prognostic subgroups. Patients with unfavorable cytogenetics and with t(9;22) have poorer outcomes.
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3

Koenecke, Christian, Gudrun Göhring, Liesbeth de Wreede, Anja van Biezen, Christof Scheid, Liisa Volin, Johan Maertens, et al. "Prognostic Value Of Five-Group Cytogenetic Risk Classification In Patients With MDS After Allogeneic Hematopoietic Stem Cell Transplantation: A Retrospective Multicenter Study Of The Chronic Malignancies Working Party Of The EBMT." Blood 122, no. 21 (November 15, 2013): 2092. http://dx.doi.org/10.1182/blood.v122.21.2092.2092.

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Abstract Introduction The only curative treatment approach for patients with myelodysplastic syndromes (MDS) is allogeneic hematopoietic stem cell transplantation (HSCT), but disease relapse after transplantation is a major concern. Predictors for disease outcome after HSCT are limited. However, unfavorable cytogenetic abnormalities have been shown to serve as predictors for MDS-relapse after transplantation. Similar to the data available in MDS-patients not undergoing HSCT (Schanz et al. J Clin Oncol 2012), there is evidence that the novel 5-group cytogenetic classification has a better predictive value for outcome after HSCT than standard IPSS cytogenetics (Deeg et al. Blood 2012). The aim of this large multicentric, international study was to retrospectively determine the impact of the new 5-group cytogenetic MDS classification on outcome after HSCT. Patients and Methods Patients were selected from the EBMT database who had received HSCT for the treatment of MDS between 1982 and 2010 and for whom sufficient cytogenetic information was available. In total, 903 patients were included into the study. At time of HSCT, 97 (10.7%) patients had untreated MDS, 218 (24.1%) patients had advanced MDS or AML evolving from MDS in complete remission, and 227 (25.1%) patients were not in remission after treatment (in 12.3% information on stage of the disease was not available). Median time between diagnosis and transplant was 6.6 months (range 0.2-359.3). Matched related donor HSCT was performed in 574 patients (63.6%), and matched unrelated donor HSCT in 329 patients (36.4%). Bone marrow (35.4%) or peripheral blood (64.6%) served as stem cell graft. Myeloablative preparative regimens were used in 582 patients (64.5%), and a non-myeloablative regimen was given to 320 patients (35.4%). Impact of cytogenetic classification was analyzed in uni- and multivariate models regarding overall survival (OS) and relapse free survival (RFS) after HSCT. Predictive performance of the 2 classifications was compared by means of the cross-validated log partial likelihood. Results Estimated 5-year RFS and OS were 32% and 36% respectively. According to the 5-group cytogenetic classification 19 (2.1%) patients had very good risk cytogenetics, 204 (22.6%) normal risk cytogenetics, 438 (48.5%) intermediate risk cytogenetics, 178 (19.7%) poor risk cytogenetics, and 64 (7.1%) very poor risk cytogenetics. Good, intermediate, and poor risk cytogenetics according to IPSS were found in 192 (38.0%), 500 (40.2%), and 211 (23.7%) patients, respectively. In univariate analysis 5-group cytogenetic information was found to be strongly associated with OS and RFS (OS: log-rank test P<.01, RFS: P<.01) (Figure 1). Further clinicopathologic factors showed a significant impact on impaired OS and RFS: Disease status at HSCT (RA/RARS no pretreatment; RAEB(t)/sAML in CR; RAEB(t)/sAML not in CR, RAEB(t)/sAML untreated) (OS: P<.01, RFS: P<.01) and IPSS cytogenetics (good; intermediate; poor) (OS: P<.01, RFS: P<.01). Patient age showed an impact for RFS (P=.05), but not for OS (P=.09). In multivariate analysis, statistically significant predictors for RFS and OS at HSCT were 5-group cytogenetics, IPSS-cytogenetics, disease status and patient's age. Using 5-group cytogenetics classification, patients with poor risk [(RFS: P=.001, HR=1.40 (95% CI: 1.15-1.71); OS: P=.003, HR=1.38 (95% CI: 1.12-1.70)] or very poor risk cytogenetics [(RFS: P<.001, HR=2.14 (95% CI: 1.6-2.9); OS: P<.001, HR=2.14 (95% CI: 1.59-2.87)] had worse RFS and OS than patients in the other 3 risk groups. Patients with very poor risk cytogenetics had worse RFS and OS compared to patients with poor risk cytogenetics [(RFS: P<.01, HR=1.53 (95-% CI: 1.11-2.11), OS: P<.01, HR=1.55 (95-% CI: 1.11-2.15)]. When comparing the predictive performance of a series of 3 models both for OS and for RFS – (1) with only classical risk factors, (2) these extended with IPSS cytogenetics, (3) extended with 5-group classification instead-, the model with 5-group cytogenetics performed best. Conclusion In this international, multicentric analysis we confirm that MDS patients with poor and very poor risk cytogenetics had significantly worse RFS and OS after HSCT than patients in the other risk groups of the 5-group cytogenetic classifier. New therapeutic strategies to prevent relapse after HSCT in patients with poor or very poor cytogenetics are urgently needed. Disclosures: No relevant conflicts of interest to declare.
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4

Kim, Sung-Yong, Jong-Wook Lee, Byung-Sik Cho, Ki-Seong Eom, Yoo-Jin Kim, Seok Lee, Chang-Ki Min, et al. "Clinical Implications of Abnormal Cytogenetics at Diagnosis of Aplastic Anemia." Blood 108, no. 11 (November 16, 2006): 986. http://dx.doi.org/10.1182/blood.v108.11.986.986.

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Abstract Because cytogenetic abnormalities of aplastic anemia at diagnosis have been reported fairly infrequently, their clinical implications have not known yet. A retrospective study was performed of the cytogenetics findings and clinical courses in patients with typical morphological and clinical features of aplastic anemia from a single institution for the years 1995 through 2005. The results of chromosome analysis of 610 patients were evaluable. Of the evaluable patients, 584 (95.7 %) had normal karyotypes and 26 (4.3 %) had abnormal karyotypes at diagnosis. The most frequent abnormality was trisomy 8 (n=13) followed by deletion 1q (n=5) and monosomy 7/deletion 7q (n=5). Other chromosome abnormalities were isochromosome 17q (n=1), trisomy 15 (n=1) and monosomy 21 (n=1). Among the 584 patients with typical aplastic anemia and no cytogenetic abnormalities, only two developed MDS/AML during the follow-up period, while 5 (19.2%) of 26 patients with typical aplastic anemia and abnormal cytogenetics subsequently developed MDS/AML. The incidence of secondary MDS/AML was statistically higher in abnormal cytogenetics group compared with normal cytogenetics group (p&lt;0.001). The incidence of secondary MDS/AML was not influenced by immunosuppressive therapy (IST) (p=0.715). The patients with trisomy 8 responded poorly to immunosuppressive therapy (IST) and showed statistically significant lower response rate compared with the patients with other cytogenetics (p=0.033). However, response rates of IST were not statistically different in the patients with normal cytogenetics group and the patients with abnormal cytogenetics other than trisomy 8 (p=1.000). Four patients with abnormal cytogenetics received allogeneic hematopoietic stem cell transplantations (allo-HSCT) with the same conditioning as the patients with normal cytogenetics. Three of them are still alive with normal peripheral blood counts. One of them died of acute GVHD and infection after successful engraftment. Our analysis suggested that cytogenetic abnormalities at diagnosis of aplastic anemia could be a risk factor for development of secondary MDS/AML and the patients with trisomy 8 at diagnosis of aplastic anemia might hardly respond to IST. Outcomes of allo-HSCT for aplastic anemia with abnormal cytogenetics probably are not different compared with aplastic anemia with normal cytogenetics.
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5

Kim, Sung-Yong, Myungshin Kim, Kyungja Han, Seok Lee, Mark Hong Lee, Jong-Wook Lee, Woo-Sung Min, and Chun-Choo Kim. "Characteristics and Clinical Outcomes of Adult Aplastic Anemia with Abnormal Cytogenetics at Diagnosis." Blood 112, no. 11 (November 16, 2008): 2039. http://dx.doi.org/10.1182/blood.v112.11.2039.2039.

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Abstract Background and methods Occasionally, patients with acquired aplastic anemia (AA) present with abnormal cytogenetics in bone marrow cells at diagnosis. The diagnosis and treatment of such patients have not been established and have been center-dependent. We have treated adult AA patients with abnormal cytogenetics in a same way as those with normal cytogenetics. Presently, the characteristics and clinical outcomes of 600 adult AA patients who had successful cytogenetics at diagnosis were retrospectively evaluated. Our aim was to determine the characteristics and clinical courses of AA patients with cytogenetic abnormalities at diagnosis who were treated as those with normal cytogenetics. Results Characteristics : Of the evaluable patients, 572 (95.3 %) had normal cytogenetics and 28 (4.7 %) had abnormal cytogenetics at diagnosis. The most frequent abnormality was trisomy 8 (n=15) followed by monosomy 7/deletion 7q (n=5) and deletion 1q (n=5). Other chromosome abnormalities were isochromosome 17q (n=1), trisomy 15 (n=1) and monosomy 21 (n=1). There was no significant statistical difference in gender (P=0.562), Hepatitis B or C infection (P=0.402), paroxysmal nocturnal hemoglobinuria (P=0.709) and severity of AA (P=0.325) between patients displaying normal cytogenetics and abnormal cytogenetics. The age of abnormal cytogenetics patients was significantly lower than normal cytogenetics patients (P&lt;0.001). Immunosuppressive therapy : A total of 334 patients received immunosuppressive therapy using antithymocyte globulin and cyclosporine. Six months after commencement of therapy, 165 (50.9 %) patients responded partially or completely. Multivariate analysis revealed abnormal cytogenetics (HR=0.250; 95% CI=0.077–0.808; P=0.021), absence of paroxysmal nocturnal hemoglobinuria and age (≥ 67) as independent predictors for the poor response to immunosuppressive therapy. Leukemic transformation : Kaplan-Meier modeling revealed that abnormal cytogenetics was also associated with higher cumulative leukemic transformation rate (P&lt;0.001) and lower leukemia-free survival (P=0.021). Of note, the cause of all deaths in non-severe AA patients with abnormal cytogenetics was leukemic transformation. Conclusion: Patients with abnormal cytogenetics at diagnosis of AA tend to respond poorly to immunosuppressive therapy and present with a high leukemic transformation risk, which suggests that cytogenetic abnormalities should be emphasized more than morphological features in diagnosis and treatment decision in AA.
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6

Larson, Melissa L., Ann M. Thomas, Nitin Goyal, Jamile M. Shammo, John J. Maciejewski, Stephanie A. Gregory, and Parameswaran Venugopal. "Efficacy of a Two Day Induction Regimen for De Novo and Secondary AML with Intermediate and Adverse Cytogenetic Profiles." Blood 112, no. 11 (November 16, 2008): 4027. http://dx.doi.org/10.1182/blood.v112.11.4027.4027.

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Abstract Background: Cytogenetic data remains one of the most powerful prognostic factors for predicting response and survival in adult AML patients. The relationship between cytogenetics and induction response to the standard “7+3” regimen has been analyzed in the past. In a CALGB study, patients with favorable cytogenetics achieved a complete remission (CR) rate of 88%, those with intermediate cytogenetics achieved a 67% CR rate and those with adverse cytogenetics had a 32% CR rate (Byrd et al. Blood100: 4325, 2002). We present a retrospective analysis of the correlation between the hierarchical cytogenetic groups and complete remission rate following induction of AML using a novel induction regimen. This regimen was developed based on the concept of timed sequential therapy. The first pulse of chemotherapy recruits leukemic cells into the cell cycle while the second pulse is given at a time of peak cell recruitment. It utilizes two highly active anti-leukemic drugs: cytarabine, a cell cycle-specific drug, and mitoxantrone, which has a favorable cardiac toxicity profile. Patients and Methods: One hundred four patients with AML were treated with two days of chemotherapy given 96 hours apart from April 1997 to April 2008. Each day consisted of two doses of cytarabine 2gm/m2 (at t=0 and t=12) followed by one dose of mitoxantrone 30 mg/m2 administered after the second cytarabine dose (t=15). Bone marrow biopsies were performed for assessment of leukemia-free state (day 14) and to document remission response. Cytogenetic results were classified into favorable, intermediate, and unfavorable categories based on CALGB data. Responses were defined per the Revised IWG Recommendations (Cheson et al, J Clin Onc21: 4642, 2003). Results: Median age of the 104 patients was 57 years [range 17–79]. There were 47 males and 57 females. Forty-two patients (40%) were 60 years of age and older, and the remaining 62 patients (60%) were younger than 60. Sixty-four patients (61.5%) had de novo AML. Five patients had favorable cytogenetics with 100% of them achieving CR. All of the patients with favorable cytogenetics were less than 60 years of age. For the 61 patients with intermediate cytogenetics, the ORR was 83.6% with a CR of 61%. In patients younger than 60, the ORR was 83.8%% (26 CR, 3 CRi, 2 CRp) with CR of 70%. For patients 60 years and older, the ORR was 83.3% (11 CR, 3 CRi, 5 CRp, 1 RMDS). In the 38 patients with unfavorable cytogenetics, the ORR was 57.9% with CR of 37%. For patients younger than 60 and 60 years and older, the overall responses were 75% and 38.8%, respectively. Of the 40 patients with secondary AML due to pre-existing MDS, the ORR was 65% with CR of 27.5%. In patients with de novo AML, the ORR was 81% with CR of 70%. Patients with prior MDS were more likely to have CRi (20% vs 1.5%), TF due to refractory disease (25% vs 15.6%) or aplasia (7.5% vs 1.5%) as compared to patients without MDS. The rates of CRp (10% vs 9%) were similar for both groups. MDS patients with intermediate cytogenetics had an ORR of 77.7% as compared to 54.5% in those with unfavorable cytogenetics. De novo patients with intermediate cytogenetics had ORR of 86% and those with unfavorable cytogenetics had ORR of 62.5%. Conclusion: Our data reflects the overall effectiveness of high dose cytarabine and mitoxantrone for induction therapy of AML. In the favorable cytogenetic group, the CR rate was higher than previously reported response rates; however, the number of patients was small. In the intermediate and unfavorable cytogenetic groups, the response rates for de novo AML compare favorably to historic controls. Patients with secondary AML respond equally well as compared to those with de novo AML; though, the influence of cytogenetics was similar to that seen in de novo AML. This regimen is very effective in producing a high response rates across cytogenetic categories.
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7

Zhang, Peng, Bernd Friebe, Bikram Gill, and R. F. Park. "Cytogenetics in the age of molecular genetics." Australian Journal of Agricultural Research 58, no. 6 (2007): 498. http://dx.doi.org/10.1071/ar07054.

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Анотація:
From the beginning of the 20th Century, we have seen tremendous advances in knowledge and understanding in almost all biological disciplines, including genetics, molecular biology, structural and functional genomics, and biochemistry. Among these advances, cytogenetics has played an important role. This paper details some of the important milestones of modern cytogenetics. Included are the historical role of cytogenetics in genetic studies in general and the genetics stocks produced using cytogenetic techniques. The basic biological questions cytogenetics can address and the important role and practical applications of cytogenetics in applied sciences, such as in agriculture and in breeding for disease resistance in cereals, are also discussed. The goal of this paper is to show that cytogenetics remains important in the age of molecular genetics, because it is inseparable from overall genome analysis. Cytogenetics complements studies in other disciplines within the field of biology and provides the basis for linking genetics, molecular biology and genomics research.
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8

Armand, Philippe, Haesook T. Kim, Daniel J. DeAngelo, Vincent T. Ho, Corey S. Cutler, Richard M. Stone, Jerome Ritz, Edwin P. Alyea, Joseph H. Antin, and Robert J. Soiffer. "Impact of Cytogenetics and Prior Therapy on Outcome of AML and MDS after Allogeneic Transplantation." Blood 108, no. 11 (November 16, 2006): 259. http://dx.doi.org/10.1182/blood.v108.11.259.259.

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Abstract Cytogenetics is an important determinant of outcome for patients with AML or MDS. However, the prognostic impact of cytogenetics in patients undergoing allogeneic stem cell transplantation (alloSCT) is less clear. Moreover, the existing cytogenetic risk groups were established on cohorts of patients treated mostly with chemotherapy, and thus may not be optimal for patients undergoing alloSCT. We retrospectively studied 556 consecutive patients with AML or MDS who received an alloSCT at our institution. Using Cox proportional hazards modeling, taking into account cytogenetics and other known prognostic factors (age, disease type and stage, HLA match, conditioning regimen, GVHD prophylaxis regimen, graft source, CMV serostatus, gender, and year of transplantation), we established a three-group cytogenetic classification scheme based on the 476 patients with de novo disease. In this system, patients with AML and t(15;17), t(8;21) alone, or inv(16)/t(16;16) were classified as favorable risk; patients with AML and complex karyotype, t(9;22), or t(6;9), as well as patients with MDS and complex karyotype or abnormality of 7, were classified as adverse risk. Cytogenetics for all other AML and MDS patients were classified as intermediate risk. Patients with AML and abnormal 3q, and patients with MDS and 5q- or 20q-, could not be assigned to a risk group due to inadequate representation in our study. The figure below shows the overall survival of all de novo AML and MDS patients when stratified according to this cytogenetic grouping scheme. Figure Figure In our cohort, this grouping scheme was the strongest prognostic factor (after age) for overall and disease-free survival. It applied to patients regardless of disease (AML, MDS, or AML arising from MDS) and of stage (AML in CR1 versus advanced leukemia). Furthermore, it outperformed the existing grouping schemes for AML (from MRC, CALGB and SWOG/ECOG) and the IPSS grouping scheme for MDS. Using competing risks regression analysis, we found that cytogenetics influences the risk of relapse but not the non-relapse mortality. The group of 80 patients with therapy-related MDS or AML had a higher frequency of adverse cytogenetics. In this population, cytogenetics remained a significant prognostic factor for overall survival. However, in multivariate models that accounted for cytogenetics, prior therapy by itself did not confer an additional adverse prognosis. This conclusion held true regardless of the grouping scheme used. Conclusion: cytogenetics is a key determinant of outcome for patients with AML or MDS undergoing alloSCT, whether with de novo disease or therapy-related disease. For patients with therapy-related disease, prior therapy has no additional prognostic importance after considering cytogenetic risk group. We also propose a new cytogenetic risk grouping scheme specifically applicable to this patient population, that can be validated in a multi-institutional database. Our results argue that patients entering clinical trials of transplantation should be stratified by cytogenetic risk group, and provide a means of doing so.
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9

Rashidi, Armin, and Amanda F. Cashen. "A Cytogenetic Model Predicts Relapse Risk and Survival in Patients with Acute Myeloid Leukemia Undergoing Hematopoietic Stem Cell Transplantation in Morphologic Complete Remission." Blood 124, no. 21 (December 6, 2014): 2545. http://dx.doi.org/10.1182/blood.v124.21.2545.2545.

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Abstract Objectives: Up to one third of patients with acute myeloid leukemia (AML) and abnormal cytogenetics have persistent cytogenetic abnormalities (pCytAbnl) at morphologic complete remission (mCR). We hypothesized that the prognostic significance of pCytAbnl in patients undergoing allogeneic hematopoietic stem cell transplantation (allo-HSCT) in mCR varies with the cytogenetic risk group. Previous studies on the subject have been small, inconclusive, or inconsistent. Methods: We analyzed the data from a large cohort of patients (n = 118) with AML and abnormal cytogenetics who underwent allo-HSCT in mCR, and developed a simple risk stratification model based on pCytAbnl and cytogenetic risk group to compare time to relapse (TTR), relapse-free survival (RFS), and overall survival (OS). Results: The mean (standard deviation) age of patients was 51 (14) years, and 58% were male. AML was therapy-related in 21 (31%) patients. The most frequent FAB subtypes were M0/M1/M2 (46%), followed by M4/M5 (26%). Favorable, intermediate and unfavorable cytogenetic risk disease was present in 18%, 28%, and 54% of patients, respectively. The majority (73%) of patients were in CR1. Conditioning was myeloablative in 67% of patients and reduced-intensity in the remainder. The groups with or without pCytAbnl were similar in all baseline and transplant characteristics except age, CR number and cytogenetic risk group. Specifically, patients with pCytAbnl were significantly older (56 ± 12 vs. 48 ± 15 years; P = 0.004), were in first CR more frequently (86% vs. 67%; P = 0.042), and were more likely to have unfavorable risk cytogenetics (P = 0.027) than patients without pCytAbnl. Univariate analysis was performed using the following variables: age, gender, therapy-related AML (present vs. absent), pCytAbnl (present vs. absent), cytogenetic risk group (unfavorable vs. intermediate/favorable), CR number (≥2 vs. 1), conditioning regimen (myeloablative vs. reduced intensity), and donor type (matched unrelated vs. sibling). There was a significant association between outcome (OS, RFS, and TTR) and the following variables: pCytAbnl, cytogenetic risk group, and the conditioning regimen. Additionally, CR number was significantly associated with TTR. In multivariate regression analysis with these four variables (Table 1), only pCytAbnl, cytogenetic risk group, and the conditioning regimen had a significant impact on outcome. A risk scoring system was then built using pCytAbnl and cytogenetic risk group. The model distinguished 3 groups of patients with distinct outcomes (Figure 1). The group with pCytAbnl and unfavorable risk cytogenetics (R2, n = 24) had the shortest median TTR (3 months), RFS (3 months), and OS (7 months). The group with favorable/intermediate risk cytogenetics and without pCytAbnl (R0, n = 47) had the longest median TTR (not reached), RFS (57 months), and OS (57 months). The group with pCytAbnl and favorable/intermediate risk cytogenetics, or without pCytAbnl but with unfavorable risk cytogenetics (R1, n = 47) experienced intermediate TTR (18 months), RFS (9 months), and OS (14 months). Conclusions: A composite cytogenetic risk model identifies patients with AML in mCR with distinct relapse, RFS, and OS rates following allo-HSCT. Table 1:Multivariate analysis for survival outcomes using variables with a significant association in univariate analysis OS RFS TTRHR (95% CI)PHR (95% CI)PHR (95% CI)PpCytAbnl + vs. -0.54 (0.32-0.91)0.0200.53 (0.32-0.86)0.0100.44 (0.24-0.80)0.007Cytogenetic risk U vs. F/I0.60 (0.36-0.99)0.0470.55 (0.34-0.98)0.0140.45 (0.23-0.95)0.023CR number ≥2 vs. 1----1.51 (0.58-3.95)0.404Conditioning MA vs. RI1.71 (1.04-2.81)0.0352.04 (1.27-3.27)0.0032.85 (1.57-5.15)0.001 CI: confidence interval; F/I: Favorable/Intermediate; HR: hazard ratio; MA: myeloablative; RI: reduced intensity; U: unfavorable Figure 1: Cumulative risk of relapse (A), relapse free survival (B) and overall survival (C) based on persistent cytogenetic abnormalities and cytogenetics. R0, R1, and R2 are defined in the text. Figure 1:. Cumulative risk of relapse (A), relapse free survival (B) and overall survival (C) based on persistent cytogenetic abnormalities and cytogenetics. R0, R1, and R2 are defined in the text. Disclosures No relevant conflicts of interest to declare.
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Mellors, Patrick, Moritz Binder, Rhett P. Ketterling, Patricia Griepp, Linda B. Baughn, Francis K. Buadi, Martha Q. Lacy, et al. "Metaphase Cytogenetics for Risk Stratification in Newly Diagnosed Multiple Myeloma." Blood 134, Supplement_1 (November 13, 2019): 4396. http://dx.doi.org/10.1182/blood-2019-122291.

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Introduction: Abnormal metaphase cytogenetics are associated with inferior survival in newly diagnosed multiple myeloma (MM). These abnormalities are only detected in one third of cases due to the low proliferative rate of plasma cells. It is unknown if metaphase cytogenetics improve risk stratification when using contemporary prognostic models such as the revised international staging system (R-ISS), which incorporates interphase fluorescence in situ hybridization (FISH). Aims: The aims of this study were to 1) characterize the association between abnormalities on metaphase cytogenetics and overall survival (OS) in newly diagnosed MM treated with novel agents and 2) evaluate whether the addition of metaphase cytogenetics to R-ISS, age, and plasma cell labeling index (PCLI) improves model discrimination with respect to OS. Methods: We analyzed a retrospective cohort of 483 newly diagnosed MM patients treated with proteasome inhibitors (PI) and/or immunomodulators (IMID) who had metaphase cytogenetics performed prior to initiation of therapy. Abnormal metaphase cytogenetics were defined as MM specific abnormalities, while normal metaphase cytogenetics included constitutional cytogenetic variants, age-related Y chromosome loss, and normal metaphase karyotypes. Multivariable adjusted proportional hazards regression models were fit for the association between known prognostic factors and OS. Covariates associated with inferior OS on multivariable analysis included R-ISS stage, age ≥ 70, PCLI ≥ 2, and abnormal metaphase cytogenetics. We devised a risk scoring system weighted by their respective hazard ratios (R-ISS II +1, R-ISS III + 2, age ≥ 70 +2, PCLI ≥ 2 +1, metaphase cytogenetic abnormalities + 1). Low (LR), intermediate (IR), and high risk (HR) groups were established based on risk scores of 0-1, 2-3, and 4-5 in modeling without metaphase cytogenetics, and scores of 0-1, 2-3, and 4-6 in modeling incorporating metaphase cytogenetics, respectively. Survival estimates were calculated using the Kaplan-Meier method. Survival analysis was stratified by LR, IR, and HR groups in models 1) excluding metaphase cytogenetics 2) including metaphase cytogenetics and 3) including metaphase cytogenetics, with IR stratified by presence and absence of metaphase cytogenetic abnormalities. Survival estimates were compared between groups using the log-rank test. Harrell's C was used to compare the predictive power of risk modeling with and without metaphase cytogenetics. Results: Median age at diagnosis was 66 (31-95), 281 patients (58%) were men, median follow up was 5.5 years (0.04-14.4), and median OS was 6.4 years (95% CI 5.7-6.8). Ninety-seven patients (20%) were R-ISS stage I, 318 (66%) stage II, and 68 (14%) stage III. One-hundred and fourteen patients (24%) had high-risk abnormalities by FISH, and 115 (24%) had abnormal metaphase cytogenetics. Three-hundred and thirteen patients (65%) received an IMID, 119 (25%) a PI, 51 (10%) received IMID and PI, and 137 (28%) underwent upfront autologous hematopoietic stem cell transplantation (ASCT). On multivariable analysis, R-ISS (HR 1.59, 95% CI 1.29-1.97, p < 0.001), age ≥ 70 (HR 2.32, 95% CI 1.83-2.93, p < 0.001), PCLI ≥ 2, (HR 1.52, 95% CI 1.16-2.00, p=0.002) and abnormalities on metaphase cytogenetics (HR 1.35, 95% CI 1.05-1.75, p=0.019) were associated with inferior OS. IR and HR groups experienced significantly worse survival compared to LR groups in models excluding (Figure 1A) and including (Figure 1B) the effect of metaphase cytogenetics (p < 0.001 for all comparisons). However, the inclusion of metaphase cytogenetics did not improve discrimination. Likewise, subgroup analysis of IR patients by the presence or absence of metaphase cytogenetic abnormalities did not improve risk stratification (Figure 1C) (p < 0.001). The addition of metaphase cytogenetics to risk modeling with R-ISS stage, age ≥ 70, and PCLI ≥ 2 did not improve prognostic performance when evaluated by Harrell's C (c=0.636 without cytogenetics, c=0.642 with cytogenetics, absolute difference 0.005, 95% CI 0.002-0.012, p=0.142). Conclusions: Abnormalities on metaphase cytogenetics at diagnosis are associated with inferior OS in MM when accounting for the effects of R-ISS, age, and PCLI. However, the addition of metaphase cytogenetics to prognostic modeling incorporating these covariates did not significantly improve risk stratification. Disclosures Lacy: Celgene: Research Funding. Dispenzieri:Akcea: Consultancy; Intellia: Consultancy; Alnylam: Research Funding; Celgene: Research Funding; Janssen: Consultancy; Pfizer: Research Funding; Takeda: Research Funding. Kapoor:Celgene: Honoraria; Sanofi: Consultancy, Research Funding; Janssen: Research Funding; Cellectar: Consultancy; Takeda: Honoraria, Research Funding; Amgen: Research Funding; Glaxo Smith Kline: Research Funding. Leung:Prothena: Membership on an entity's Board of Directors or advisory committees; Takeda: Research Funding; Omeros: Research Funding; Aduro: Membership on an entity's Board of Directors or advisory committees. Kumar:Celgene: Consultancy, Research Funding; Janssen: Consultancy, Research Funding; Takeda: Research Funding.
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Дисертації з теми "Cytogenetics"

1

Fantes, Judith Ann. "Molecular cytogenetics of 11p." Thesis, Open University, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388443.

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Marshall, Jillian Annette. "Molecular cytogenetics of Lycopersicon Mill." Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310839.

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Slater, Sarah. "The role of cytogenetics in leukaemia." Thesis, Queen Mary, University of London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398923.

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Xin, Mao. "Molecular cytogenetics of primary cutaneous lymphomas." Thesis, King's College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408664.

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Johansson, Soller Maria. "Cytogenetic studies of lung tumors." Lund : Dept. of Clinical Genetics, University of Lund, 1994. http://catalog.hathitrust.org/api/volumes/oclc/39068855.html.

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Sun, Li. "Molecular cytogenetics of oral squamous cell carcinoma." Click to view the E-thesis via HKUTO, 2002. http://sunzi.lib.hku.hk/HKUTO/record/B38627887.

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Loveday, Ruth Louise. "Molecular cytogenetics of breast cancer : clinical perspectives." Thesis, University of Hull, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322556.

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鄺沃林 and Yok-lam Kwong. "Cytogenetics and molecular genetics of haematological disorders." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1995. http://hub.hku.hk/bib/B31981550.

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Sun, Li, and 孫莉. "Molecular cytogenetics of oral squamous cell carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B36544267.

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Kwong, Yok-lam. "Cytogenetics and molecular genetics of haematological disorders." Hong Kong : University of Hong Kong, 1995. http://sunzi.lib.hku.hk/hkuto/record.jsp?B14036423.

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Книги з теми "Cytogenetics"

1

Liehr, Thomas. Cytogenetics and Molecular Cytogenetics. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003223658.

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Obe, Günter, and Armin Basler, eds. Cytogenetics. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72802-0.

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Singh, Ram J. Plant cytogenetics. Boca Raton: CRC Press, 1993.

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Singh, Ram J. Plant Cytogenetics. Third edition. | Boca Raton : Taylor & Francis, 2017.: CRC Press, 2016. http://dx.doi.org/10.1201/9781315374611.

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Fan, Yao-Shan. Molecular Cytogenetics. New Jersey: Humana Press, 2002. http://dx.doi.org/10.1385/1592593003.

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Swansbury, John. Cancer Cytogenetics. New Jersey: Humana Press, 2003. http://dx.doi.org/10.1385/1592593631.

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Wan, Thomas S. K., ed. Cancer Cytogenetics. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6703-2.

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Heim, Sverre, and Felix Mitelman, eds. Cancer Cytogenetics. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9781118010136.

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Kianian, Shahryar F., and Penny M. Avoles Kianian, eds. Plant Cytogenetics. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3622-9.

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Kato, Takamitsu A., and Paul F. Wilson, eds. Radiation Cytogenetics. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9432-8.

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Частини книг з теми "Cytogenetics"

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Moorman, Anthony V., and Christine J. Harrison. "Cytogenetics." In Adult Acute Lymphocytic Leukemia, 61–75. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-707-5_5.

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Sompalaym, Ramakrishna, Kokilamani A. Lingarajaiah, Raju G. Narayanappa, Jayaprakash, and Venkatachalaiah Govindaiah. "Cytogenetics." In Mealybugs and their Management in Agricultural and Horticultural crops, 19–54. New Delhi: Springer India, 2016. http://dx.doi.org/10.1007/978-81-322-2677-2_3.

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Guenet, Jean-Louis, Fernando Benavides, Jean-Jacques Panthier, and Xavier Montagutelli. "Cytogenetics." In Genetics of the Mouse, 51–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-44287-6_3.

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Raca, Gordana, Jo-Anne van der Krogt, Michelle M. Le Beau, and Iwona Wlodarska. "Cytogenetics." In Rare Lymphomas, 17–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-39590-1_2.

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Lozano-Kühne, Jingky. "Cytogenetics." In Encyclopedia of Systems Biology, 513. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_1293.

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Bailey, Ernest, and Samantha A. Brooks. "Cytogenetics." In Horse genetics, 168–80. Wallingford: CABI, 2020. http://dx.doi.org/10.1079/9781786392589.0168.

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Gorczyca, Wojciech. "Cytogenetics." In Atlas of Differential Diagnosis in Neoplastic Hematopathology, 158–82. 4th ed. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781003120445-07.

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Fletcher, Jonathan A. "Cytogenetics." In Multidisciplinary Treatment of Soft Tissue Sarcomas, 23–35. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3082-4_2.

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Gardner, Aaron, Sarah Stauffer, Lindsay Petley-Ragan, Philip Wismer, and Dewi Ayu Kencana Ungu. "Cytogenetics." In Labster Virtual Lab Experiments: Genetics of Human Diseases, 29–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-58744-7_2.

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Ramage, R. T. "Cytogenetics." In Agronomy Monographs, 127–54. Madison, WI, USA: American Society of Agronomy, Crop Science Society of America, Soil Science Society of America, 2015. http://dx.doi.org/10.2134/agronmonogr26.c6.

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Тези доповідей конференцій з теми "Cytogenetics"

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Ainsbury, Elizabeth, David Lloyd, Beverly Karplus Hartline, Renee K. Horton, and Catherine M. Kaicher. "Dose Estimation in Radiation Cytogenetics." In WOMEN IN PHYSICS: Third IUPAP International Conference on Women in Physics. AIP, 2009. http://dx.doi.org/10.1063/1.3137775.

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Yang, Xiaoli, Wei Wu, Ding Wen, Bin Chen, Jason Lacny, and Charles Tseng. "Virtual chromosome modeling for learning human cytogenetics." In 2010 8th IEEE International Conference on Control and Automation (ICCA). IEEE, 2010. http://dx.doi.org/10.1109/icca.2010.5524141.

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Muthappa Achandira, Udayakumar. "Follicular Dendritic Cell Sarcoma: Cytogenetics And Pathological Findings." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2014. http://dx.doi.org/10.5339/qfarc.2014.hbpp0414.

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"Genetic diversity of Triticum araraticum assessed using cytogenetics." In Plant Genetics, Genomics, Bioinformatics, and Biotechnology. Novosibirsk ICG SB RAS 2021, 2021. http://dx.doi.org/10.18699/plantgen2021-013.

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Vera Laceiras, Maria Silvia, Jaqueline Caffetti, and Maria Ines Pisarello. "Digital processing of cytogenetics images for classification and segmentation." In 2020 IEEE Congreso Bienal de Argentina (ARGENCON). IEEE, 2020. http://dx.doi.org/10.1109/argencon49523.2020.9505369.

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He, Jie, Jeffrey Gardner, James X. Sun, Omar Abdel-Wahab, Andrew M. Intlekofer, Michelle K. Nahas, Jo-Anne Vergilio, et al. "Abstract 4927: Next-generation sequencing enables new approach to molecular cytogenetics." 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.am2015-4927.

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"Quantitative real-time PCR as a supplementary tool for molecular cytogenetics." In Plant Genetics, Genomics, Bioinformatics, and Biotechnology. Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 2019. http://dx.doi.org/10.18699/plantgen2019-044.

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Russell, Nigel, and Marten Dooper. "No survival benefit of CPX-351 over FLAG-Ida in AML patients with adverse cytogenetics." In EHA2022 Hybrid Congress, edited by Rachel Giles. Baarn, the Netherlands: Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/942a78ab.

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Baker, Angela S., Esteban Braggio, Susana Jacobus, Sungwon Jung, Dirk Larson, Terry Therneau, Angela Dispenzieri, et al. "Abstract 2021: Characterization of myeloma tumors from a multi-ethnic cohort using cytogenetics and genomic analysis." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2021.

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Anderson, Christopher B., Michael Lipsky, Subhadra V. Nandula, Freeman E. Christopher, Matthews Thomas, Caitlin E. Walsh, Gen Li, et al. "Abstract 3415: Cytogenetics of renal oncocytomas identify three distinct and mutually exclusive diagnostic classes of chromosome aberrations." 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.am2018-3415.

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Звіти організацій з теми "Cytogenetics"

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Turner, Jill. Cytogenetics of Delphinium (Ranunculaceae) Species Native to Oregon. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.6450.

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Greulich-Bode, Karin M., Mei Wang, Andreas P. Rhein, Jingly F. Weier, and Heinz-Ulli G. Weier. Validation of DNA probes for molecular cytogenetics by mapping onto immobilized circular DNA. Office of Scientific and Technical Information (OSTI), December 2008. http://dx.doi.org/10.2172/982916.

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SRI INTERNATIONAL MENLO PARK CA. LPI845 Liquid Gun Propellant Dermal Toxicity Studies. An Assessment of the LP1846 Utilizing the Mammalian Cell Cytogenetics Assay With Chinese Hamster Ovary (CHO) Cells. Fort Belvoir, VA: Defense Technical Information Center, February 1990. http://dx.doi.org/10.21236/ada238250.

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Tel-Zur, Neomi, and Jeffrey J. Doyle. Role of Polyploidy in Vine Cacti Speciation and Crop Domestication. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7697110.bard.

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1. Abstract: Over the past 25 years, vine cacti of the genera Hylocereus and Selenicereus have been introduced into Israel and southern California as new exotic fruit crops. The importance of these crops lies in their high water use efficiency and horticultural potential as exotic fruit crops. Our collaboration focused on the cytological, molecular and evolutionary aspects of vine cacti polyploidization to confront the agricultural challenge of genetic improvement, ultimately to improve success of vine cacti as commercial fruit crop plants. More specifically, we worked on the: 1- Identification of the putative ancestor(s) of the tetraploid H. megalanthus; 2- Determination of the number of origins of H. megalanthus (single vs. multiple origins of polyploidy); 3- Cytogenetic analysis of BC1 and F1 hybrids; 4- Determination of important agricultural traits and the selection of superior hybrids for cultivation. The plant material used in this study comprised interspecific Hylocereus F1 and first backcross (BC1) hybrids, nine Hylocereus species (58 genotypes), nine Selenicereus species (14 genotypes), and four Epiphyllum genotypes. Two BC1 hexaploids (BC-023 and BC-031) were obtained, a high ploidy level that can be explained only by a fertilization event between one unreduced female gamete from the triploid hybrid and a balanced gamete from the pollen donor, the diploid H. monacanthus. These findings are scientific evidence that support the possibility that “hybridization followed by chromosome doubling” could also occur in nature. Cytomixis, the migration of chromatin between adjacent cells through connecting cytoplasmatic channels, was observed in vine cacti hybrids and may thus imply selective DNA elimination in response to the allopolyploidization process. Evidence from plastid and nrDNA internal transcribed spacers (ITS) sequences support the placement of H. megalanthus within a monophyletic Hylocereus group. Furthermore, both plastid and ITS datasets are most consistent with a conclusion that this tetraploid species is an autopolyploid, despite observations that the species appears to be morphologically intermediate between Hylocereus and Selenicereus. Although the possibility of very narrow allopolyploidly (i.e., derivation from parents that are barely diverged from each other such as closely related species in the same genus) cannot be ruled out entirely based on our data (in part due to the unavailability of Hylocereus species considered to be morphologically the closest relatives of H. megalanthus), the possibility of H. megalanthus representing an intergeneric cross (i.e., Hylocereus × Selenicereus) seems extremely unlikely. Interestingly, the process of homogenization of ITS sequences (concerted evolution) is either incomplete or lacking in both Hylocereus and Selenicereus, and the inclusion of several artificial hybrids in the molecular study revealed the potential for biparental plastid inheritance in Hylocereus. The most important agricultural implication of this research project was the information collected for F1 and BC1 hybrids. Specifically, this project concluded with the selection of four superior hybrids in terms of fruit quality and potential yields under extreme high temperatures. These selected hybrids are self-compatible, avoiding the need for hand cross pollination to set fruits, thus reducing manpower costs. We recently offered these hybrids to growers in Israel for prioritized rapid evaluation and characterization.
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