About

Dr. Suhu Liu is a hematologist and medical oncologist specializing in the diagnosis and treatment of hematologic malignancies, with a research focus in acute myeloid leukemia. She received her M.D. and Ph.D. degrees from Xi’an Jiaotong University in China, and subsequently pursued postdoctoral research training at Dana-Farber Cancer Institute of Harvard Medical School in Boston. Her clinical training includes an Internal Medicine residency at Montefiore of Albert Einstein College of Medicine and a Hematology & Oncology fellowship at Stony Brook University Hospital. Dr. Liu has extensive experience in cancer research and deeply appreciates how research has transformed patient care. She has received several awards, including the abstract achievement award from the American Society of Hematology in 2012, the Ruth L. Kirschstein National Research Service Award (NRSA) from 2012 to 2016, and the CAHON Young Investigator Award in 2022. She is dedicated to providing the best care for her patients, aiming to help them live their lives with as much normalcy as possible despite a cancer diagnosis. Additionally, she closely collaborates with scientists to enhance understanding of the pathogenesis of hematological malignancies and to develop novel biomarkers and therapeutic approaches.

Research topics

• Cell biology
• Medicine
• Biology
• Immunology
• Cancer research
• Internal medicine

Selected publications

• Retrospective analysis of R-CDOP efficacy and safety in frail patients with DLBCL compared to R-CHOP in fit patients

  Blood · 2025-11-03

  articleOpen access

  Abstract Introduction: R-CHOP (Rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone) remains a frontline treatment for DLBCL. However, toxicity in older patients remains a challenge. Pegylated liposomal doxorubicin (PLD) compared with doxorubicin has demonstrated a more favorable hematologic toxicity profile in breast cancer treatment. Further data is needed to better establish efficacy and relative safety for PLD substitution in the R-CHOP regimen (R-CDOP). Patients and Methods: A retrospective review was conducted on patients with DLBCL not otherwise specified (NOS) who received treatment with either R-CHOP or R-CDOP at Stony Brook University Hospital between 2014 and 2025. Patients were identified by ICD-10 code C83.3 for DLBCL via TriNetX query. Three independent reviewers manually verified records and excluded cases other than DLBCL NOS such as DLBCL transformed from indolent lymphoma and high-grade B cell lymphoma or other entities. Patient demographics, response rate, overall survival (OS), disease free survival (DFS; events defined as radiographic progression; deaths without confirmed progression were censored), cell counts of baseline, start of cycle, and nadir counts were assessed. Significance testing was performed using the log-rank test for OS and DFS, two tailed t-test for quantitative variables, and Fisher's exact test for categorical variables without adjustment for multiple comparison. Results: Of 450 records screened, 18 patients treated with R-CHOP and 10 with R-CDOP were included for analysis. Patients in the R-CDOP group were older compared to the R-CHOP group (75.4 years vs 57.4 years at diagnosis; p < 0.01), and more likely to have non-GCB subtype (70% versus 44%, p = 0.03). The R-CDOP group had lower baseline ejection fraction (EF) than the R-CHOP group (59% versus 63%, p = 0.04). There was no significant difference in gender, IPI score, LDH, or BMI between the two populations. Each patient in the R-CHOP group completed 6 cycles and 8 in the R-CDOP group completed 6 cycles, one 5 cycles and one 4 cycles. Median OS and DFS were not reached in either group. 5-year DFS was similar (75% for R-CDOP vs 88% for R-CHOP) while OS was significantly lower in the R-CDOP group (5-year OS: 53% vs 94% for R-CHOP; p = 0.01). Rates of any-grade observed adverse events were comparable between R-CDOP and R-CHOP: anemia (100% vs 94%), thrombocytopenia (60% vs 56%), neutropenia (80% vs 72%), and heart failure exacerbation (10% vs 0%). Grade ≥3 toxicities were also similar: anemia (50% vs 22%), thrombocytopenia (40% vs 11%), neutropenia (60% vs 56%), and febrile neutropenia (20% vs 11%). In R-CDOP, neutrophil count declined from 9.67 to 4.14 k/μL by cycle 6 (p = 0.01), with no significant changes in hemoglobin, platelets, or nadir counts between cycles 1 and 6. Conclusions: Patients in the R-CDOP group demonstrated greater age, lower EF, and more aggressive disease subtype than those in the R-CHOP group. There was no evidence of increased hematopoietic or cardiac adverse events in the R-CDOP group compared to the R-CHOP group. DFS was comparable while the OS was lower in the R-CDOP group, suggesting death from non-relapse etiologies.

  PublisherOA PDFDOI

• Revisiting the therapeutic potential of fenretinide in acute erythroid and acute megakaryoblastic leukemias

  Blood · 2025-11-03

  articleSenior author

  Abstract N-(4-hydroxyphenyl)retinamide (4-HPR, also known as Fenretinide) is a synthetic derivative of vitamin A with well-established anti-cancer properties. These properties include the rapid generation of reactive oxygen species, induction of stress responses and apoptosis, and repression of NF-κB and Wnt signaling pathways. Here, we report the transcription factor GATA1 as a novel target of Fenretinide, positioning Fenretinide as a promising therapeutic candidate for two aggressive subtypes of acute myeloid leukemia (AML): acute erythroleukemia (M6) and acute megakaryocytic leukemia (M7). These subtypes of AML have the poorest prognosis, with a median survival of only a few months despite active treatment. Using data from the Cancer Cell Line Encyclopedia and CRISPR screening from DepMap, we found that M6 and M7 AMLs exhibit high expression of GATA1 and are dependent on it for survival. GATA1 has been implicated in promoting AML cell proliferation and conferring resistance to chemotherapy. Despite its importance, GATA1 has long been considered “undruggable.” Here, we demonstrate that Fenretinide inhibits GATA1 expression in both M6/M7 AML cell lines and primary M6/M7 patient samples at concentrations as low as 0.35-2 µM, concentrations readily achievable in vivo with Fenretinide. GATA1 knockdown induces cytotoxicity comparable to low-dose Fenretinide treatment, while GATA1 overexpression rescues cells from low-dose Fenretinide-induced cytotoxicity. Furthermore, Fenretinide sensitizes M6/M7 AML cells to standard-of-care (SOC) therapies, particularly the Bcl-2 inhibitor venetoclax. Mechanistically, combination treatment with 4-HPR and SOC therapies leads to downregulation of BCL-XL, an anti-apoptotic protein known to contribute to M6/M7 resistance to Bcl-2 inhibitors. Interestingly, gene expression analysis following GATA1 knockdown reveals modulation of genes involved in immune-related pathways. Given the availability of clinical formulations, well documented clinical tolerability, and the lack of effective therapeutic options for M6/M7 AML, we propose that the therapeutic potential of Fenretinide warrants further exploration in patients with these aggressive subtypes of AML.

  PublisherDOI

• Tolerability and long-term survival of fragile or older patients with diffuse large B cell lymphoma (DLBCL) not otherwise specified by R-CDOP

  Blood · 2025-11-03

  article

  Abstract Introduction: According to Surveillance, Epidemiology, and End Results data, Diffuse Large B-Cell Lymphoma (DLBCL) is diagnosed at the median age of 67. Treatment decisions amongst older patients, especially over 75-year-old are challenging due to the poor tolerability of standard R-CHOP and the compromised efficacy of R-mini-CHOP. Patients and Methods: We retrospectively analyzed data from patients with DLBCL not otherwise specified (NOS) who were treated with frontline R-CDOP. The regimen included Rituximab 375mg/m2, Cyclophosphamide 750mg/m2, liposomal doxorubicin 30mg/m2 on day 1 and prednisone 100mg day 1-5, every 21 days a cycle, followed by granulocyte colony stimulating factor and preventive antibiotics support. Patients with transformed or other entities of DLBCL, or RCDOP as second line were excluded from this study. Clinical data included complete blood counts with differential, chemistry and clinical signs of cardiac failure, transfusion requirement, hospitalizations, positron emission tomography scans and clinical signs and symptoms of disease were analyzed. Deaths without evidence of disease relapse were counted as events Results: Ten patients' data (2 females, 8 males; 1 diagnosed at age of 47 with heart failure, the other 9, age from 71-86) were analyzed, 1 patients completed 4 cycles, one 5 cycles and the other 8 completed 6 cycles, none was given dose reduction. There was no worsening of cardiac congestion noted or events that compromised treatment. One showed partial response, the other 9 showed durable complete response. Three patients died without evidence of disease relapse (one from demenitia and 2 from secondary malignancies), 2 died from disease relapse. Overall survival and relapse-free survival at 5 years are both 50%. No patient died from the treatment. Conclusions: RCDOP as frontline appears tolerable for olderly with DLBCL NOS and gives durable response and long-term survival.

  PublisherDOI

• Fenretinide targets GATA1 to induce cytotoxicity in GATA1 positive Acute Erythroid and Acute Megakaryoblastic Leukemic cells

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-01-22 · 1 citations

  preprintOpen access

  ABSTRACT Patients with Acute Myeloid Leukemia (AML) subtypes, acute erythroleukemia and acute megakaryocytic leukemia (M6 and M7 AMLs, respectively) have a median survival of only a few months with no targeted effective treatment. Our gene expression analysis using the Cancer Cell Line Encyclopedia and CRISPR screen from DepMap showed that M6/M7 AMLs have high levels of the transcription factor GATA1 and depend on GATA1 for survival. While GATA1 was shown to support AML cell proliferation and resistance to chemotherapy, GATA1 has long been considered “undruggable”. Here, we identify the small molecule N-(4-hydroxyphenyl)retinamide (4-HPR, Fenretinide) as a novel GATA1 targeting agent in M6 and M7 AML cells, with nM to low μM concentrations of 4-HPR causing loss of GATA1. In M6 AML OCIM1 cells, knock-down of GATA1 induced cytotoxicity similarly to low doses 4-HPR while overexpression of GATA1 significantly protected cells from 4-HPR-induced cytotoxicity. In M6 AML cells resistant to current standard-of-care (SOC) Azacytidine plus Venetoclax, 4-HPR synergized with SOC overcoming cell resistance to the drugs. As single-agent, 4-HPR outperformed SOC. In M6 AML cells sensitive to SOC, 4-HPR enhanced and prolonged the growth inhibitory effect of SOC. 4-HPR is a synthetic derivative of vitamin A, and numerous clinical trials have supported its safe profile in cancer patients; therefore, targeted use of 4-HPR against M6 and M7 AMLs may represent a novel therapeutic window. Key Points - Fenretinide (4-HPR) targets the transcription factor GATA1, which was previously thought to be “undruggable” and induces GATA1 loss. - M6 and M7 Acute Myeloid Leukemias (AML) have enriched expression of GATA1 and they can be considered GATA1 positive. - Loss of GATA1 contributes significantly to 4-HPR cytotoxicity in M6 OCIM1 cells. - 4-HPR treatment overcomes chemotherapeutic resistance in M6 Acute Myeloid Leukemia cells, synergizes with standard-of-care and outperforms standard-of-care as a single agent.

  PublisherOA PDFDOI

• Prospective Study of CLL1 and CD45RA As Biomarkers of Leukemic Stem Cells to Predict Therapeutic Response in Acute Myeloid Leukemia

  Blood · 2024-11-05 · 1 citations

  articleSenior author

  Background: Acute myeloid leukemia (AML) is an aggressive hematologic malignancy characterized by the clonal expansion of immature myeloblasts from leukemic stem cells (LSCs) and the disruption of normal hematopoiesis by hematopoietic stem cells (HSCs). Currently, treatment response is evaluated at the end of induction therapy (Days 28 ± 7). Despite an overall remission rate of about 70% for newly diagnosed AML and 30-50% for relapsed/refractory AML, many patients endure toxic treatments without clinical benefit. There is a need for biomarkers that enable timely evaluation of treatment response and facilitate real-time therapy adjustments that optimize therapeutic benefit while minimizing unnecessary toxicity. Our prior retrospective study at Stony Brook University Hospital (SBUH) evaluated the dynamic changes of LSC versus HSC in AML patients using flow cytometric markers. Among the five LSC markers studied, changes in LSC/HSC subsets identified by CLL1 and CD45RA showed the strongest correlation with treatment response. Moreover, the presence of CLL1+ or CD45RA+ LSC/HSC subsets in peripheral blood correlated highly with bone marrow aspirate findings, suggesting that peripheral blood monitoring of LSC/HSC subsets could be a timely, non-invasive method to track LSC/HSC dynamics during AML treatment. Aims: The primary aims of this study are to assess: 1) the feasibility of tracking changes in LSC/HSC subsets using peripheral blood CLL1 and CD45RA as biomarkers on Days 3, 5, and 7 of induction therapy in AML patients, and 2) the feasibility of using LSC/HSC subsets to predict therapeutic response as evaluated by bone marrow examination at the end of induction cycle (Days 28 ± 7). Methods: This pilot prospective study plans to recruit 20 AML patients from SBUH who are 18 years or older, with newly diagnosed or relapsed/refractory AML and pre-treatment LSC marker (CLL1 and/or CD45RA) expression ≥50% of total HSCs. Following informed consent, peripheral blood samples are collected and processed for multicolor flow cytometry (MFC) on Days 3, 5, and 7 of induction therapy. The HSC population is defined as CD45dim/SSC and CD34+CD38low/-. CLL1 or CD45RA positive HSCs are identified as LSCs. LSC/HSC subsets are calculated as the percentage of CLL1+ or CD45RA+ cells within the HSC population. Changes in LSC/HSC subsets from pre-treatment will be evaluated and compared between patients with persistent disease and those achieving complete remission after induction chemotherapy. This study is registered at ClinicalTrials.gov (NCT06297551). Results: To date, 7 patients with newly diagnosed or relapsed AML have been enrolled. In the 4 patients who achieved complete remission, LSC/HSC subsets changed by an average of -14.22 ± 18.70% on Day 3, -65.19 ± 29.65% on Day 5, and -78.26 ± 20.76% on Day 7 compared to pre-treatment levels (normalized as 0% change). In the 3 patients with persistent disease after induction therapy, LSC/HSC subsets changed by an average of +19.30 ± 23.55% on Day 3, +11.60 ± 18.34% on Day 5, and -2.57 ± 5.11% on Day 7. Conclusions: Our preliminary results indicate that measuring the change in peripheral blood CLL1+ or CD45RA+ LSC/HSC subsets on Days 5 to 7 of induction therapy is feasible and may predict therapeutic outcome in AML. A significant decrease in CLL1+ or CD45RA+ LSC/HSC subsets in peripheral blood was observed as early as Days 5 to 7 of induction therapy, and this decrease in LSC/HSC subset biomarkers appears to be associated with complete remission by the end of the treatment cycle. Conversely, a lack of reduction in these subsets was seen in patients with persistent disease post induction therapy. Recruitment is ongoing, and we hope that additional data will further refine our findings for this study. In future studies, we hope to determine the optimal threshold of CLL1+ and CD45RA+ LSC/HSC subset change on Days 5 to 7 of induction therapy that is associated with remission versus disease persistence.

  PublisherDOI

• Supplementary Tables 1 to 3 and Supplementary Figures 1 to 7 from Targeting STAT5 in Hematologic Malignancies through Inhibition of the Bromodomain and Extra-Terminal (BET) Bromodomain Protein BRD2

  2023-04-03

  supplementary-materialsOpen access1st authorCorresponding

  <p>PDF - 128K, Supplemental Table 1: Clinical and molecular characteristics of cell lines; Supplemental Table 2: Sequences of primers used for Q-RT-PCR and CHIP; Supplemental Table 3: Targeting sequences of shRNA constructs; Supplemental Figure S1: JQ1 inhibits STAT5-dependent gene expression; Supplemental Figure S2: JQ1 inhibits expression of endogenous STAT5 target genes; Supplemental Figure S3: RNA interference constructs targeting bromodomain proteins show specificity; Supplemental Figure S4: Among bromodomain proteins, only inhibition of Brd2 reduces STAT5 transcriptional function; Supplemental Figure S5: Brd2 depletion reduces expression of STAT5 target genes only in cells with constitutively active STAT5. shRNA to Brd2 or GFP (as a control) was introduced into cells with (A) or without (B) activated STAT5, and quantitative RT-PCR analysis was performed for the indicated genes; Supplemental Figure S6: A. JQ1 reduces viability of T lymphocytic leukemia cells. B. JQ1 reduces Myc protein expression in T-ALL; Supplemental Figure S7. A. JQ1 has minimal effects on the viability of mononuclear cells from human cord blood. B. Kinase inhibitors have minimal effects on the viability of mononuclear cells from human cord blood.</p>

  PublisherDOI

• Data from Targeting STAT5 in Hematologic Malignancies through Inhibition of the Bromodomain and Extra-Terminal (BET) Bromodomain Protein BRD2

  2023-04-03

  preprintOpen access1st authorCorresponding

  <div>Abstract<p>The transcription factor signal STAT5 is constitutively activated in a wide range of leukemias and lymphomas, and drives the expression of genes necessary for proliferation, survival, and self-renewal. Thus, targeting STAT5 is an appealing therapeutic strategy for hematologic malignancies. Given the importance of bromodomain-containing proteins in transcriptional regulation, we considered the hypothesis that a pharmacologic bromodomain inhibitor could inhibit STAT5-dependent gene expression. We found that the small-molecule bromodomain and extra-terminal (BET) bromodomain inhibitor JQ1 decreases STAT5-dependent (but not STAT3-dependent) transcription of both heterologous reporter genes and endogenous STAT5 target genes. JQ1 reduces STAT5 function in leukemia and lymphoma cells with constitutive STAT5 activation, or inducibly activated by cytokine stimulation. Among the BET bromodomain subfamily of proteins, it seems that BRD2 is the critical mediator for STAT5 activity. In experimental models of acute T-cell lymphoblastic leukemias, where activated STAT5 contributes to leukemia cell survival, Brd2 knockdown or JQ1 treatment shows strong synergy with tyrosine kinase inhibitors (TKI) in inducing apoptosis in leukemia cells. In contrast, mononuclear cells isolated form umbilical cord blood, which is enriched in normal hematopoietic precursor cells, were unaffected by these combinations. These findings indicate a unique functional association between BRD2 and STAT5, and suggest that combinations of JQ1 and TKIs may be an important rational strategy for treating leukemias and lymphomas driven by constitutive STAT5 activation. <i>Mol Cancer Ther; 13(5); 1194–205. ©2014 AACR</i>.</p></div>

  PublisherDOI

• Data from Targeting STAT5 in Hematologic Malignancies through Inhibition of the Bromodomain and Extra-Terminal (BET) Bromodomain Protein BRD2

  2023-04-03

  preprintOpen access1st authorCorresponding

  <div>Abstract<p>The transcription factor signal STAT5 is constitutively activated in a wide range of leukemias and lymphomas, and drives the expression of genes necessary for proliferation, survival, and self-renewal. Thus, targeting STAT5 is an appealing therapeutic strategy for hematologic malignancies. Given the importance of bromodomain-containing proteins in transcriptional regulation, we considered the hypothesis that a pharmacologic bromodomain inhibitor could inhibit STAT5-dependent gene expression. We found that the small-molecule bromodomain and extra-terminal (BET) bromodomain inhibitor JQ1 decreases STAT5-dependent (but not STAT3-dependent) transcription of both heterologous reporter genes and endogenous STAT5 target genes. JQ1 reduces STAT5 function in leukemia and lymphoma cells with constitutive STAT5 activation, or inducibly activated by cytokine stimulation. Among the BET bromodomain subfamily of proteins, it seems that BRD2 is the critical mediator for STAT5 activity. In experimental models of acute T-cell lymphoblastic leukemias, where activated STAT5 contributes to leukemia cell survival, Brd2 knockdown or JQ1 treatment shows strong synergy with tyrosine kinase inhibitors (TKI) in inducing apoptosis in leukemia cells. In contrast, mononuclear cells isolated form umbilical cord blood, which is enriched in normal hematopoietic precursor cells, were unaffected by these combinations. These findings indicate a unique functional association between BRD2 and STAT5, and suggest that combinations of JQ1 and TKIs may be an important rational strategy for treating leukemias and lymphomas driven by constitutive STAT5 activation. <i>Mol Cancer Ther; 13(5); 1194–205. ©2014 AACR</i>.</p></div>

  PublisherDOI

• Use of CLL1 and CD45RA As Biomarkers for Leukemia Stem Cells in Acute Myeloid Leukemia Re-Induction Therapy Decision Making

  Blood · 2023-11-02

  articleSenior author

  Background: The decision to re-induce patients with newly diagnosed acute myeloid leukemia (AML) currently relies on morphological evaluation of leukemia blasts in post treatment bone marrow, with more than 5% bone marrow blast counts indicating necessity of re-induction therapy. Our previous study showed that changes in Leukemia Stem Cell (LSC) subsets, identified by CLL1 (CD371) or CD45RA as specific markers, are highly correlated with therapeutic outcome. In this study, we focus on newly diagnosed AML patients undergoing induction therapy to determine whether information gained from LSC subset analysis can aid in decision making for re-induction therapy. Methods: We analyzed flow cytometry data from bone marrow aspirate in patients with newly diagnosed AML of all types except acute promyelocytic leukemia (M3) before and after induction therapy from a single institution. “Leukemic blasts” were identified by morphology and leukemia-associated immunophenotype by Multicolor Flow cytometry (MFC). Hematopoietic stem cells (HSCs) gating was based on CD45 dim/SSC and CD34 +CD38 low/- expression. Leukemic stem cells (LSC) subset was analyzed using % of CD371 (CLL-1) or CD45RA positive cells over total HSCs (%CLL1 +/CD34 +CD38 - or %CD45RA +/CD34 +CD38 -). Newly diagnosed AML with >50% (CLL1 +/CD34 +CD38 - or CD45RA +/CD34 +CD38 -) on diagnosis was selected for further study. Fold change of LSC subset was calculated using LSC percentage post-induction divided by LSC percentage on diagnosis. Chart review was conducted to determine correlation between LSC subset change, bone marrow blasts count and clinical course. Mann-Whitney test was used for statistical analysis. Results: Forty-eight newly diagnosed AML (non-M3) cases, who received at least one cycle of induction therapy with both pre- and post-treatment bone marrow biopsy were reviewed. Twenty-seven cases were identified with CLL1 +/CD34 +CD38 - or CD45RA +/CD34 +CD38 - above the 50% threshold on diagnosis. Four cases were later excluded due to inadequate CD34 +CD38 - cellular events on flow cytometry (<20) in post-treatment bone marrow samples. As shown in figure 1, in all the 9 patients with post induction blasts counts of less than 5% (complete remission, CR), post induction LSC subset is reduced to less than 0.5× of LSC subset on diagnosis. Thus, post induction LSC subset less than 0.5× of diagnosis is used as cut off for “adequate reduction”. In 14 patients with residual blasts of more than 5%, there is a wide range of LSC subset change. Interestingly, 6 of them showed adequate reduction of LSC subsets, similar to patients who achieved CR. Among them, one was observed and showed CR on repeat bone marrow biopsy at a later time point without further therapy. The other 5 patients were given re-induction and achieved CR after a second cycle. Eight patients with residual blasts did not achieve adequate reduction of LSC subset (residual LSC subset > 0.5× of diagnosis). Five achieved CR on subsequent re-induction. Three had persistent disease and failed to achieve CR despite 3 cycles of induction therapy. Conclusion: In newly diagnosed AML with high percent of CLL1 +/CD34 +CD38 - or CD45RA +/CD34 +CD38 - LSC subset on diagnosis, monitoring LSC subset offers additional information regarding efficacy of induction therapy. All the patients with CR showed residual LSC subset of 0.5-fold or less compared to LSC subset on diagnosis (defined as “adequate reduction” of LSC subset). For patients who did not achieve remission but adequately reduced LSC subset, which indicates efficacy of induction therapy, observation with repeat bone marrow biopsy, or re-induction with similar regimen can be considered. For patients with no adequate reduction of LSC subset, intensified chemotherapy or alternative therapy with different mechanism of action needs to be considered to maximize the possibility of achieving CR on re-induction. A multi-institutional study with more patients is needed to confirm these findings and validate these LSC biomarkers for this important treatment decision making in AML.

  PublisherDOI

• Supplementary Tables 1 to 3 and Supplementary Figures 1 to 7 from Targeting STAT5 in Hematologic Malignancies through Inhibition of the Bromodomain and Extra-Terminal (BET) Bromodomain Protein BRD2

  2023-04-03

  supplementary-materialsOpen access1st authorCorresponding

  <p>PDF - 128K, Supplemental Table 1: Clinical and molecular characteristics of cell lines; Supplemental Table 2: Sequences of primers used for Q-RT-PCR and CHIP; Supplemental Table 3: Targeting sequences of shRNA constructs; Supplemental Figure S1: JQ1 inhibits STAT5-dependent gene expression; Supplemental Figure S2: JQ1 inhibits expression of endogenous STAT5 target genes; Supplemental Figure S3: RNA interference constructs targeting bromodomain proteins show specificity; Supplemental Figure S4: Among bromodomain proteins, only inhibition of Brd2 reduces STAT5 transcriptional function; Supplemental Figure S5: Brd2 depletion reduces expression of STAT5 target genes only in cells with constitutively active STAT5. shRNA to Brd2 or GFP (as a control) was introduced into cells with (A) or without (B) activated STAT5, and quantitative RT-PCR analysis was performed for the indicated genes; Supplemental Figure S6: A. JQ1 reduces viability of T lymphocytic leukemia cells. B. JQ1 reduces Myc protein expression in T-ALL; Supplemental Figure S7. A. JQ1 has minimal effects on the viability of mononuclear cells from human cord blood. B. Kinase inhibitors have minimal effects on the viability of mononuclear cells from human cord blood.</p>

  PublisherOA PDFDOI

Frequent coauthors

• David A. Frank

  Emory University

  120 shared

• Sarah R. Walker

  University of New Hampshire

  90 shared

• Patricia A. Toniolo

  64 shared

• Michael Xiang

  Jinshan Hospital of Fudan University

  39 shared

• Erik A. Nelson

  37 shared

• Jennifer Yeh

  Stanford University

  35 shared

• Adam I. Riker

  Precision Spine (United States)

  33 shared

• Darwin Q. Ye

  Harvard University

  30 shared

Education

• M.D.

  Xi'an Jiaotong University

• Ph.D.

  Xi'an Jiaotong University

• Other

  Dana-Farber Cancer Institute of Harvard Medical School

• Other

  Montefiore of Albert Einstein College of Medicine

• Other

  Stony Brook University Hospital

Awards & honors

• Abstract achievement award from American Society of Hematolo…
• Ruth L. Kirschstein National Research Service Award (NRSA) (…
• CAHON Young Investigator Award (YIA) in 2022