Christopher J. Patterson
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View article: Long-term follow-up of venetoclax monotherapy in previously treated patients with Waldenström macroglobulinemia.
Long-term follow-up of venetoclax monotherapy in previously treated patients with Waldenström macroglobulinemia. Open
Venetoclax is highly active in previously treated Waldenström macroglobulinemia (WM). However, data on the long-term durability and retreatment with venetoclax remain limited. Herein, we present an update of a prospective clinical trial of…
View article: Assessing ChatGPT's capability in understanding and reporting antiretroviral therapy drug–drug interaction effects: Quantitative and qualitative results from the ACCURATE‐DDI study
Assessing ChatGPT's capability in understanding and reporting antiretroviral therapy drug–drug interaction effects: Quantitative and qualitative results from the ACCURATE‐DDI study Open
View article: The Evolution and Subtypes of Waldenstrom Macroglobulinemia: Findings from a Multi-omic Analysis of 249 Treatment Naive MYD88L265P Mutated Patients.
The Evolution and Subtypes of Waldenstrom Macroglobulinemia: Findings from a Multi-omic Analysis of 249 Treatment Naive MYD88L265P Mutated Patients. Open
To study the heterogeneity of transcriptional and genomic traits that underlie the clinical presentation of untreated Waldenstrom’s Macroglobulinemia (WM), we performed multi-omic studies in 249 treatment-naive patients with WM. For all pa…
View article: Development and characterization of the novel <i>MYD88</i> mutated, 6q deleted <scp>BCWM</scp>.2 cell line for Waldenström macroglobulinaemia
Development and characterization of the novel <i>MYD88</i> mutated, 6q deleted <span>BCWM</span>.2 cell line for Waldenström macroglobulinaemia Open
Summary Cell lines have enabled a comprehensive understanding of disease biology and the advancement of new therapeutics in Waldenström macroglobulinaemia (WM). Herein, we report the development of BCWM.2, a novel WM cell line derived from…
View article: A randomized, placebo-controlled trial of the BTK inhibitor zanubrutinib in hospitalized patients with COVID-19 respiratory distress: immune biomarker and clinical findings
A randomized, placebo-controlled trial of the BTK inhibitor zanubrutinib in hospitalized patients with COVID-19 respiratory distress: immune biomarker and clinical findings Open
Background Cytokine release triggered by a hyperactive immune response is thought to contribute to severe acute respiratory syndrome coronavirus 2019 (SARS-CoV-2)–related respiratory failure. Bruton tyrosine kinase (BTK) is involved in inn…
View article: Identification of robust predictors for ibrutinib response by multiomics in MYD88-mutated Waldenström macroglobulinemia
Identification of robust predictors for ibrutinib response by multiomics in MYD88-mutated Waldenström macroglobulinemia Open
View article: An Addendum to NeBula: Toward Extending Team CoSTAR’s Solution to Larger Scale Environments
An Addendum to NeBula: Toward Extending Team CoSTAR’s Solution to Larger Scale Environments Open
This paper presents an appendix to the original NeBula autonomy solution developed by the TEAM CoSTAR (Collaborative SubTerranean Autonomous Robots), participating in the DARPA Subterranean Challenge. Specifically, this paper presents exte…
View article: Ibrutinib and venetoclax as primary therapy in symptomatic, treatment-naïve Waldenström macroglobulinemia
Ibrutinib and venetoclax as primary therapy in symptomatic, treatment-naïve Waldenström macroglobulinemia Open
Concurrent Bruton tyrosine kinase and BCL2 inhibition has not yet been investigated in Waldenström macroglobulinemia (WM). We performed an investigator-initiated trial of ibrutinib and venetoclax in symptomatic treatment-naïve patients wit…
View article: A new role for the SRC family kinase HCK as a driver of SYK activation in MYD88 mutated lymphomas
A new role for the SRC family kinase HCK as a driver of SYK activation in MYD88 mutated lymphomas Open
The SRC family kinase (SFK) HCK is transcriptionally upregulated and activated by mutated MYD88 (MYD88Mut), a key adaptor for Toll-receptor signaling. HCK activates BTK, AKT, and ERK in MYD88Mut lymphomas. SYK, a B-cell receptor (BCR) comp…
View article: Response and survival predictors in a cohort of 319 patients with Waldenström macroglobulinemia treated with ibrutinib monotherapy
Response and survival predictors in a cohort of 319 patients with Waldenström macroglobulinemia treated with ibrutinib monotherapy Open
Bruton tyrosine kinase (BTK) inhibitors are the only FDA-approved treatments for Waldenström macroglobulinemia (WM). Factors prognostic of survival and predictive of response to BTK inhibitors remained to be clarified. We evaluated 319 pat…
View article: Long-term follow-up of ibrutinib monotherapy in treatment-naive patients with Waldenstrom macroglobulinemia
Long-term follow-up of ibrutinib monotherapy in treatment-naive patients with Waldenstrom macroglobulinemia Open
Herein, we present the final report of a single-center, prospective phase II study evaluating ibrutinib 420 mg once daily in 30 treatment-naive patients with Waldenstrom macroglobulinemia (WM). The present study is registered with Clinical…
View article: Phase 1 study of ibrutinib and the CXCR4 antagonist ulocuplumab in CXCR4-mutated Waldenström macroglobulinemia
Phase 1 study of ibrutinib and the CXCR4 antagonist ulocuplumab in CXCR4-mutated Waldenström macroglobulinemia Open
MYD88 and CXCR4 mutations are common in Waldenström macroglobulinemia (WM). Mutated CXCR4 (CXCR4Mut) impacts BTK-inhibitor response. We conducted a phase 1 trial of the CXCR4-antagonist ulocuplumab with ibrutinib in this first-ever study t…
View article: Diagnostic Next-generation Sequencing Frequently Fails to Detect MYD88L265P in Waldenström Macroglobulinemia
Diagnostic Next-generation Sequencing Frequently Fails to Detect MYD88L265P in Waldenström Macroglobulinemia Open
Mutations in MYD88 (MYD88MUT) are present in approximately 93%–97% of patients with Waldenström macroglobulinemia (WM), nearly all of which correspond to the c.978T>C transversion resulting in a p.Leu265Pro (L265P) substitution at the prot…
View article: Natural history of Waldenström macroglobulinemia following acquired resistance to ibrutinib monotherapy
Natural history of Waldenström macroglobulinemia following acquired resistance to ibrutinib monotherapy Open
Ibrutinib is highly active and produces long-term responses in patients with Waldenström macroglobulinemia (WM), but acquired resistance can occur with prolonged treatment. We therefore evaluated the natural history and treatment outcomes …
View article: The HCK/BTK inhibitor KIN-8194 is active in MYD88-driven lymphomas and overcomes mutated BTKCys481 ibrutinib resistance
The HCK/BTK inhibitor KIN-8194 is active in MYD88-driven lymphomas and overcomes mutated BTKCys481 ibrutinib resistance Open
Activating mutations in MYD88 promote malignant cell growth and survival through hematopoietic cell kinase (HCK)–mediated activation of Bruton tyrosine kinase (BTK). Ibrutinib binds to BTKCys481 and is active in B-cell malignancies driven …
View article: Volcanic Caves as Priority Sites for Astrobiology Science
Volcanic Caves as Priority Sites for Astrobiology Science Open
We have the technological capability-today-to map and explore mines and caves on Earth.The purpose of this white paper is to urge NASA's support for development of technology needed to enter a planetary cave with a scientific payload for l…
View article: Bone marrow involvement and subclonal diversity impairs detection of mutated <i>CXCR4</i> by diagnostic next‐generation sequencing in Waldenström macroglobulinaemia
Bone marrow involvement and subclonal diversity impairs detection of mutated <i>CXCR4</i> by diagnostic next‐generation sequencing in Waldenström macroglobulinaemia Open
Summary CXCR4 mutations impact disease presentation and treatment outcomes in Waldenström macroglobulinaemia (WM). Non‐uniform testing for CXCR4 mutations may account for discordant findings in WM clinical trials. We compared two approache…
View article: Comparative genomics of CXCR4MUT and CXCR4WT single cells in Waldenström’s macroglobulinemia
Comparative genomics of CXCR4MUT and CXCR4WT single cells in Waldenström’s macroglobulinemia Open
Key Points Single-cell whole-genome amplification can be used to interrogate the genomic architecture of Waldenström’s macroglobulinemia. The mutational signature of CXCR4MUT cells may be associated with alterations in DNA repairing genes …
View article: Long-Term Follow-Up of Ibrutinib Monotherapy in Symptomatic, Previously Treated Patients With Waldenström Macroglobulinemia
Long-Term Follow-Up of Ibrutinib Monotherapy in Symptomatic, Previously Treated Patients With Waldenström Macroglobulinemia Open
PURPOSE We report the long-term findings and final analysis of a pivotal multicenter trial of ibrutinib monotherapy in previously treated patients with Waldenström macroglobulinemia (WM). PATIENTS AND METHODS Sixty-three symptomatic patien…
View article: Ixazomib, dexamethasone, and rituximab in treatment-naive patients with Waldenström macroglobulinemia: long-term follow-up
Ixazomib, dexamethasone, and rituximab in treatment-naive patients with Waldenström macroglobulinemia: long-term follow-up Open
Proteasome inhibition is a standard of care for the primary treatment of patients with Waldenström macroglobulinemia (WM). We present the long-term follow-up of a prospective, phase II clinical trial that evaluated the combination of ixazo…
View article: Response and Survival Outcomes to Ibrutinib Monotherapy for Patients With Waldenström Macroglobulinemia on and off Clinical Trials
Response and Survival Outcomes to Ibrutinib Monotherapy for Patients With Waldenström Macroglobulinemia on and off Clinical Trials Open
Ibrutinib is the first approved therapy for symptomatic patients with Waldenström macroglobulinemia (WM). The approval was based on a single, multicenter, phase II trial in previously treated WM patients. We sought to evaluate whether ther…
View article: Genomic Landscape of Waldenström Macroglobulinemia and Its Impact on Treatment Strategies
Genomic Landscape of Waldenström Macroglobulinemia and Its Impact on Treatment Strategies Open
Next-generation sequencing has revealed recurring somatic mutations in Waldenström macroglobulinemia (WM), including MYD88 (95%-97%), CXCR4 (30%-40%), ARID1A (17%), and CD79B (8%-15%). Deletions involving chromosome 6q are common in patien…
View article: SYK is activated by mutated MYD88 and drives pro-survival signaling in MYD88 driven B-cell lymphomas
SYK is activated by mutated MYD88 and drives pro-survival signaling in MYD88 driven B-cell lymphomas Open
View article: <scp>CXCR4</scp> mutational status does not impact outcomes in patients with <scp>W</scp>aldenström macroglobulinemia treated with proteasome inhibitors
<span>CXCR4</span> mutational status does not impact outcomes in patients with <span>W</span>aldenström macroglobulinemia treated with proteasome inhibitors Open
View article: Expression of the prosurvival kinase HCK requires PAX5 and mutated MYD88 signaling in MYD88-driven B-cell lymphomas
Expression of the prosurvival kinase HCK requires PAX5 and mutated MYD88 signaling in MYD88-driven B-cell lymphomas Open
Hematopoietic cell kinase (HCK) is an SRC family member that is aberrantly upregulated in B-cell neoplasms dependent on MYD88-activating mutations and supports their growth and survival. We showed herein that activation of Toll-like recept…
View article: Deepening of response after completing rituximab‐containing therapy in patients with Waldenstrom macroglobulinemia
Deepening of response after completing rituximab‐containing therapy in patients with Waldenstrom macroglobulinemia Open
Rituximab‐containing regimens are commonly used for frontline therapy in patients with symptomatic Waldenström macroglobulinemia (WM). We had observed that a portion of WM patients experienced deepening of response months to years after th…
View article: CXCR4 S338X clonality is an important determinant of ibrutinib outcomes in patients with Waldenström macroglobulinemia
CXCR4 S338X clonality is an important determinant of ibrutinib outcomes in patients with Waldenström macroglobulinemia Open
Key Points CXCR4 S338X clonality ≥25% is associated with lower very good partial response and shorter progression-free survival to ibrutinib. CXCR4 S338X clonality assessment represents a novel biomarker to predict outcomes to ibrutinib in…
View article: <i>CXCR4</i> mutation subtypes impact response and survival outcomes in patients with Waldenström macroglobulinaemia treated with ibrutinib
<i>CXCR4</i> mutation subtypes impact response and survival outcomes in patients with Waldenström macroglobulinaemia treated with ibrutinib Open
Summary Ibrutinib is associated with response rate of 90% and median progression‐free survival (PFS) in excess of 5 years in Waldenström macroglobulinaemia (WM) patients. CXCR4 mutations are detected in 30–40% of patients with WM and assoc…
View article: IBRUTINIB MONOTHERAPY PRODUCES LONG‐TERM DISEASE CONTROL IN PREVIOUSLY TREATED WALDENSTROM'S MACROGLOBULINEMIA. FINAL REPORT OF THE PIVOTAL TRIAL (NCT01614821).
IBRUTINIB MONOTHERAPY PRODUCES LONG‐TERM DISEASE CONTROL IN PREVIOUSLY TREATED WALDENSTROM'S MACROGLOBULINEMIA. FINAL REPORT OF THE PIVOTAL TRIAL (NCT01614821). Open
Adverse events (Grade >2) in >5% of patients during active follow-up were: neutropenia (22%); thrombocytopenia (14%), pneumonia (9%); GERD (8%); hypertension (8%); anemia (6%); and skin infection (5%). Seven patients (11%) had an atrial ar…
View article: Insights into the genomic landscape of MYD88 wild-type Waldenström macroglobulinemia
Insights into the genomic landscape of MYD88 wild-type Waldenström macroglobulinemia Open
Activating MYD88 mutations are present in 95% of Waldenström macroglobulinemia (WM) patients, and trigger NF-κB through BTK and IRAK. The BTK inhibitor ibrutinib is active in MYD88-mutated (MYD88MUT) WM patients, but shows lower activity i…