Sophia Adamia

ORCID: 0000-0001-5704-6040
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Chronic Myeloid Leukemia Treatments
  • Chronic Lymphocytic Leukemia Research
  • Acute Myeloid Leukemia Research
  • Drug Transport and Resistance Mechanisms
  • RNA Interference and Gene Delivery
  • Multiple Myeloma Research and Treatments
  • Protein Degradation and Inhibitors
  • RNA Research and Splicing
  • Cancer therapeutics and mechanisms
  • RNA modifications and cancer
  • Glycosylation and Glycoproteins Research
  • MicroRNA in disease regulation
  • Lymphoma Diagnosis and Treatment
  • DNA and Nucleic Acid Chemistry
  • Proteoglycans and glycosaminoglycans research
  • Cancer Mechanisms and Therapy
  • Ferrocene Chemistry and Applications
  • Histone Deacetylase Inhibitors Research
  • Microfluidic and Capillary Electrophoresis Applications
  • Peptidase Inhibition and Analysis
  • Immunodeficiency and Autoimmune Disorders
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • CAR-T cell therapy research
  • Biochemical and Molecular Research
  • PARP inhibition in cancer therapy

Harvard University
2013-2024

Dana-Farber Cancer Institute
2015-2024

Beth Israel Deaconess Medical Center
2013-2024

Ilia State University
2022-2023

Inserm
2013

Boston Medical Center
2011

Dana-Farber Brigham Cancer Center
2010

Brigham and Women's Hospital
2010

University of Alberta
2001-2008

Cancer Institute (WIA)
2003-2008

Nucleoside analogs (NAs) are considered as appropriate agents in the treatment of Waldenström macroglobulinemia (WM), a lymphoplasmacytic lymphoma. Sporadic reports on increased incidence transformation to high-grade non-Hodgkin's lymphoma and development therapy-related myelodysplasia/acute leukemia (t-MDS/AML) among patients with WM treated NAs prompted us examine such events large population WM.We examined these 439 WM, 193 136 whom were previously without an NA, respectively, 110 had...

10.1200/jco.2007.15.1530 article EN Journal of Clinical Oncology 2008-12-09

Despite new treatments, acute myeloid leukemia (AML) remains an incurable disease. More effective drug design requires expanded view of the molecular complexity that underlies AML. Alternative splicing RNA is used by normal cells to generate protein diversity. Growing evidence indicates aberrant genes plays a key role in cancer. We investigated genome-wide abnormalities AML and based on these abnormalities, we aimed identify novel potential biomarkers therapeutic targets.We alternative...

10.1158/1078-0432.ccr-13-0956 article EN Clinical Cancer Research 2013-11-28

Fluorescently labeled peanut lectin agglutinin (PNA-FITC) was used to identify a subtype of mitochondria-rich (MR) cells in the gills freshwater rainbow trout. In situ binding PNA-FITC visualized by inverted fluorescence microscopy and found bind on trailing edge filament epithelium as demonstrated differential interference contrast optics. The amount increased with cortisol pretreatment concomitant an chloride cell fractional area scanning electron microscopy. Dispersed gill were isolated...

10.1152/ajpregu.2001.281.5.r1718 article EN AJP Regulatory Integrative and Comparative Physiology 2001-11-01

Abstract Deregulated microRNA (miR)/transcription factor (TF)-based networks represent a hallmark of cancer. We report here novel c-Myc/miR-23b/Sp1 feed-forward loop with critical role in multiple myeloma (MM) and Waldenstrom’s macroglobulinemia (WM) cell growth survival. have found miR-23b to be downregulated MM WM cells especially the presence components tumor bone marrow milieu. Promoter methylation is one mechanism suppression myeloma. In gain-of-function studies using mimics-transfected...

10.1038/bcj.2015.106 article EN cc-by Blood Cancer Journal 2016-01-15

Mutations in two type-3 receptor tyrosine kinases (RTKs), KIT and FLT3, are common both acute myeloid leukaemia (AML) systemic mastocytosis (SM) lead to hyperactivation of key signalling pathways. A large number kinase inhibitors (TKIs) have been developed that target either FLT3 or significant clinical benefit has demonstrated multiple trials. Given the structural similarity KIT, it is not surprising some these TKIs inhibit receptors. This typified by midostaurin, which approved US Food...

10.1111/bjh.16092 article EN British Journal of Haematology 2019-07-15

Abstract In many cancers, mortality is associated with the emergence of relapse multidrug resistance (MDR). Thus far, investigation cancer mechanisms has largely focused on acquired genetic mutations. Using acute myeloid leukemia (AML) patient-derived xenografts (PDX), we systematically elucidated a basis MDR and identified drug sensitivity in relapsed AML. We derived pharmacologic for 22 AML PDX models using dynamic BH3 profiling (DBP), together genomics transcriptomics. vivo resistant...

10.1158/2643-3230.bcd-24-0001 article EN Blood Cancer Discovery 2024-03-05

Abstract Clinical studies of patients with chronic myeloid leukemia revealed that a common pattern response is dramatic fall in the circulating population blast cells, minimal or delayed decrease marrow blasts, suggesting protective environment. These observations suggest greater understanding interaction stromal cells leukemic essential. Here, we present an vivo system for monitoring relative tumor accumulation mice and residual disease treated tyrosine kinase inhibitor vitro identifying...

10.1158/1535-7163.mct-07-2331 article EN Molecular Cancer Therapeutics 2008-04-30

Objectives Clinical responses achieved with FLT3 kinase inhibitors in acute myeloid leukemia (AML) are typically transient and partial. Thus, there is a need for identification of molecular mechanisms clinical resistance to these drugs. In response, we characterized MOLM13 AML cell lines made resistant two structurally-independent inhibitors. Methods cells were drug via prolonged exposure midostaurin HG-7-85-01, respectively. Cell proliferation was determined by Trypan blue exclusion....

10.1371/journal.pone.0025351 article EN cc-by PLoS ONE 2011-09-28
Coming Soon ...