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Article: A Gut Instinct on Leukaemia: A New Mechanistic Hypothesis for Microbiota-Immune Crosstalk in Disease Progression and Relapse.

Pagani, Ilaria S / Poudel, Govinda / Wardill, Hannah R

2022 Volume 10, Issue 4

Abstract: Despite significant advances in the treatment of Chronic Myeloid and Acute Lymphoblastic Leukaemia (CML and ALL, respectively), disease progression and relapse remain a major problem. Growing evidence indicates the loss of immune surveillance of residual ...

Abstract	Despite significant advances in the treatment of Chronic Myeloid and Acute Lymphoblastic Leukaemia (CML and ALL, respectively), disease progression and relapse remain a major problem. Growing evidence indicates the loss of immune surveillance of residual leukaemic cells as one of the main contributors to disease recurrence and relapse. More recently, there was an appreciation for how the host's gut microbiota predisposes to relapse given its potent immunomodulatory capacity. This is especially compelling in haematological malignancies where changes in the gut microbiota have been identified after treatment, persisting in some patients for years after the completion of treatment. In this hypothesis-generating review, we discuss the interaction between the gut microbiota and treatment responses, and its capacity to influence the risk of relapse in both CML and ALL We hypothesize that the gut microbiota contributes to the creation of an immunosuppressive microenvironment, which promotes tumour progression and relapse.
Language	English
Publishing date	2022-03-25
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720891-6
ISSN	2076-2607
ISSN	2076-2607
DOI	10.3390/microorganisms10040713
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Article: Mechanisms of Resistance and Implications for Treatment Strategies in Chronic Myeloid Leukaemia.

Poudel, Govinda / Tolland, Molly G / Hughes, Timothy P / Pagani, Ilaria S

Cancers

2022 Volume 14, Issue 14

Abstract: Tyrosine kinase inhibitors (TKIs) have revolutionised the management of chronic myeloid leukaemia (CML), with the disease now having a five-year survival rate over 80%. The primary focus in the treatment of CML has been on improving the specificity and ... ...

Abstract	Tyrosine kinase inhibitors (TKIs) have revolutionised the management of chronic myeloid leukaemia (CML), with the disease now having a five-year survival rate over 80%. The primary focus in the treatment of CML has been on improving the specificity and potency of TKIs to inhibit the activation of the BCR::ABL1 kinase and/or overcoming resistance driven by mutations in the BCR::ABL1 oncogene. However, this approach may be limited in a significant proportion of patients who develop TKI resistance despite the effective inhibition of BCR::ABL1. These patients may require novel therapeutic strategies that target both BCR::ABL1-dependent and BCR::ABL1-independent mechanisms of resistance. The combination treatment strategies that target alternative survival signalling, which may contribute towards BCR::ABL1-independent resistance, could be a successful strategy for eradicating residual leukaemic cells and consequently increasing the response rate in CML patients.
Language	English
Publishing date	2022-07-06
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14143300
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Article ; Online: Lineage-specific detection of residual disease predicts relapse in patients with chronic myeloid leukemia stopping therapy.

Pagani, Ilaria S / Shanmuganathan, Naranie / Dang, Phuong / Saunders, Verity A / Grose, Randall / Kok, Chung H / James, Jane / Tolland, Molly / Braley, Jodi A / Altamura, Haley K / Yeung, David T / Branford, Susan / Yong, Agnes S M / Hughes, Timothy P / Ross, David M

Blood

2023 Volume 142, Issue 25, Page(s) 2192–2197

Abstract: Abstract: Patients with chronic myeloid leukemia who are eligible for treatment-free remission (TFR) may still relapse after tyrosine kinase inhibitor (TKI) cessation. There is a need for accurate predictors of outcome to enable patients with a ... ...

Abstract	Abstract: Patients with chronic myeloid leukemia who are eligible for treatment-free remission (TFR) may still relapse after tyrosine kinase inhibitor (TKI) cessation. There is a need for accurate predictors of outcome to enable patients with a favorable profile to proceed while avoiding futile attempts. Sensitive detection of residual disease in total leukocytes at treatment cessation is associated with relapse but is not highly discriminatory, likely because it is a composite measure of residual leukemia derived from different cell lineages, whereas only some lineages are relevant for relapse. We prospectively measured BCR::ABL1 DNA as a predictive yes/no binary test in 5 cellular fractions from 48 patients meeting conventional criteria for TKI discontinuation. The median BCR::ABL1 DNA level was higher in granulocytes and T cells, but not in other lineages, in patients who relapsed. Among the 40 patients undergoing their first TFR attempt, we defined 3 groups with differing relapse risk: granulocyte-positive group (100%), granulocyte-negative/T-cell-positive group (67%), and granulocyte-negative /T-cell-negative group (25%). These data show the critical importance of lineage-specific assessment of residual disease in the selection of patients who can attempt to achieve TFR with a high expectation of success and, concurrently, defer patients who have a high probability of relapse.
MeSH term(s)	Humans ; Fusion Proteins, bcr-abl/genetics ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/diagnosis ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics ; Protein Kinase Inhibitors ; Recurrence ; Remission Induction ; DNA
Chemical Substances	Fusion Proteins, bcr-abl (EC 2.7.10.2) ; Protein Kinase Inhibitors ; DNA (9007-49-2)
Language	English
Publishing date	2023-08-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2023021119
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Article ; Online: Clinical utility of genomic DNA Q-PCR for the monitoring of a patient with atypical e19a2

Pagani, Ilaria S / Dang, Phuong / Saunders, Verity A / Braley, Jodi / Thieleke, Angelica / Branford, Susan / Hughes, Timothy P / Ross, David M

Leukemia & lymphoma

2020 Volume 61, Issue 10, Page(s) 2527–2529

MeSH term(s)	DNA ; Fusion Proteins, bcr-abl/genetics ; Genomics ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/diagnosis ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics ; Polymerase Chain Reaction
Chemical Substances	DNA (9007-49-2) ; Fusion Proteins, bcr-abl (EC 2.7.10.2)
Language	English
Publishing date	2020-06-06
Publishing country	United States
Document type	Letter
ZDB-ID	1042374-6
ISSN	1029-2403 ; 1042-8194
ISSN (online)	1029-2403
ISSN	1042-8194
DOI	10.1080/10428194.2020.1772476
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Article ; Online: Impact of additional genetic abnormalities at diagnosis of chronic myeloid leukemia for first-line imatinib-treated patients receiving proactive treatment intervention.

Shanmuganathan, Naranie / Wadham, Carol / Shahrin, NurHezrin / Feng, Jinghua / Thomson, Daniel / Wang, Paul / Saunders, Verity / Kok, Chung Hoow / King, Rob M / Kenyon, Rosalie R / Lin, Ming / Pagani, Ilaria S / Ross, David M / Yong, Agnes S M / Grigg, Andrew P / Mills, Anthony K / Schwarer, Anthony P / Braley, Jodi / Altamura, Haley /

Yeung, David T / Scott, Hamish S / Schreiber, Andreas W / Hughes, Timothy P / Branford, Susan

Haematologica

2023 Volume 108, Issue 9, Page(s) 2380–2395

Abstract: The BCR::ABL1 gene fusion initiates chronic myeloid leukemia (CML); however, evidence has accumulated from studies of highly selected cohorts that variants in other cancer-related genes are associated with treatment failure. Nevertheless, the true ... ...

Abstract	The BCR::ABL1 gene fusion initiates chronic myeloid leukemia (CML); however, evidence has accumulated from studies of highly selected cohorts that variants in other cancer-related genes are associated with treatment failure. Nevertheless, the true incidence and impact of additional genetic abnormalities (AGA) at diagnosis of chronic phase (CP)-CML is unknown. We sought to determine whether AGA at diagnosis in a consecutive imatinib-treated cohort of 210 patients enrolled in the TIDEL-II trial influenced outcome despite a highly proactive treatment intervention strategy. Survival outcomes including overall survival, progression-free survival, failure-free survival, and BCR::ABL1 kinase domain mutation acquisition were evaluated. Molecular outcomes were measured at a central laboratory and included major molecular response (MMR, BCR::ABL1 ≤0.1%IS), MR4 (BCR::ABL1 ≤0.01%IS), and MR4.5 (BCR::ABL1 ≤0.0032%IS). AGA included variants in known cancer genes and novel rearrangements involving the formation of the Philadelphia chromosome. Clinical outcomes and molecular response were assessed based on the patient's genetic profile and other baseline factors. AGA were identified in 31% of patients. Potentially pathogenic variants in cancer-related genes were detected in 16% of patients at diagnosis (including gene fusions and deletions) and structural rearrangements involving the Philadelphia chromosome (Ph-associated rearrangements) were detected in 18%. Multivariable analysis demonstrated that the combined genetic abnormalities plus the EUTOS long-term survival clinical risk score were independent predictors of lower molecular response rates and higher treatment failure. Despite a highly proactive treatment intervention strategy, first-line imatinib-treated patients with AGA had poorer response rates. These data provide evidence for the incorporation of genomically-based risk assessment for CML.
MeSH term(s)	Humans ; Imatinib Mesylate/therapeutic use ; Antineoplastic Agents/therapeutic use ; Philadelphia Chromosome ; Fusion Proteins, bcr-abl/genetics ; Fusion Proteins, bcr-abl/metabolism ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/diagnosis ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics ; Leukemia, Myeloid, Chronic-Phase/drug therapy ; Protein Kinase Inhibitors/therapeutic use
Chemical Substances	Imatinib Mesylate (8A1O1M485B) ; Antineoplastic Agents ; Fusion Proteins, bcr-abl (EC 2.7.10.2) ; Protein Kinase Inhibitors
Language	English
Publishing date	2023-09-01
Publishing country	Italy
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2022.282184
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Article ; Online: Early BCR-ABL1 kinetics are predictive of subsequent achievement of treatment-free remission in chronic myeloid leukemia.

Shanmuganathan, Naranie / Pagani, Ilaria S / Ross, David M / Park, Sahee / Yong, Agnes S M / Braley, Jodi A / Altamura, Haley K / Hiwase, Devendra K / Yeung, David T / Kim, Dong-Wook / Branford, Susan / Hughes, Timothy P

Blood

2020 Volume 137, Issue 9, Page(s) 1196–1207

Abstract: With treatment-free remission (TFR) rapidly becoming the ultimate goal of therapy in chronic myeloid leukemia (CML), there is a need to develop strategies to maximize sustained TFR by improving our understanding of its key determinants. Chronic-phase CML ...

Abstract	With treatment-free remission (TFR) rapidly becoming the ultimate goal of therapy in chronic myeloid leukemia (CML), there is a need to develop strategies to maximize sustained TFR by improving our understanding of its key determinants. Chronic-phase CML patients attempting TFR were evaluated to identify the impact of multiple variables on the probability of sustained TFR. Early molecular response dynamics were included as a predictive variable, assessed by calculating the patient-specific halving time of BCR-ABL1 after commencing tyrosine kinase inhibitor (TKI) therapy. Overall, 115 patients attempted TFR and had ≥12 months of follow-up. The probability of sustained TFR, defined as remaining in major molecular response off TKI therapy for 12 months, was 55%. The time taken for the BCR-ABL1 value to halve was the strongest independent predictor of sustained TFR: 80% in patients with a halving time of <9.35 days (first quartile) compared with only 4% if the halving time was >21.85 days (last quartile) (P < .001). The e14a2 BCR-ABL1 transcript type and duration of TKI exposure before attempting TFR were also independent predictors of sustained TFR. However, the BCR-ABL1 value measured at 3 months of TKI was not an independent predictor of sustained TFR. A more rapid initial BCR-ABL1 decline after commencing TKI also correlated with an increased likelihood of achieving TFR eligibility. The association between sustained TFR and the time taken for BCR-ABL1 to halve after commencing TKI was validated using an independent dataset. These data support the critical importance of the initial kinetics of BCR-ABL1 decline for long-term outcomes.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Female ; Fusion Proteins, bcr-abl/antagonists & inhibitors ; Fusion Proteins, bcr-abl/genetics ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/diagnosis ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics ; Male ; Middle Aged ; Prognosis ; Protein Kinase Inhibitors/therapeutic use ; Retrospective Studies ; Treatment Outcome
Chemical Substances	BCR-ABL1 fusion protein, human ; Protein Kinase Inhibitors ; Fusion Proteins, bcr-abl (EC 2.7.10.2)
Language	English
Publishing date	2020-09-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2020005514
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Article ; Online: BCR-ABL1

Pagani, Ilaria S / Dang, Phuong / Kommers, Ivar O / Goyne, Jarrad M / Nicola, Mario / Saunders, Verity A / Braley, Jodi / White, Deborah L / Yeung, David T / Branford, Susan / Hughes, Timothy P / Ross, David M

Haematologica

2018 Volume 103, Issue 12, Page(s) 2026–2032

Abstract: Accurate quantification of minimal residual disease (MRD) during treatment of chronic myeloid leukemia (CML) guides clinical decisions. The conventional MRD method, RQ-PCR ... ...

Abstract	Accurate quantification of minimal residual disease (MRD) during treatment of chronic myeloid leukemia (CML) guides clinical decisions. The conventional MRD method, RQ-PCR for
MeSH term(s)	Adolescent ; Adult ; Aged ; Aged, 80 and over ; DNA, Neoplasm/genetics ; Female ; Fusion Proteins, bcr-abl/genetics ; Gene Expression Regulation, Leukemic/drug effects ; Humans ; Imatinib Mesylate/therapeutic use ; Kinetics ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/pathology ; Male ; Middle Aged ; Neoplasm, Residual/diagnosis ; Neoplasm, Residual/genetics ; Polymerase Chain Reaction/methods ; Protein Kinase Inhibitors/therapeutic use ; Young Adult
Chemical Substances	DNA, Neoplasm ; Protein Kinase Inhibitors ; Imatinib Mesylate (8A1O1M485B) ; Fusion Proteins, bcr-abl (EC 2.7.10.2)
Language	English
Publishing date	2018-07-05
Publishing country	Italy
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2018.189787
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Article ; Online: Germline mutations in mitochondrial complex I reveal genetic and targetable vulnerability in IDH1-mutant acute myeloid leukaemia.

Bassal, Mahmoud A / Samaraweera, Saumya E / Lim, Kelly / Benard, Brooks A / Bailey, Sheree / Kaur, Satinder / Leo, Paul / Toubia, John / Thompson-Peach, Chloe / Nguyen, Tran / Maung, Kyaw Ze Ya / Casolari, Debora A / Iarossi, Diana G / Pagani, Ilaria S / Powell, Jason / Pitson, Stuart / Natera, Siria / Roessner, Ute / Lewis, Ian D /

Brown, Anna L / Tenen, Daniel G / Robinson, Nirmal / Ross, David M / Majeti, Ravindra / Gonda, Thomas J / Thomas, Daniel / D'Andrea, Richard J

Nature communications

2022 Volume 13, Issue 1, Page(s) 2614

Abstract: The interaction of germline variation and somatic cancer driver mutations is under-investigated. Here we describe the genomic mitochondrial landscape in adult acute myeloid leukaemia (AML) and show that rare variants affecting the nuclear- and ... ...

Abstract	The interaction of germline variation and somatic cancer driver mutations is under-investigated. Here we describe the genomic mitochondrial landscape in adult acute myeloid leukaemia (AML) and show that rare variants affecting the nuclear- and mitochondrially-encoded complex I genes show near-mutual exclusivity with somatic driver mutations affecting isocitrate dehydrogenase 1 (IDH1), but not IDH2 suggesting a unique epistatic relationship. Whereas AML cells with rare complex I variants or mutations in IDH1 or IDH2 all display attenuated mitochondrial respiration, heightened sensitivity to complex I inhibitors including the clinical-grade inhibitor, IACS-010759, is observed only for IDH1-mutant AML. Furthermore, IDH1 mutant blasts that are resistant to the IDH1-mutant inhibitor, ivosidenib, retain sensitivity to complex I inhibition. We propose that the IDH1 mutation limits the flexibility for citrate utilization in the presence of impaired complex I activity to a degree that is not apparent in IDH2 mutant cells, exposing a mutation-specific metabolic vulnerability. This reduced metabolic plasticity explains the epistatic relationship between the germline complex I variants and oncogenic IDH1 mutation underscoring the utility of genomic data in revealing metabolic vulnerabilities with implications for therapy.
MeSH term(s)	Adult ; Germ-Line Mutation ; Humans ; Isocitrate Dehydrogenase/genetics ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Mutation
Chemical Substances	Isocitrate Dehydrogenase (EC 1.1.1.41) ; IDH1 protein, human (EC 1.1.1.42.)
Language	English
Publishing date	2022-05-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-30223-9
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Article ; Online: Author Correction: Germline mutations in mitochondrial complex I reveal genetic and targetable vulnerability in IDH1-mutant acute myeloid leukaemia.

Brown, Anna L / Tenen, Daniel G / Robinson, Nirmal / Ross, David M / Majeti, Ravindra / Gonda, Thomas J / Thomas, Daniel / D'Andrea, Richard J

Nature communications

2022 Volume 13, Issue 1, Page(s) 4131

Language	English
Publishing date	2022-07-15
Publishing country	England
Document type	Published Erratum
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-31952-7
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Article ; Online: Lineage of measurable residual disease in patients with chronic myeloid leukemia in treatment-free remission.

Pagani, Ilaria S / Dang, Phuong / Saunders, Verity A / Grose, Randall / Shanmuganathan, Naranie / Kok, Chung H / Carne, Lisa / Rwodzi, Zandy / Watts, Sophie / McLean, Jennifer / Braley, Jodi / Altamura, Haley / Yeung, David T / Branford, Susan / Yong, Agnes S M / White, Deborah L / Hughes, Timothy P / Ross, David M

Leukemia

2019 Volume 34, Issue 4, Page(s) 1052–1061

Abstract: Approximately half of patients with chronic myeloid leukemia (CML) in sustained deep molecular response who discontinue tyrosine kinase inhibitors (TKIs) remain in treatment-free remission (TFR). Some of these patients have measurable residual disease ( ... ...

Abstract	Approximately half of patients with chronic myeloid leukemia (CML) in sustained deep molecular response who discontinue tyrosine kinase inhibitors (TKIs) remain in treatment-free remission (TFR). Some of these patients have measurable residual disease (MRD) by BCR-ABL1 mRNA testing, and most have detectable BCR-ABL1 DNA by highly sensitive methods. We used fluorescence-activated cell sorting and BCR-ABL1 DNA PCR to investigate the lineage of residual CML cells in TFR. Twenty patients in TFR for >1 year provided blood for sorting into granulocytes, monocytes, B cells, T cells, and NK cells. MRD was identified predominantly in the lymphoid compartment and never in granulocytes. B cells were more often BCR-ABL1 positive than T cells (18 vs 11/20 patients) and at higher levels (median 10
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Cell Lineage ; Female ; Follow-Up Studies ; Fusion Proteins, bcr-abl/antagonists & inhibitors ; Fusion Proteins, bcr-abl/genetics ; Humans ; Imatinib Mesylate/therapeutic use ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/immunology ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/pathology ; Lymphocyte Subsets/drug effects ; Lymphocyte Subsets/immunology ; Lymphocyte Subsets/metabolism ; Male ; Middle Aged ; Neoplasm, Residual/drug therapy ; Neoplasm, Residual/genetics ; Neoplasm, Residual/immunology ; Neoplasm, Residual/pathology ; Prognosis ; Protein Kinase Inhibitors/therapeutic use ; Remission Induction
Chemical Substances	Protein Kinase Inhibitors ; Imatinib Mesylate (8A1O1M485B) ; Fusion Proteins, bcr-abl (EC 2.7.10.2)
Language	English
Publishing date	2019-11-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807030-1
ISSN	1476-5551 ; 0887-6924
ISSN (online)	1476-5551
ISSN	0887-6924
DOI	10.1038/s41375-019-0647-x
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