Scholars@Duke
Sin Tiong Ong

Sin Tiong Ong

Associate Professor of Medicine
Medicine, Medical Oncology
sintiong.ong@duke-nus.edu.sg
406 Seeley Mudd Bldg, Box 3406, Durham, NC 27710
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Selected Publications

Leukaemia Exposure Alters the Transcriptional Profile and Function of Macrophages in the Bone Marrow Niche

Conference Blood · November 2, 2023 These authors contributed equally to this work: Martha M. Zarou & Amy DawsonMacrophages are fundamental cells of the innate immune system. Bone marrow (BM) resident macrophages are i ... Full text Cite

A single-cell atlas identifies pretreatment features of primary imatinib resistance in chronic myeloid leukemia.

Journal Article Blood · June 1, 2023 Primary resistance to tyrosine kinase inhibitors (TKIs) is a significant barrier to optimal outcomes in chronic myeloid leukemia (CML), but factors contributing to response heterogeneity remain unclear. Using single-cell RNA (scRNA) sequencing, we identifi ... Full text Link to item Cite

Epigenetic Dysregulation of CML

Journal Article CLINICAL LYMPHOMA MYELOMA & LEUKEMIA · 2023 Cite

Therapy Resistance and Disease Progression in CML: Mechanistic Links and Therapeutic Strategies.

Journal Article Curr Hematol Malig Rep · December 2022 PURPOSE OF REVIEW: Despite the adoption of tyrosine kinases inhibitors (TKIs) as molecular targeted therapy in chronic myeloid leukemia, some patients do not respond to treatment and even experience disease progression. This review aims to give a broad sum ... Full text Link to item Cite

A novel network pharmacology approach for leukaemia differentiation therapy using Mogrify®.

Journal Article Oncogene · November 2022 Acute myeloid leukaemia (AML) is a rapidly fatal blood cancer that is characterised by the accumulation of immature myeloid cells in the blood and bone marrow as a result of blocked differentiation. Methods which identify master transcriptional regulators ... Full text Link to item Cite

Integrating genetic and epigenetic factors in chronic myeloid leukemia risk assessment: toward gene expression-based biomarkers.

Journal Article Haematologica · February 1, 2022 Cancer treatment is constantly evolving from a one-size-fits-all towards bespoke approaches for each patient. In certain solid cancers, including breast and lung, tumor genome profiling has been incorporated into therapeutic decision-making. For chronic ph ... Full text Link to item Cite

THZ531 Induces a State of BRCAness in Multiple Myeloma Cells: Synthetic Lethality with Combination Treatment of THZ 531 with DNA Repair Inhibitors.

Journal Article Int J Mol Sci · January 21, 2022 Multiple myeloma (MM) is a hematological disease marked by abnormal growth of B cells in bone marrow. Inherent chromosomal instability and DNA damage are major hallmarks of MM, which implicates an aberrant DNA repair mechanism. Studies have implicated a ro ... Full text Link to item Cite

RCA2: a scalable supervised clustering algorithm that reduces batch effects in scRNA-seq data.

Journal Article Nucleic Acids Res · September 7, 2021 The transcriptomic diversity of cell types in the human body can be analysed in unprecedented detail using single cell (SC) technologies. Unsupervised clustering of SC transcriptomes, which is the default technique for defining cell types, is prone to grou ... Full text Link to item Cite

SRSF1 mediates cytokine-induced impaired imatinib sensitivity in chronic myeloid leukemia.

Journal Article Leukemia · July 2020 Patients with chronic myeloid leukemia (CML) who are treated with tyrosine kinase inhibitors (TKIs) experience significant heterogeneity regarding depth and speed of responses. Factors intrinsic and extrinsic to CML cells contribute to response heterogenei ... Full text Link to item Cite

An integrative model of pathway convergence in genetically heterogeneous blast crisis chronic myeloid leukemia.

Journal Article Blood · June 25, 2020 Targeted therapies against the BCR-ABL1 kinase have revolutionized treatment of chronic phase (CP) chronic myeloid leukemia (CML). In contrast, management of blast crisis (BC) CML remains challenging because BC cells acquire complex molecular alterations t ... Full text Link to item Cite

Phase I study of vorinostat with gefitinib in BIM deletion polymorphism/epidermal growth factor receptor mutation double-positive lung cancer.

Journal Article Cancer Sci · February 2020 Patients with epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer (NSCLC) harboring BIM deletion polymorphism (BIM deletion) have poor responses to EGFR TKI. Mechanistically, the BIM deletion induces preferential splicing of the non- ... Full text Link to item Cite

Resminostat, a histone deacetylase inhibitor, circumvents tolerance to EGFR inhibitors in EGFR-mutated lung cancer cells with BIM deletion polymorphism.

Journal Article J Med Invest · 2020 Drug-tolerant cells are mediators of acquired resistance. BIM-intron2 deletion polymorphism (BIM-del) is one of the mechanisms underlying the resistance to epidermal growth factor tyrosine kinase inhibitor (EGFR-TKI)-mediated apoptosis that induces drug to ... Full text Link to item Cite

Laying the foundation for genomically-based risk assessment in chronic myeloid leukemia.

Journal Article Leukemia · August 2019 Outcomes for patients with chronic myeloid leukemia (CML) have substantially improved due to advances in drug development and rational treatment intervention strategies. Despite these significant advances there are still unanswered questions on patient man ... Full text Link to item Cite

Viable Mice with Extensive Gene Humanization (25-kbp) Created Using Embryonic Stem Cell/Blastocyst and CRISPR/Zygote Injection Approaches.

Journal Article Sci Rep · October 9, 2018 Here, we describe an expansion of the typical DNA size limitations associated with CRISPR knock-in technology, more specifically, the physical extent to which mouse genomic DNA can be replaced with donor (in this case, human) DNA at an orthologous locus by ... Full text Link to item Cite

Optimization of Selective Mitogen-Activated Protein Kinase Interacting Kinases 1 and 2 Inhibitors for the Treatment of Blast Crisis Leukemia.

Journal Article J Med Chem · May 24, 2018 Chronic myeloid leukemia (CML) is a myeloproliferative disease caused by bcr-abl1, a constitutively active tyrosine kinase fusion gene responsible for an abnormal proliferation of leukemic stem cells (LSCs). Inhibition of BCR-ABL1 kinase activity offers lo ... Full text Link to item Cite

The arginase inhibitor Nω-hydroxy-nor-arginine (nor-NOHA) induces apoptosis in leukemic cells specifically under hypoxic conditions but CRISPR/Cas9 excludes arginase 2 (ARG2) as the functional target.

Journal Article PLoS One · 2018 Cancer cells, including in chronic myeloid leukemia (CML), depend on the hypoxic response to persist in hosts and evade therapy. Accordingly, there is significant interest in drugging cancer-specific hypoxic responses. However, a major challenge in leukemi ... Full text Link to item Cite

Leukaemia Exposure Alters the Transcriptional Profile and Function of Macrophages in the Bone Marrow Niche

Conference Blood · November 2, 2023 These authors contributed equally to this work: Martha M. Zarou & Amy DawsonMacrophages are fundamental cells of the innate immune system. Bone marrow (BM) resident macrophages are i ... Full text Cite

A single-cell atlas identifies pretreatment features of primary imatinib resistance in chronic myeloid leukemia.

Journal Article Blood · June 1, 2023 Primary resistance to tyrosine kinase inhibitors (TKIs) is a significant barrier to optimal outcomes in chronic myeloid leukemia (CML), but factors contributing to response heterogeneity remain unclear. Using single-cell RNA (scRNA) sequencing, we identifi ... Full text Link to item Cite

Epigenetic Dysregulation of CML

Journal Article CLINICAL LYMPHOMA MYELOMA & LEUKEMIA · 2023 Cite

Therapy Resistance and Disease Progression in CML: Mechanistic Links and Therapeutic Strategies.

Journal Article Curr Hematol Malig Rep · December 2022 PURPOSE OF REVIEW: Despite the adoption of tyrosine kinases inhibitors (TKIs) as molecular targeted therapy in chronic myeloid leukemia, some patients do not respond to treatment and even experience disease progression. This review aims to give a broad sum ... Full text Link to item Cite

A novel network pharmacology approach for leukaemia differentiation therapy using Mogrify®.

Journal Article Oncogene · November 2022 Acute myeloid leukaemia (AML) is a rapidly fatal blood cancer that is characterised by the accumulation of immature myeloid cells in the blood and bone marrow as a result of blocked differentiation. Methods which identify master transcriptional regulators ... Full text Link to item Cite

Integrating genetic and epigenetic factors in chronic myeloid leukemia risk assessment: toward gene expression-based biomarkers.

Journal Article Haematologica · February 1, 2022 Cancer treatment is constantly evolving from a one-size-fits-all towards bespoke approaches for each patient. In certain solid cancers, including breast and lung, tumor genome profiling has been incorporated into therapeutic decision-making. For chronic ph ... Full text Link to item Cite

THZ531 Induces a State of BRCAness in Multiple Myeloma Cells: Synthetic Lethality with Combination Treatment of THZ 531 with DNA Repair Inhibitors.

Journal Article Int J Mol Sci · January 21, 2022 Multiple myeloma (MM) is a hematological disease marked by abnormal growth of B cells in bone marrow. Inherent chromosomal instability and DNA damage are major hallmarks of MM, which implicates an aberrant DNA repair mechanism. Studies have implicated a ro ... Full text Link to item Cite

RCA2: a scalable supervised clustering algorithm that reduces batch effects in scRNA-seq data.

Journal Article Nucleic Acids Res · September 7, 2021 The transcriptomic diversity of cell types in the human body can be analysed in unprecedented detail using single cell (SC) technologies. Unsupervised clustering of SC transcriptomes, which is the default technique for defining cell types, is prone to grou ... Full text Link to item Cite

SRSF1 mediates cytokine-induced impaired imatinib sensitivity in chronic myeloid leukemia.

Journal Article Leukemia · July 2020 Patients with chronic myeloid leukemia (CML) who are treated with tyrosine kinase inhibitors (TKIs) experience significant heterogeneity regarding depth and speed of responses. Factors intrinsic and extrinsic to CML cells contribute to response heterogenei ... Full text Link to item Cite

An integrative model of pathway convergence in genetically heterogeneous blast crisis chronic myeloid leukemia.

Journal Article Blood · June 25, 2020 Targeted therapies against the BCR-ABL1 kinase have revolutionized treatment of chronic phase (CP) chronic myeloid leukemia (CML). In contrast, management of blast crisis (BC) CML remains challenging because BC cells acquire complex molecular alterations t ... Full text Link to item Cite

Phase I study of vorinostat with gefitinib in BIM deletion polymorphism/epidermal growth factor receptor mutation double-positive lung cancer.

Journal Article Cancer Sci · February 2020 Patients with epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer (NSCLC) harboring BIM deletion polymorphism (BIM deletion) have poor responses to EGFR TKI. Mechanistically, the BIM deletion induces preferential splicing of the non- ... Full text Link to item Cite

Resminostat, a histone deacetylase inhibitor, circumvents tolerance to EGFR inhibitors in EGFR-mutated lung cancer cells with BIM deletion polymorphism.

Journal Article J Med Invest · 2020 Drug-tolerant cells are mediators of acquired resistance. BIM-intron2 deletion polymorphism (BIM-del) is one of the mechanisms underlying the resistance to epidermal growth factor tyrosine kinase inhibitor (EGFR-TKI)-mediated apoptosis that induces drug to ... Full text Link to item Cite

Laying the foundation for genomically-based risk assessment in chronic myeloid leukemia.

Journal Article Leukemia · August 2019 Outcomes for patients with chronic myeloid leukemia (CML) have substantially improved due to advances in drug development and rational treatment intervention strategies. Despite these significant advances there are still unanswered questions on patient man ... Full text Link to item Cite

Viable Mice with Extensive Gene Humanization (25-kbp) Created Using Embryonic Stem Cell/Blastocyst and CRISPR/Zygote Injection Approaches.

Journal Article Sci Rep · October 9, 2018 Here, we describe an expansion of the typical DNA size limitations associated with CRISPR knock-in technology, more specifically, the physical extent to which mouse genomic DNA can be replaced with donor (in this case, human) DNA at an orthologous locus by ... Full text Link to item Cite

Optimization of Selective Mitogen-Activated Protein Kinase Interacting Kinases 1 and 2 Inhibitors for the Treatment of Blast Crisis Leukemia.

Journal Article J Med Chem · May 24, 2018 Chronic myeloid leukemia (CML) is a myeloproliferative disease caused by bcr-abl1, a constitutively active tyrosine kinase fusion gene responsible for an abnormal proliferation of leukemic stem cells (LSCs). Inhibition of BCR-ABL1 kinase activity offers lo ... Full text Link to item Cite

The arginase inhibitor Nω-hydroxy-nor-arginine (nor-NOHA) induces apoptosis in leukemic cells specifically under hypoxic conditions but CRISPR/Cas9 excludes arginase 2 (ARG2) as the functional target.

Journal Article PLoS One · 2018 Cancer cells, including in chronic myeloid leukemia (CML), depend on the hypoxic response to persist in hosts and evade therapy. Accordingly, there is significant interest in drugging cancer-specific hypoxic responses. However, a major challenge in leukemi ... Full text Link to item Cite

Overcoming imatinib resistance conferred by the BIM deletion polymorphism in chronic myeloid leukemia with splice-switching antisense oligonucleotides.

Journal Article Oncotarget · September 29, 2017 Many tyrosine kinase-driven cancers, including chronic myeloid leukemia (CML), are characterized by high response rates to specific tyrosine kinase inhibitors (TKIs) like imatinib. In East Asians, primary imatinib resistance is caused by a deletion polymor ... Full text Link to item Cite

Mnk1/2 and Abl inhibitions for the treatment of blast crisis chronic myelogenous leukemia

Conference ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY · August 20, 2017 Link to item Cite

A systematic review and meta-analysis of individual patient data on the impact of the BIM deletion polymorphism on treatment outcomes in epidermal growth factor receptor mutant lung cancer.

Journal Article Oncotarget · June 20, 2017 BACKGROUND: A germline deletion in the BIM (BCL2L11) gene has been shown to impair the apoptotic response to tyrosine kinase inhibitors (TKIs) in vitro but its association with poor outcomes in TKI-treated non-small cell lung cancer (NSCLC) patients remain ... Full text Link to item Cite

Histone Deacetylase 3 Inhibition Overcomes BIM Deletion Polymorphism-Mediated Osimertinib Resistance in EGFR-Mutant Lung Cancer.

Journal Article Clin Cancer Res · June 15, 2017 Purpose: The BIM deletion polymorphism is associated with apoptosis resistance to EGFR tyrosine kinase inhibitors (EGFR-TKI), such as gefitinib and erlotinib, in non-small cell lung cancer (NSCLC) harboring EGFR mutations. Here, we investigated whether the ... Full text Link to item Cite

The HDAC inhibitor SB939 overcomes resistance to BCR-ABL kinase Inhibitors conferred by the BIM deletion polymorphism in chronic myeloid leukemia.

Journal Article PLoS One · 2017 Chronic myeloid leukemia (CML) treatment has been improved by tyrosine kinase inhibitors (TKIs) such as imatinib mesylate (IM) but various factors can cause TKI resistance in patients with CML. One factor which contributes to TKI resistance is a germline i ... Full text Link to item Cite

Structure-Activity Relationship Studies of Mitogen Activated Protein Kinase Interacting Kinase (MNK) 1 and 2 and BCR-ABL1 Inhibitors Targeting Chronic Myeloid Leukemic Cells.

Journal Article J Med Chem · April 14, 2016 Clinically used BCR-ABL1 inhibitors for the treatment of chronic myeloid leukemia do not eliminate leukemic stem cells (LSC). It has been shown that MNK1 and 2 inhibitors prevent phosphorylation of eIF4E and eliminate the self-renewal capacity of LSCs. Her ... Full text Link to item Cite

The BIM deletion polymorphism: A paradigm of a permissive interaction between germline and acquired TKI resistance factors in chronic myeloid leukemia.

Journal Article Oncotarget · January 19, 2016 Both germline polymorphisms and tumor-specific genetic alterations can determine the response of a cancer to a given therapy. We previously reported a germline deletion polymorphism in the BIM gene that was sufficient to mediate intrinsic resistance to tyr ... Full text Link to item Cite

The Genomic and Epigenomic Landscapes of Blast Crisis Transformation in Chronic Myeloid Leukemia

Conference Blood · December 3, 2015 AbstractThe transition from chronic phase (CP) to blast crisis (BC) chronic myeloid leukemia (CML) is characterized by reprogramming of the CML transcriptome (Radich et al. PNAS 2006), and shortened survival ... Full text Cite

Molecular mechanism of TKI resistance and potential approaches to overcome resistance

Chapter · January 1, 2015 There has been a remarkable improvement in the survival of patients with chronic myeloid leukaemia (CML) in chronic phase since the introduction of tyrosine kinase inhibitors (TKIs). However there are a significant proportion of patients with CML who are r ... Full text Cite

A novel Bcr-Abl-mTOR-eIF4A axis regulates IRES-mediated translation of LEF-1.

Journal Article Open Biol · November 2014 Internal ribosome entry sites (IRESs) in cellular mRNAs direct expression of growth-promoting factors through an alternative translation mechanism that has yet to be fully defined. Lymphoid enhancer factor-1 (LEF-1), a Wnt-mediating transcription factor im ... Full text Link to item Cite

The BCL2 inhibitor ABT-199 significantly enhances imatinib-induced cell death in chronic myeloid leukemia progenitors.

Journal Article Oncotarget · October 15, 2014 BCR-ABL1-specific tyrosine kinase inhibitors prolong the life of patients with chronic myeloid leukemia (CML) but cannot completely eradicate CML progenitors. The BH3 mimetic, ABT-263, targets prosurvival BCL2 family members, and has activity against CML p ... Full text Link to item Cite

Heritable resistance to tyrosine kinase inhibitors.

Journal Article Clin Adv Hematol Oncol · July 2014 Link to item Cite

Physiologic hypoxia promotes maintenance of CML stem cells despite effective BCR-ABL1 inhibition.

Conference Blood · May 22, 2014 C-abl oncogene 1, nonreceptor tyrosine kinase (ABL1) kinase inhibitors such as imatinib mesylate (imatinib) are effective in managing chronic myeloid leukemia (CML) but incapable of eliminating leukemia stem cells (LSCs), suggesting that kinase-independent ... Full text Link to item Cite

Identification of cis-acting elements and splicing factors involved in the regulation of BIM Pre-mRNA splicing.

Journal Article PLoS One · 2014 Aberrant changes in the expression of the pro-apoptotic protein, BCL-2-like 11 (BIM), can result in either impaired or excessive apoptosis, which can contribute to tumorigenesis and degenerative disorders, respectively. Altering BIM pre-mRNA splicing is an ... Full text Link to item Cite

Multi-agent chemotherapy overcomes glucocorticoid resistance conferred by a BIM deletion polymorphism in pediatric acute lymphoblastic leukemia.

Journal Article PLoS One · 2014 A broad range of anti-cancer agents, including glucocorticoids (GCs) and tyrosine kinase inhibitors (TKIs), kill cells by upregulating the pro-apoptotic BCL2 family member, BIM. A common germline deletion in the BIM gene was recently shown to favor the pro ... Full text Link to item Cite

Targeting of the MNK-eIF4E axis in blast crisis chronic myeloid leukemia inhibits leukemia stem cell function.

Journal Article Proc Natl Acad Sci U S A · June 18, 2013 Chronic myeloid leukemia responds well to therapy targeting the oncogenic fusion protein BCR-ABL1 in chronic phase, but is resistant to treatment after it progresses to blast crisis (BC). BC is characterized by elevated β-catenin signaling in granulocyte m ... Full text Link to item Cite

Abstract 4958: Identification of cis-regulatory elements in a BIM deletion polymorphism that regulate splicing and generation of non-apoptotic BIM isoforms

Journal Article Cancer Research · April 15, 2012 AbstractBIM is a pro-apoptotic member of the BCL-2 family of proteins that trigger apoptosis by either opposing the pro-survival members of the family (BCL-2, BCL-xL, MCL1), or by directly binding the distal ... Full text Cite

A common BIM deletion polymorphism mediates intrinsic resistance and inferior responses to tyrosine kinase inhibitors in cancer.

Journal Article Nat Med · March 18, 2012 Tyrosine kinase inhibitors (TKIs) elicit high response rates among individuals with kinase-driven malignancies, including chronic myeloid leukemia (CML) and epidermal growth factor receptor-mutated non-small-cell lung cancer (EGFR NSCLC). However, the exte ... Full text Link to item Cite

The role of protein phosphorylation in therapy resistance and disease progression in chronic myelogenous leukemia.

Journal Article Prog Mol Biol Transl Sci · 2012 This review focuses on the central role that protein phosphorylation plays in the pathogenesis of chronic myelogenous leukemia (CML). It will cover the signaling pathways that are dysregulated by the oncogenic tyrosine kinase, BCR-ABL1, which both defines ... Full text Link to item Cite

Effective and selective targeting of leukemia cells using a TORC1/2 kinase inhibitor.

Journal Article Nat Med · February 2010 Targeting the mammalian target of rapamycin (mTOR) protein is a promising strategy for cancer therapy. The mTOR kinase functions in two complexes, TORC1 (target of rapamycin complex-1) and TORC2 (target of rapamycin complex-2); however, neither of these co ... Full text Link to item Cite

Inhibition of polysome assembly enhances imatinib activity against chronic myelogenous leukemia and overcomes imatinib resistance.

Journal Article Mol Cell Biol · October 2008 Dysregulated mRNA translation is implicated in the pathogenesis of many human cancers including chronic myelogenous leukemia (CML). Because our prior work has specifically implicated translation initiation in CML, we tested compounds that could modulate tr ... Full text Link to item Cite

A Fas-associated death domain protein/caspase-8-signaling axis promotes S-phase entry and maintains S6 kinase activity in T cells responding to IL-2.

Journal Article J Immunol · October 15, 2007 Fas-associated death domain protein (FADD) constitutes an essential component of TNFR-induced apoptotic signaling. Paradoxically, FADD has also been shown to be crucial for lymphocyte development and activation. In this study, we report that FADD is necess ... Full text Link to item Cite

A novel mechanism for Bcr-Abl action: Bcr-Abl-mediated induction of the eIF4F translation initiation complex and mRNA translation.

Journal Article Oncogene · February 22, 2007 The oncogenic kinase Bcr-Abl is thought to cause chronic myelogenous leukemia (CML) by altering the transcription of specific genes with growth- and survival-promoting functions. Recently, Bcr-Abl has also been shown to activate an important regulator of p ... Full text Link to item Cite

Multiple joint effusions associated with high-dose imatinib therapy in a patient with chronic myelogenous leukaemia.

Journal Article Eur J Haematol · May 2006 Imatinib mesylate is a small molecule tyrosine kinase inhibitor that has significant efficacy in the treatment of chronic myelogenous leukaemia (CML). However, it is likely that patients with CML will require prolonged and perhaps life-long therapy. In gen ... Full text Link to item Cite

Bcr-Abl kinase modulates the translation regulators ribosomal protein S6 and 4E-BP1 in chronic myelogenous leukemia cells via the mammalian target of rapamycin.

Journal Article Cancer Res · September 15, 2003 Identification of signaling pathways downstream of Abl tyrosine kinase may increase our understanding of the pathogenesis of chronic myelogenous leukemia (CML) and suggest strategies to improve clinical treatment of the disease. By combining the use of a p ... Link to item Cite

Expression profiling of a transformed thymocyte cell line undergoing maturation in vitro identifies multiple genes involved in positive selection.

Journal Article Cell Immunol · January 2003 Biochemical and genetic studies of thymocyte maturation would be facilitated by the development of cultured cell lines that reflect stages of positive selection. We have derived a CD4(+)CD8(+)TCR(+) T-lymphoid cell line (M20) from a murine thymic tumor ind ... Full text Link to item Cite

Aberrant FHIT mRNA transcripts are present in malignant and normal haematopoiesis, but absence of FHIT protein is restricted to leukaemia.

Journal Article Oncogene · January 7, 1999 Aberrant FHIT mRNA transcripts are present in malignant and normal haematopoiesis, but absence of FHIT protein is restricted to leukaemia Alterations of the recently cloned fragile histidine triad (FHIT) gene at chromosome 3p14.2 are frequent in a variety ... Full text Link to item Cite

Chromosomal abnormalities and molecular genetics of non-Hodgkin's lymphoma.

Journal Article Semin Oncol · August 1998 A number of recurring cytogenetic abnormalities have been identified in lymphomas that correlate with clinical, morphologic, and immunophenotypic features. For example, the t(14;18) is observed in a high proportion of follicular small cleaved cell lymphoma ... Link to item Cite

Lymphadenopathy, splenomegaly, and altered immunoglobulin production in BCL3 transgenic mice.

Journal Article Oncogene · May 7, 1998 The candidate proto-oncogene BCL3 was isolated through its involvement in the t(14;19) found in chronic lymphocytic leukemia and other B-cell neoplasms. As a member of the I kappaB family, BCL3 plays a role in the immune response by interactions with the N ... Full text Link to item Cite

Precise localization of the FHIT gene to the common fragile site at 3p14.2 (FRA3B) and characterization of homozygous deletions within FRA3B that affect FHIT transcription in tumor cell lines.

Journal Article Genes Chromosomes Cancer · September 1997 Chromosomal or allelic losses at 3p14 are common in a variety of human tumors, including those of the lung, breast, kidney, and head and neck. This suggests the existence of a tumor suppressor gene in this band. A promising candidate is the recently cloned ... Full text Link to item Cite

FHIT and FRA3B 3p14.2 allele loss are common in lung cancer and preneoplastic bronchial lesions and are associated with cancer-related FHIT cDNA splicing aberrations.

Journal Article Cancer Res · June 1, 1997 We evaluated primary lung cancers, tumor cell lines, and preneoplastic bronchial lesions for molecular genetic abnormalities in the candidate tumor suppressor gene FHIT, which spans the FRA3B fragile site at 3p14.2. 3p14.2 allele loss was very frequent in ... Link to item Cite

The sixth Lugano conference: Basic science papers

Journal Article Annals of Oncology · January 1, 1997 Full text Cite

Direct cloning of DNA sequences from the common fragile site region at chromosome band 3p14.2.

Journal Article Genomics · July 1, 1996 Despite several lines of evidence suggesting that common chromosomal fragile sites are biologically important as hot spots for recombination, their structure remains unknown. We showed previously that the plasmid pSV2neo preferentially integrates into band ... Full text Link to item Cite

Chemotherapy in malignant pleural mesothelioma. A review.

Journal Article J Clin Oncol · March 1996 PURPOSE AND DESIGN: We reviewed the published literature of clinical studies in malignant pleural mesothelioma, including phase II trials of the newer antifolates and plant derivatives, as well as older single-agent and combination chemotherapy trials. We ... Full text Link to item Cite

Current management of acute lymphoblastic leukemia in adults.

Journal Article Oncology (Williston Park) · May 1995 Intensive remission chemotherapy followed by post-remission consolidation and maintenance therapies has achieved complete remission rates of 75% to 90% and 3-year survival rates of 25% to 50% in adults with acute lymphoblastic leukemia (ALL). These results ... Link to item Cite

Hepatic candidiasis: persistent pyrexia in a patient with acute myeloid leukaemia after recovery from consolidation therapy-induced neutropenia.

Journal Article Ann Acad Med Singap · March 1993 Fever, a frequent manifestation in acute leukaemia patients who develop treatment-induced neutropenia, usually resolves when the neutrophil count returns to normal irrespective of whether an infective agent is isolated or not. A persistent pyrexia followin ... Link to item Cite