scholarly journals Synchronous Plasma Cell Myeloma and Acute Myeloid Leukemia in a Therapy-Naïve Patient: A Rare Occurrence

2015 ◽  
Vol 32 (S1) ◽  
pp. 168-172 ◽  
Author(s):  
Rajesh Kumar ◽  
Vishrut K. Srinivasan ◽  
Prashant Sharma ◽  
Ritu Aggarwal ◽  
Gaurav Prakash ◽  
...  
2018 ◽  
Vol 74 ◽  
pp. 130-136 ◽  
Author(s):  
Tomas Radivoyevitch ◽  
Robert M. Dean ◽  
Bronwen E. Shaw ◽  
Ruta Brazauskas ◽  
Heather R. Tecca ◽  
...  

2016 ◽  
Vol 5 (4) ◽  
pp. 333 ◽  
Author(s):  
SmithaCarol Saldanha ◽  
Govind Babu ◽  
MallekavuSuresh Babu ◽  
LakshmaiahChinnagiriyappa Kuntegowdanahalli ◽  
LakkavalliKrishnappa Rajeev ◽  
...  

Author(s):  
Deepshi Thakral ◽  
Ritu Gupta ◽  
Ranjit Kumar Sahoo ◽  
Pramod Verma ◽  
Indresh Kumar ◽  
...  

The clonal evolution of acute myeloid leukemia (AML), an oligoclonal hematological malignancy, is driven by a plethora of cytogenetic abnormalities, gene mutations, abnormal epigenetic patterns, and aberrant gene expressions. These alterations in the leukemic blasts promote clinically diverse manifestations with common characteristics of high relapse and drug resistance. Defining and real-time monitoring of a personalized panel of these predictive genetic biomarkers is rapidly being adapted in clinical setting for diagnostic, prognostic, and therapeutic decision-making in AML. A major challenge remains the frequency of invasive biopsy procedures that can be routinely performed for monitoring of AML disease progression. Moreover, a single-site biopsy is not representative of the tumor heterogeneity as it is spatially and temporally constrained and necessitates the understanding of longitudinal and spatial subclonal dynamics in AML. Hematopoietic cells are a major contributor to plasma cell-free DNA, which also contain leukemia-specific aberrations as the circulating tumor-derived DNA (ctDNA) fraction. Plasma cell-free DNA analysis holds immense potential as a minimally invasive tool for genomic profiling at diagnosis as well as clonal evolution during AML disease progression. With the technological advances and increasing sensitivity for detection of ctDNA, both genetic and epigenetic aberrations can be qualitatively and quantitatively evaluated. However, challenges remain in validating the utility of liquid biopsy tools in clinics, and universal recommendations are still awaited towards reliable diagnostics and prognostics. Here, we provide an overview on the scope of ctDNA analyses for prognosis, assessment of response to treatment and measurable residual disease, prediction of disease relapse, development of acquired resistance and beyond in AML.


Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 21-21
Author(s):  
Can Can ◽  
Lu Ding ◽  
Yuxin Tan ◽  
Balu Wu ◽  
Dongdong Zhang ◽  
...  

Objective: To investigate the efficacy and safety of recombinant human thrombopoietin(rhTPO) in the treatment of thrombocytopenia after chemotherapy for acute myeloid leukemia in vivo and in vitro. Methods: A retrospective collection of 95 patients with acute myeloid leukemia who suffered thrombocytopenia after chemotherapy in Zhongnan hospital from July 2014 to April 2019 were collected. The patients were divided into two groups according to different medications, one group was treated with reorganized human thrombopoietin, the other one with recombinant IL-11, the platelet counts between two groups was analyzed and the platelet recovery under different ages, medical conditions and other factors were analyzed; mice patient derived xenograft model of acute myeloid leukemia with thrombocytopenia after chemotherapy was established to verify the efficacy and the mechanism of rhTPO. Results: Since the platelet counts began to recover, the platelet increase in rhTPO group was significantly greater than that in IL-11 group, the platelet count is significantly higher than IL-11 group at Day42 (P<0.05). Age and whether it is chemotherapy-naive patient has no significant effect on the function of rhTPO in restoring platelet counts. It is verified that rhTPO can increase platelet counts, but has no significant effect on leukocytes, erythrocytes. The injection of rhTPO leads to more synthesis of TPO in liver by activating the JAK2-STAT3 pathway. Conclusion: Our work has paved the way for further study on the clinical application of rhTPO in managing thrombocytopenia for AML after chemotherapy. Disclosures No relevant conflicts of interest to declare.


2015 ◽  
Vol 33 (15_suppl) ◽  
pp. e18056-e18056
Author(s):  
Abhishek Avinash Mangaonkar ◽  
Rohini Chintalapally ◽  
Ashis Mondal ◽  
Ravindra B. Kolhe ◽  
Vamsi Kota

Blood ◽  
2016 ◽  
Vol 127 (19) ◽  
pp. 2359-2359
Author(s):  
Erika M. Moore ◽  
Christine G. Roth

2020 ◽  
Vol 4 (3) ◽  
Author(s):  
Michael T Milano ◽  
Paul C Dinh ◽  
Hongmei Yang ◽  
Mohammad Abu Zaid ◽  
Sophie D Fossa ◽  
...  

Abstract Background No large US population-based study focusing on recent decades, to our knowledge, has comprehensively examined risks of second malignant solid and hematological neoplasms (solid-SMN and heme-SMN) after testicular cancer (TC), taking into account initial therapy and histological type. Methods Standardized incidence ratios (SIR) vs the general population and 95% confidence intervals (CI) for solid-SMN and heme-SMN were calculated for 24 900 TC survivors (TCS) reported to the National Cancer Institute’s Surveillance, Epidemiology, and End Results registries (1973–2014). All statistical tests were two-sided. Results The median age at TC diagnosis was 33 years. Initial management comprised chemotherapy (n = 6340), radiotherapy (n = 9058), or surgery alone (n = 8995). During 372 709 person-years of follow-up (mean = 15 years), 1625 TCS developed solid-SMN and 228 (107 lymphomas, 92 leukemias, 29 plasma cell dyscrasias) developed heme-SMN. Solid-SMN risk was increased 1.06-fold (95% CI = 1.01 to 1.12), with elevated risks following radiotherapy (SIR = 1.13, 95% CI = 1.06 to 1.21) and chemotherapy (SIR = 1.36, 95% CI = 1.12 to 1.41) but not surgery alone (SIR = 0.83, 95% CI = 0.75 to 0.92). Corresponding risks for seminoma were 1.13 (95% CI = 1.06 to 1.21), 1.28 (95% CI = 1.02 to 1.58), and 0.87 (95% CI = 0.74 to 1.01) and for nonseminoma were 1.05 (95% CI = 0.67 to 1.56), 1.25 (95% CI = 1.08 to 1.43), and 0.80 (95% CI = 0.70 to 0.92), respectively. Thirty-year cumulative incidences of solid-SMN after radiotherapy, chemotherapy, and surgery alone were 16.9% (95% CI = 15.7% to 18.1%), 10.1% (95% CI = 8.8% to 11.5%), and 8.8% (95% CI = 7.8% to 9.9%), respectively (P < .0001). Increased leukemia risks after chemotherapy (SIR = 2.68, 95% CI = 1.70 to 4.01) were driven by statistically significant sevenfold excesses of acute myeloid leukemia 1 to 10 years after TC diagnosis. Risks for lymphoma and plasma cell dyscrasias were not elevated. Conclusions We report statistically significant excesses of solid-SMN affecting 1 in 6 TCS 30 years after radiotherapy, and 2.7-fold risks of leukemias after chemotherapy, mostly acute myeloid leukemia. Efforts to minimize chemotherapy and radiotherapy exposures for TC should continue. TCS should be counseled about cancer prevention and screening.


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