2-chloro-3'-deoxyadenosine: do not confuse with 2-chloro-2'-deoxyadenosine which is CLADRIBINE [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]
| ID Source | ID |
|---|---|
| PubMed CID | 3034808 |
| CHEMBL ID | 3110073 |
| SCHEMBL ID | 3436977 |
| MeSH ID | M0157304 |
| Synonym |
|---|
| adenosine, 2-chloro-3'-deoxy- |
| 2-chloro-3'-deoxyadenosine |
| 3'-deoxy-2-chloroadenosine |
| (2r,3r,5s)-2-(6-amino-2-chloropurin-9-yl)-5-(hydroxymethyl)oxolan-3-ol |
| 115044-75-2 |
| unii-jyw18y92up |
| jyw18y92up , |
| CHEMBL3110073 |
| adenosine,2-chloro-3'-deoxy- |
| SCHEMBL3436977 |
| DTXSID90150942 |
| 2-chloro-3/'-deoxyadenosine |
| Q27281750 |
| (2r,3r,5s)-2-(6-amino-2-chloro-9h-purin-9-yl)-5-(hydroxymethyl)tetrahydrofuran-3-ol |
| (2r,3r,5s)-2-(6-amino-2-chloro-9h-purin-9-yl)-5-(hydroxymethyl)oxolan-3-ol |
| F86907 |
| Excerpt | Reference | Relevance |
|---|---|---|
| " We analyzed the induction of apoptosis by 2-CdA alone (n=5) and in combination with other drugs in peripheral lymphocytes from 25 patients with leukemic low-grade lymphomas and from 25 healthy volunteers." | ( Induction of apoptosis by 2-chloro-2'deoxyadenosine (2-CdA) alone and in combination with other cytotoxic drugs: synergistic effects on normal and neoplastic lymphocytes by addition of doxorubicin and mitoxantrone. Boehrer, S; Chow, KU; Hoelzer, D; Jantschke, P; Martin, H; Mitrou, PS; Napieralski, S; Pourebrahim, F; Ries, J; Rummel, MJ; Stein, J; Weidmann, E, 2000) | 0.31 |
| Excerpt | Reference | Relevance |
|---|---|---|
| " The bioavailability of 2-CDA after subcutaneous injection is 100%, but the concentration-time profile is completely different compared to continuous intravenous administration." | ( [2-CDA in treatment of hairy cell leukemia: a comparison between intravenous and subcutaneous administration. Swiss Study Group of Applied Cancer Research]. Bacchi, M; Betticher, DC; Cerny, T; Hess, U; Ratschiller, D; Sperb, RA; Tichelli, A; Tobler, A; von Rohr, A, 1998) | 0.3 |
| Assay ID | Title | Year | Journal | Article |
|---|---|---|---|---|
| AID1065714 | Trypanocidal activity against bloodstream stage of Trypanosoma brucei brucei AnTat1.1E after 72 hrs by WST-1 assay | 2013 | Journal of medicinal chemistry, Dec-27, Volume: 56, Issue:24 | Structure-activity relationships of synthetic cordycepin analogues as experimental therapeutics for African trypanosomiasis. |
| AID1065710 | Displacement of [2,8-3H]-adenosine from Trypanosoma brucei AT1/P2 expressed in bloodstream stage of Trypanosoma brucei brucei B48 | 2013 | Journal of medicinal chemistry, Dec-27, Volume: 56, Issue:24 | Structure-activity relationships of synthetic cordycepin analogues as experimental therapeutics for African trypanosomiasis. |
| [information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023] | ||||
| Timeframe | Studies, This Drug (%) | All Drugs % |
|---|---|---|
| pre-1990 | 2 (4.55) | 18.7374 |
| 1990's | 21 (47.73) | 18.2507 |
| 2000's | 16 (36.36) | 29.6817 |
| 2010's | 5 (11.36) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| [information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023] | ||
According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be weak demand-to-supply ratio for research on this compound.
| This Compound (11.52) All Compounds (24.57) |
| Publication Type | This drug (%) | All Drugs (%) |
|---|---|---|
| Trials | 5 (10.64%) | 5.53% |
| Reviews | 6 (12.77%) | 6.00% |
| Case Studies | 8 (17.02%) | 4.05% |
| Observational | 0 (0.00%) | 0.25% |
| Other | 28 (59.57%) | 84.16% |
| [information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023] | ||
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| CLAG-M or FLAG-Ida Chemotherapy Followed Immediately by Related/Unrelated Reduced-Intensity Conditioning (RIC) Allogeneic Hematopoietic Cell Transplantation for Adults With Myeloid Malignancies at High Risk of Relapse: A Phase 1 Study [NCT04375631] | Phase 1 | 120 participants (Anticipated) | Interventional | 2020-12-03 | Recruiting | ||
| Addition of Sorafenib to G-CSF, Cladribine, Cytarabine and Mitoxantrone (G-CLAM) in Adults With Newly-Diagnosed Acute Myeloid Leukemia (AML) Independent of FLT3-ITD Status: A Phase 1/2 Study [NCT02728050] | Phase 1/Phase 2 | 84 participants (Actual) | Interventional | 2016-12-01 | Completed | ||
| Phase Ib/II Study of Uproleselan Added to Cladribine Plus Low Dose Cytarabine (LDAC) Induction Followed by Consolidation With Uproleselan Plus Cladribine Plus LDAC in Patients With Treated Secondary AML (TS-AML) [NCT04848974] | Phase 1/Phase 2 | 37 participants (Anticipated) | Interventional | 2021-06-11 | Recruiting | ||
| Allogeneic Transplantation Using Venetoclax, Timed Sequential Busulfan,Cladribine, and Fludarabine Conditioning in Patients With AML and MDS [NCT02250937] | Phase 2 | 116 participants (Anticipated) | Interventional | 2014-10-27 | Active, not recruiting | ||
| Phase II Study of 2-Chlorodeoxyadenosine (2CDA) Followed by Rituximab in Hairy Cell Leukemia [NCT00412594] | Phase 2 | 150 participants (Anticipated) | Interventional | 2004-06-10 | Recruiting | ||
| Phase II Study of Cladribine Plus Idarubicin Plus Cytarabine (ARAC) in Patients With AML, HR MDS, or Myeloid Blast Phase of CML [NCT02115295] | Phase 2 | 458 participants (Anticipated) | Interventional | 2014-05-19 | Recruiting | ||
| Phase II Study of Vorinostat (SAHA), Cladribine, and Rituximab (SCR) in Mantle Cell Lymphoma, Chronic Lymphocytic Leukemia, and Relapsed B Cell Non-Hodgkin Lymphoma [NCT00764517] | Phase 2 | 57 participants (Actual) | Interventional | 2008-08-31 | Completed | ||
| Impact of Treatment Intensity on Survival, Quality of Life, and Resource Utilization in Medically Less Fit Adults With Acute Myeloid Leukemia and Analogous Myeloid Neoplasms: A Randomized Pilot Study [NCT03012672] | Phase 2 | 50 participants (Actual) | Interventional | 2016-12-30 | Completed | ||
| Venetoclax to Improve Outcomes of Fractionated Busulfan Regimen in Patients With High-Risk AML and MDS [NCT04708054] | Phase 2 | 100 participants (Anticipated) | Interventional | 2021-10-21 | Recruiting | ||
| Dose-Finding (Phase 1) Study of Continuous Infusion Cladribine, Cytarabine and Mitoxantrone (CI-CLAM) for Adults With Relapsed/Refractory Acute Myeloid Leukemia or Other High-Grade Myeloid Neoplasms Treated at UW/SCCA [NCT04196010] | Phase 1 | 13 participants (Actual) | Interventional | 2020-05-08 | Terminated(stopped due to Terminated due to unfavorable risk-benefit ratio of investigational regimen.) | ||
| Four-Arm Randomized Phase II Study of SGI-110: 5 Days, Versus 10 Days, Versus 5 Days + Idarubicin, Versus 5 Days + Cladribine, in Previously Untreated Patients >/= 70 Years With Acute Myeloid Leukemia [NCT02096055] | Phase 2 | 44 participants (Actual) | Interventional | 2014-04-04 | Completed | ||
| Cardioprotection With Dexrazoxane in Acute Myeloid Leukemia (AML), High-Risk Myelodysplastic Syndrome (MDS), Myeloid Blast Phase of Chronic Myeloid Leukemia (CML), Ph+ AML, and Myeloid Blast Phase of Myeloproliferative Neoplasms [NCT03589729] | Phase 2 | 100 participants (Anticipated) | Interventional | 2018-09-19 | Recruiting | ||
| "A Feasibility Study of Early Allogeneic Hematopoietic Cell Transplantation for Relapsed or Refractory High-Grade Myeloid Neoplasms" [NCT02756572] | Phase 2 | 30 participants (Actual) | Interventional | 2016-09-22 | Completed | ||
| Phase 1/2 Study of Concurrent Decitabine in Combination With G-CSF, Cladribine, Cytarabine, and Mitoxantrone (G-CLAM) in Adults With Newly Diagnosed Acute Myeloid Leukemia (AML) or High-Risk Myelodysplastic Syndromes (MDS) [NCT02921061] | Phase 1/Phase 2 | 28 participants (Actual) | Interventional | 2016-11-17 | Completed | ||
| Phase II Study of Venetoclax Added to Cladribine Plus Low Dose Cytarabine (LDAC) Induction Followed by Consolidation With Cladribine Plus LDAC Alternating With 5-Azacitidine With Venetoclax in Patients With Untreated AML [NCT03586609] | Phase 2 | 145 participants (Anticipated) | Interventional | 2018-10-25 | Recruiting | ||
| A Phase 1/2 Trial of G-CSF, Cladribine, Cytarabine, and Dose-Escalated Mitoxantrone (G-CLAM) in Adults With Newly Diagnosed or Relapsed/Refractory Acute Myeloid Leukemia (AML) or High-Risk Myelodysplastic Syndromes (MDS) [NCT02044796] | Phase 1/Phase 2 | 199 participants (Actual) | Interventional | 2014-01-23 | Completed | ||
| A Phase 1 Single-Center Trial Combining Venetoclax With G-CSF, Cladribine, Cytarabine, and Mitoxantrone (CLAG-M) for Patients With AML and High-Grade Myeloid Neoplasms [NCT04797767] | Phase 1 | 20 participants (Anticipated) | Interventional | 2022-02-04 | Recruiting | ||
| A Single-Center Phase 1/2 Study of Single- or Fractioned-Dose Gemtuzumab Ozogamicin in Combination With G-CSF, Cladribine, Cytarabine, and Mitoxantrone for Previously Untreated Adult Acute Myeloid Leukemia or High-Grade Myeloid Neoplasm [NCT03531918] | Phase 1/Phase 2 | 66 participants (Actual) | Interventional | 2018-09-14 | Completed | ||
| A Combination of Cladribine, Idarubicin, Cytarabine (CLIA) and Quizartinib for the Treatment of Patients With Newly Diagnosed or Relapsed/Refractory Acute Myeloid Leukemia (AML) and High-Risk Myelodysplastic Syndrome (MDS)) [NCT04047641] | Phase 1/Phase 2 | 80 participants (Anticipated) | Interventional | 2019-10-22 | Recruiting | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
"Time from treatment start until disease progression, death, or discontinuation of treatment for adverse event (toxicity)~Estimated using the Kaplan-Meier method. A logrank test will be used to compare progression-free survival between Group I and Group II. A p-value less that 0.05 will be considered statistically significant." (NCT00764517)
Timeframe: Up to 5 years
| Intervention | Months (Median) |
|---|---|
| Previously Untreated | 39.0 |
| Relapsed | 19.5 |
ORR defined as the percentage of patients who achieved a complete response (CR) or a partial response (PR). Assessed per the revised Cheson criteria. Response definitions per revised International Working Group Response Criteria. 95% confidence interval will be provided. Definitions: Complete response (CR) = disappearance of all evidence of disease; Partial response (PR) = regression of measurable disease and no new sites. (NCT00764517)
Timeframe: 2 years
| Intervention | percentage of participants (Number) |
|---|---|
| Previously Untreated | 97 |
| Relapsed | 39 |
"Time from treatment start until disease progression or death.~Estimated using the Kaplan-Meier method. A logrank test will be used to compare progression-free survival between Group I and Group II. A p-value less that 0.05 will be considered statistically significant." (NCT00764517)
Timeframe: Up to 5 years
| Intervention | Months (Median) |
|---|---|
| Previously Untreated | NA |
| Relapsed | 19.5 |
Tolerability is determined to be the percentage of patients who completed the full duration of treatment (all 6 cycles) regardless of adverse event status. % tolerability shows the rate of patients that tolerated the treatment for the full duration. (NCT00764517)
Timeframe: 6 months
| Intervention | percentage of participants (Number) |
|---|---|
| Previously Untreated | 62 |
| Relapsed | 22 |
Toxicity is determined percentage of patients that experienced an adverse event (AE) grade 3 or higher during the time frame, assessed using the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) version 4.0. Grade refers to the severity of the AE increasing from Grade 1 to 5. Generally, Grade 1 = Mild; Grade 2 = Moderate; Grade 3 = Severe or medically significant but not immediately life-threatening; Grade 4 = Life-threatening consequences; Grade 5 = Death related to AE. (NCT00764517)
Timeframe: 6 months
| Intervention | percentage of participants (Number) |
|---|---|
| Previously Untreated | 90 |
| Relapsed | 83 |
Remission Rate defined as Recist Category of Complete Resposne (CR) Disappearance of all non-target lesions and normalization of tumor marker level. All lymph nodes must be non-pathological in size(<10 mm short axis). (NCT02044796)
Timeframe: Up to day 45 after start of second course of induction chemotherapy
| Intervention | Participants (Count of Participants) |
|---|---|
| Newly Diagnosed Group | 95 |
| Relapsed/Refractory | 22 |
Defined as the highest dose studied in which the incidence of dose-limiting toxicity is < 33%, graded according to NCI Common Terminology Criteria for Adverse Events version 4.0 (NCT02044796)
Timeframe: Up to day 45 after start of induction chemotherapy
| Intervention | Participants (Count of Participants) |
|---|---|
| Newly Diagnosed Group | 1 |
| Relapsed/Refractory Group | 2 |
Number of subjects that have survived (NCT02044796)
Timeframe: From date of randomization until the date of death from any cause, assessed up to 12 months
| Intervention | Participants (Number) |
|---|---|
| Phase 2 Newly Diagnosed Group 18 mg/m^2 | 66 |
| Phase 2 Relapsed/Refractory Group 16 mg/m^2 | 13 |
(NCT02044796)
Timeframe: Up to 5 years
| Intervention | Participants (Count of Participants) |
|---|---|
| Phase 2 Relapsed/Refractory Group 16 mg/m^2 | 24 |
Complete Response = Complete Remission (CR) + Complete Remission without blood count recovery (CRi) - CR: Neutrophil count >/= 1.0 x 10^9/L and platelet count >/= 100 x 10^9/L, and normal bone marrow differential (NCT02096055)
Timeframe: Up to 4 years, 3 months
| Intervention | Participants (Count of Participants) |
|---|---|
| Arm I (Guadecitabine) x 5 Days | 5 |
| Arm II (CLOSED) (Guadecitabine) x 10 Days | 5 |
| Arm III (Guadecitabine, Idarubicin) | 10 |
| Arm IV (CLOSED) (Guadecitabine, Cladribine) | 0 |
Survival time will be estimated using the Kaplan-Meier method. The two-sided log-rank test will be used to assess the differences of time to events between groups. Time from date of treatment start until the date of first objective documentation of disease-relapse. (NCT02096055)
Timeframe: Up to 4 years, 3 months
| Intervention | Months (Median) |
|---|---|
| Arm I (Guadecitabine) x 5 Days | 4.2 |
| Arm II (CLOSED) (Guadecitabine) x 10 Days | 10.0 |
| Arm III (Guadecitabine, Idarubicin) | 7.4 |
| Arm IV (CLOSED) (Guadecitabine, Cladribine) | 4.3 |
The date of Complete Response to the date of loss of response or last follow-up. (NCT02096055)
Timeframe: Up to 4 years, 3 months
| Intervention | Months (Median) |
|---|---|
| Arm I (Guadecitabine) x 5 Days | 7.4 |
| Arm II (CLOSED) (Guadecitabine) x 10 Days | 14.2 |
| Arm III (Guadecitabine, Idarubicin) | 5.3 |
Survival time will be estimated using the Kaplan-Meier method. The two-sided log-rank test will be used to assess the differences of time to events between groups. (NCT02096055)
Timeframe: Up to 4 years, 3 months
| Intervention | Months (Median) |
|---|---|
| Arm I (Guadecitabine) x 5 Days | 13.1 |
| Arm II (CLOSED) (Guadecitabine) x 10 Days | 13.0 |
| Arm III (Guadecitabine, Idarubicin) | 15.4 |
| Arm IV (CLOSED) (Guadecitabine, Cladribine) | 11.9 |
The most frequently reported adverse events will be determined by the Principal Investigator. The number of participants who experienced the most frequent grade 3 or 4 adverse events will be reported. (NCT02096055)
Timeframe: Up to 4 years, 3 months
| Intervention | Participants (Count of Participants) | ||
|---|---|---|---|
| Infection/Sepsis | Febrile Neutropenia | Fatigue | |
| Arm I (Guadecitabine) x 5 Days | 4 | 5 | 0 |
| Arm II (CLOSED) (Guadecitabine) x 10 Days | 8 | 2 | 0 |
| Arm III (Guadecitabine, Idarubicin) | 8 | 4 | 3 |
| Arm IV (CLOSED) (Guadecitabine, Cladribine) | 9 | 9 | 0 |
Will be assessed using National Cancer Institute Common Terminology Criteria for Adverse Events version 5.0. (NCT02728050)
Timeframe: Up to 5 years
| Intervention | Participants (Count of Participants) |
|---|---|
| Phase 1, Dose Level 1 | 6 |
| Phase 1, Dose Level 2 | 6 |
| Phase 1, Dose Level 3 | 11 |
| Phase 1, Dose Level 4 | 8 |
| Phase 1, Dose Level 5 | 9 |
| Phase 1, Dose Level 6 | 7 |
| Phase 2, Dose Level 6 | 32 |
ORR, defined as CR+CRi, rates of patients treated with CLAG-M with sorafenib. (NCT02728050)
Timeframe: Up to 5 years
| Intervention | Participants (Count of Participants) |
|---|---|
| Phase 1, Dose Level 1 | 6 |
| Phase 1, Dose Level 2 | 6 |
| Phase 1, Dose Level 3 | 8 |
| Phase 1, Dose Level 4 | 5 |
| Phase 1, Dose Level 5 | 9 |
| Phase 1, Dose Level 6 | 7 |
| Phase 2, Dose Level 6 | 34 |
12-month overall survival (NCT02728050)
Timeframe: 12 months
| Intervention | percentage of participants (Number) |
|---|---|
| CLAGM+Sorafenib Phase 2 | 86 |
MTD/RP2D will be defined as the highest dose studied in which the incidence of dose-limiting toxicity (DLT) is < 33% assuming at least 6 patients have been treated at this dose. DLTs were defined as: 1) grade ≥3 non-hematologic toxicity lasting >48 hours leading to >7-day delay of the next cycle; 2) grade ≥4 non-hematologic toxicity if no recovery to grade ≤2 in 14 days (both excluding febrile neutropenia/ infection); 3) Absolute neutrophil count <500/ µL or platelet count <50,000/µL for >49 days after CLAGM+S without marrow evidence of AML. Doses were escalated up to dose level six if <2/6 patients out of each cohort of 6 had a DLT (some cohorts were expanded to 12 patients while awaiting completion of DLT monitoring period). The dose level at which dose escalation was stopped was the recommended phase 2 dose (RP2D). (NCT02728050)
Timeframe: First 28 days of treatment
| Intervention | mg/m^2 (Number) |
|---|---|
| CLAGM+Sorafenib Phase 1 | 18 |
MTD/RP2D will be defined as the highest dose studied in which the incidence of dose-limiting toxicity (DLT) is < 33% assuming at least 6 patients have been treated at this dose. DLTs were defined as: 1) grade ≥3 non-hematologic toxicity lasting >48 hours leading to >7-day delay of the next cycle; 2) grade ≥4 non-hematologic toxicity if no recovery to grade ≤2 in 14 days (both excluding febrile neutropenia/ infection); 3) Absolute neutrophil count <500/ µL or platelet count <50,000/µL for >49 days after CLAGM+S without marrow evidence of AML. Doses were escalated up to dose level six if <2/6 patients out of each cohort of 6 had a DLT (some cohorts were expanded to 12 patients while awaiting completion of DLT monitoring period). The dose level at which dose escalation was stopped was the recommended phase 2 dose (RP2D). (NCT02728050)
Timeframe: First 28 days of treatment
| Intervention | mg BID (Number) |
|---|---|
| CLAGM+Sorafenib Phase 1 | 400 |
We will determine if the addition of sorafenib to CLAG-M improves the rate of MRDneg CR compared to our institution's historical control of CLAG-M alone in adults with newly-diagnosed AML/high-risk MDS. (NCT02728050)
Timeframe: 56 days (2 cycles of induction chemotherapy)
| Intervention | Participants (Count of Participants) |
|---|---|
| Phase 1, Dose Level 1 | 3 |
| Phase 1, Dose Level 2 | 6 |
| Phase 1, Dose Level 3 | 8 |
| Phase 1, Dose Level 4 | 4 |
| Phase 1, Dose Level 5 | 9 |
| Phase 1, Dose Level 6 | 7 |
| Phase 2, Dose Level 6 | 31 |
12-month event free survival (NCT02728050)
Timeframe: 12 months
| Intervention | percentage of participants (Number) |
|---|---|
| CLAGM+Sorafenib Phase 2 | 81 |
12-month relapse free survival (RFS) (NCT02728050)
Timeframe: 12 months
| Intervention | percentage of participants (Number) |
|---|---|
| CLAGM+Sorafenib Phase 2 | 82 |
Patients who receive early transplant will be compared to those that don't using the Wilcoxon rank sum test for the quantitative variable of age. (NCT02756572)
Timeframe: From time of subject's study enrollment to time of subject's feasibility success assessment (i.e. when subject received transplant within 60 days or when it was determined subject would not proceed with transplant on study)
| Intervention | years (Median) |
|---|---|
| Received Allogeneic HCT on Study | 55 |
| Did Not Receive Allogeneic HCT on Study | 57 |
"Patients who receive early transplant will be compared to those that don't using the Wilcoxon rank sum test for the quantitative variable of treatment-related mortality (TRM). This outcome measure is intended to report a predicted TRM score assessed at the time of feasibility evaluation. The TRM score is used to measure treatment-related mortality, or likelihood of death within 28 days of initiation of induction chemotherapy for patients with AML. The score is normalized from 0 to 100, so that a score of 0 demonstrates the patient has a very low likelihood of TRM and a score of 100 a very high likelihood of death. A calculation is used to predict TRM using age, performance status, if they have secondary AML, albumin, creatinine, platelet count, white blood cell count, and peripheral blood blast percentage. The higher the TRM score, the higher the risk of TRM. Calculator and table of relationship between TRM score and TRM probability found here: https://trmcalculator.fredhutch.org/." (NCT02756572)
Timeframe: From time of subject's study enrollment to time of subject's feasibility success assessment (i.e. when subject received transplant within 60 days or when it was determined subject would not proceed with transplant on study)
| Intervention | units on a scale (Median) |
|---|---|
| Received Allogeneic HCT on Study | 2.15 |
| Did Not Receive Allogeneic HCT on Study | 3.045 |
Overall survival among patients who did not receive early allogeneic HCT on study as estimated with the Kaplan-Meier method. (NCT02756572)
Timeframe: Up to 100 days after induction day 1
| Intervention | Percentage of participants (Number) |
|---|---|
| Did Not Receive Allogeneic HCT on Study | 75 |
Overall survival among patients who did not receive early allogeneic HCT on study as estimated with the Kaplan-Meier method. (NCT02756572)
Timeframe: Up to 6 months after induction day 1
| Intervention | Percentage of participants (Number) |
|---|---|
| Did Not Receive Allogeneic HCT on Study | 62 |
Overall survival among patients who received early allogeneic HCT on study as estimated with the Kaplan-Meier method. (NCT02756572)
Timeframe: Up to 100 days post-transplant
| Intervention | Percentage of participants (Number) |
|---|---|
| Received Allogeneic HCT on Study | 91 |
Overall survival among patients who received early allogeneic HCT on study as estimated with the Kaplan-Meier method. (NCT02756572)
Timeframe: Up to 6 months post-transplant
| Intervention | Percentage of participants (Number) |
|---|---|
| Received Allogeneic HCT on Study | 82 |
Relapse-free survival among patients who received early allogeneic HCT on study as estimated with the Kaplan-Meier method. (NCT02756572)
Timeframe: Up to 100 days post-transplant
| Intervention | Percentage of participants (Number) |
|---|---|
| Received Allogeneic HCT on Study | 91 |
Relapse-free survival among patients who received early allogeneic HCT on study as estimated with the Kaplan-Meier method. (NCT02756572)
Timeframe: Up to 6 months post-transplant
| Intervention | Percentage of participants (Number) |
|---|---|
| Received Allogeneic HCT on Study | 82 |
Treatment related mortality calculated among patients who received early allogeneic HCT on study vs patients who did not receive early transplant on study. (NCT02756572)
Timeframe: At day 100
| Intervention | Percentage of participants (Number) |
|---|---|
| Received Allogeneic HCT on Study | 9 |
| Did Not Receive Allogeneic HCT on Study | 23.8 |
The amount of returned patient-reported outcome questionnaires will be summarized for each collection timepoint using percent collection from surviving patients for PRO timepoints. (NCT02756572)
Timeframe: Up to 12 months post-HCT
| Intervention | Participants (Count of Participants) | ||||
|---|---|---|---|---|---|
| Enrollment PROs returned | Post G-CLAM PROs returned | Pre-HCT PROs returned | 6 months post-HCT PROs returned | 12 months post-HCT PROs returned | |
| Treatment (Chemotherapy, HCT) | 27 | 23 | 8 | 4 | 3 |
Patients who receive early transplant will be compared to those that don't using the Fisher's exact test for the categorical variables of gender. (NCT02756572)
Timeframe: From time of subject's study enrollment to time of subject's feasibility success assessment (i.e. when subject received transplant within 60 days or when it was determined subject would not proceed with transplant on study)
| Intervention | Participants (Count of Participants) | |
|---|---|---|
| Female | Male | |
| Did Not Receive Allogeneic HCT on Study | 10 | 11 |
| Received Allogeneic HCT on Study | 8 | 1 |
Success will be defined as enrollment of at least 30 patients with transplants occurring in 15 of these 30 (50%) within 60 days of enrollment or start of induction chemotherapy with G-CLAM, whichever is earlier. (NCT02756572)
Timeframe: Up to 60 days after start of chemotherapy
| Intervention | Participants (Count of Participants) | |
|---|---|---|
| Received allogeneic HCT on study within 60 days (feasibility success) | Did not receive allogeneic HCT on study within 60 days (feasibility failure) | |
| Treatment (Chemotherapy, HCT) | 9 | 21 |
Success will be defined as observing a 40% of higher 6-month relapse-free survival among patients who received early transplant on study. (NCT02756572)
Timeframe: 6 months after early allogeneic HCT on study
| Intervention | Participants (Count of Participants) | |
|---|---|---|
| No relapse within 6 months post-HCT (feasibility success) | Relapse within 6 months post-HCT (feasibility failure) | |
| Received Early Allogeneic HCT on Study | 6 | 2 |
"Complete Remission (CR), defined as <5% blasts in bone marrow with hematologic recovery (ANC>1000/ul and platelets >100,000/ml).~CRi, defined as complete remission with insufficient hematologic recovery (ANC<1000/ul or platelets<100,000/ul).~CRp, defined as complete remission but platelets <100,000/ul. Minimal residual disease (MRD), defined as any detectable disease by flow cytometry, cytogenetics, FISH or PCR in a patient otherwise fulfilling remission criteria.~Morphologic leukemia-free state (MLFS), defined as <5% blasts in bone marrow with no hematologic recovery.~Relapse, defined as >5% blasts in bone marrow, flow cytometry, or manual differential; OR treatment for active relapsed disease." (NCT02756572)
Timeframe: Approximately 28 days after early allogeneic HCT
| Intervention | Participants (Count of Participants) | ||||||
|---|---|---|---|---|---|---|---|
| CR with MRD | CR without MRD | CRi with MRD | CRi without MRD | MLFS with MRD | MLFS without MRD | Relapse | |
| Received Allogeneic HCT on Study | 0 | 7 | 0 | 1 | 0 | 0 | 0 |
"Complete Remission (CR), defined as <5% blasts in bone marrow with hematologic recovery (ANC>1000/ul and platelets >100,000/ml).~CRi, defined as complete remission with insufficient hematologic recovery (ANC<1000/ul or platelets<100,000/ul).~CRp, defined as complete remission but platelets <100,000/ul. Minimal residual disease (MRD), defined as any detectable disease by flow cytometry, cytogenetics, FISH or PCR in a patient otherwise fulfilling remission criteria.~Morphologic leukemia-free state (MLFS), defined as <5% blasts in bone marrow with no hematologic recovery.~Relapse, defined as >5% blasts in bone marrow, flow cytometry, or manual differential; OR treatment for active relapsed disease." (NCT02756572)
Timeframe: Approximately 84 days after early allogeneic HCT
| Intervention | Participants (Count of Participants) | ||||||
|---|---|---|---|---|---|---|---|
| CR with MRD | CR without MRD | CRi with MRD | CRi without MRD | MLFS with MRD | MLFS without MRD | Relapse | |
| Received Allogeneic HCT on Study | 0 | 4 | 0 | 2 | 0 | 0 | 2 |
Acute graft versus host disease (graded II, III, or IV) among patients who received early allogeneic HCT on study. (NCT02756572)
Timeframe: At day 100
| Intervention | Participants (Count of Participants) |
|---|---|
| Received Allogeneic HCT on Study | 0 |
The amount of days of hospitalization (the major driver of costs within the first year) will be collected for resource utilization. (NCT02756572)
Timeframe: Within the first year of induction chemotherapy on study
| Intervention | days (Median) |
|---|---|
| Treatment (Chemotherapy, HCT) | 49 |
Event-free survival among patients who received early allogeneic HCT on study as estimated with the Kaplan-Meier method. Events included death, relapse, and grade 3-4 acute graft vs host disease. (NCT02756572)
Timeframe: Up to 100 days post-transplant
| Intervention | Percentage of participants (Number) |
|---|---|
| Received Allogeneic HCT on Study | 91 |
Event-free survival among patients who received early allogeneic HCT on study as estimated with the Kaplan-Meier method. Events included death, relapse, and grade 3-4 acute graft vs host disease. (NCT02756572)
Timeframe: Up to 6 months post-transplant
| Intervention | Percentage of participants (Number) |
|---|---|
| Received Allogeneic HCT on Study | 82 |
(NCT02921061)
Timeframe: Up to 1 year
| Intervention | participants (Number) |
|---|---|
| Treatment (Decitabine 20 mg/m2 and G-CLAM) | 9 |
(NCT02921061)
Timeframe: Up to 1 year
| Intervention | participants (Number) |
|---|---|
| Treatment (Decitabine 20 mg/m2 and G-CLAM) | 8 |
"Evaluated according to National Cancer Institute Common Terminology Criteria for Adverse Events version 4.0. MTD is defined as the highest dose studied in which the incidence of DLT is < 33%. Each participant was monitored for DLTs in the first 20 days of treatment. DLTs monitored included~any grade 3 non-hematologic toxicity lasting more than 48 hours that resulted in more than a 7 day delay of the subsequent treatment cycle (except for febrile neutropenia or infection)~any grade 4 or greater non-hematologic toxicity (except febrile neutropenia and infection unless a direct consequence of a treatment-related toxicity, and except constitutional symptoms if they recovered to grade 2 or less within 14 days)~lack of recovery of the absolute neutrophil count to 500/microliter or greater and lack of self-sustained platelet count of at least 50,000/microliter by treatment day +49 with no evidence of residual leukemia" (NCT02921061)
Timeframe: Up to 49 days
| Intervention | Participants (Count of Participants) |
|---|---|
| Treatment (Decitabine 20 mg/m2 and G-CLAM) | 3 |
(NCT02921061)
Timeframe: Up to 1 year
| Intervention | participants (Number) |
|---|---|
| Treatment (Decitabine 20 mg/m2 and G-CLAM) | 13 |
(NCT02921061)
Timeframe: Up to 1 year
| Intervention | participants (Number) |
|---|---|
| Treatment (Decitabine 20 mg/m2 and G-CLAM) | 8 |
Compared to historical controls of filgrastim, cladribine, cytarabine, and mitoxantrone hydrochloride (G-CLAM) alone. A Simon Minimax two-stage design will be used. (NCT02921061)
Timeframe: Up to 1 year
| Intervention | participants (Number) |
|---|---|
| Treatment (Decitabine 20 mg/m2 and G-CLAM) | 13 |
"As a summary of adverse events (captured on trial using the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) version 5.0), 30-day all cause mortality is reported as a percent of patients treated at the MTD/RP2D.~Will be estimated and 95% confidence intervals will be calculated. Regression models (logistic regression for binary endpoints, Cox regression for time-to-event endpoints [Cox models for the hazard of the subdistribution for events with competing risks]) will be used to compare outcomes with patients who have received GCLAM without GO at our institution, controlling for measured prognostic factors." (NCT03531918)
Timeframe: Up to 5 years. 30-day all-cause mortality is reported
| Intervention | proportion died on/before day 30 (Number) |
|---|---|
| GO3 Dose Level Includes Phase 1 and Phase 2 | .03 |
Defined as the highest dose studied in which the incidence of Dose Limiting Toxicity (DLT) is ≤33% (≤4 of 12 patients experiencing DLT), defined as any Grade 3 non-hematologic toxicity lasting >48 hours that results in >7-day delay of the subsequent treatment cycle, with the exception of febrile neutropenia or infection or toxicities secondary to febrile neutropenia or infection, or any Grade ≥4 non-hematologic toxicity except febrile neutropenia/infection (or toxicities secondary to febrile neutropenia or infection) unless felt to be a direct consequence of treatment-related toxicity (e.g. intestinal infection following mucosal barrier breakdown), and with the exception of constitutional symptoms if recovery to Grade ≤2 within 14 days. The National Cancer Institute Common Terminology Criteria for Adverse Events v5.0 will be used. (NCT03531918)
Timeframe: At time of count recovery, second cycle of treatment, response assessment or removal from protocol (at approximately 1 month).
| Intervention | Participants (Count of Participants) |
|---|---|
| GO1 Dose Level Phase 1 | NA |
| GO3 Dose Level Includes Phase 1 and Phase 2 | NA |
"Will be estimated and 95% confidence intervals will be calculated. Regression models (logistic regression for binary endpoints, Cox regression for time-to-event endpoints [Cox models for the hazard of the subdistribution for events with competing risks]) will be used to compare outcomes with patients who have received GCLAM without GO at our institution, controlling for measured prognostic factors.~o Aplasia rate is defined in this protocol as frequency of patients without blood count recovery after chemotherapy and bone marrow examination showing hypocellularity not meeting cellularity criteria for morphologic leukemia free state (MLFS). MRD negative (MRDneg) status is defined as negative for leukemic markers by multiparameter flow cytometry.~Aplasia was defined as absence of tumoral cells but cellularity not meeting criteria for MLFS.~Statistical significance tests were not performed." (NCT03531918)
Timeframe: 90 days
| Intervention | Participants (Count of Participants) |
|---|---|
| GO1 Dose Level Phase 1 | 0 |
| GO3 Dose Level Includes Phase 1 and Phase 2 | 2 |
"Will be estimated and 95% confidence intervals will be calculated. Regression models (logistic regression for binary endpoints, Cox regression for time-to-event endpoints [Cox models for the hazard of the subdistribution for events with competing risks]) will be used to compare outcomes with patients who have received GCLAM without GO at our institution, controlling for measured prognostic factors.~Complete response (CR) + complete response with incomplete hematologic recovery (CRi) rate is defined as the frequency of patients achieving CR or CRi per the European LeukemiaNet 2017 criteria as defined above. MRD negative (MRDneg) status is defined as negative for leukemic markers by multiparameter flow cytometry.~Aplasia was defined as absence of tumoral cells but cellularity not meeting criteria for MLFS.~Statistical significance tests were not performed." (NCT03531918)
Timeframe: 90 days
| Intervention | Participants (Count of Participants) |
|---|---|
| GO1 Dose Level Phase 1 | 5 |
| GO3 Dose Level Includes Phase 1 and Phase 2 | 52 |
"Will be estimated and 95% confidence intervals will be calculated. Regression models (logistic regression for binary endpoints, Cox regression for time-to-event endpoints [Cox models for the hazard of the subdistribution for events with competing risks]) will be used to compare outcomes with patients who have received GCLAM without GO at our institution, controlling for measured prognostic factors.~Complete response with incomplete hematologic recovery (CRi) rate is defined as the frequency of patients achieving CRi, which is defined by the European LeukemiaNet 2017 guidelines as all CR criteria except for residual neutropenia (ANC <1.0 x 109/L [1000/mL]) or thrombocytopenia (platelet count <100 x 109/L [100,000/mL]). MRD negative (MRDneg) status is defined as negative for leukemic markers by multiparameter flow cytometry.~Aplasia was defined as absence of tumoral cells but cellularity not meeting criteria for MLFS.~Statistical significance tests were not performed." (NCT03531918)
Timeframe: 90 days
| Intervention | Participants (Count of Participants) |
|---|---|
| GO1 Dose Level Phase 1 | 1 |
| GO3 Dose Level Includes Phase 1 and Phase 2 | 7 |
"Will be estimated and 95% confidence intervals will be calculated. Regression models (logistic regression for binary endpoints, Cox regression for time-to-event endpoints [Cox models for the hazard of the subdistribution for events with competing risks]) will be used to compare outcomes with patients who have received GCLAM without GO at our institution, controlling for measured prognostic factors.~Morphologic leukemia free state (MLFS) rate is defined as the frequency of patients achieving MLFS, which is defined by the European LeukemiaNet guidelines as bone marrow blasts <5%; absence of blasts with Auer rods; absence of extramedullary disease; no hematologic recovery required. At least 200 cells should be enumerated or cellularity should be at least 10%. MRD negative (MRDneg) status is defined as negative for leukemic markers by multiparameter flow cytometry.~Aplasia was defined as absence of tumoral cells but cellularity not meeting criteria for MLFS.~Statistical significance" (NCT03531918)
Timeframe: 90 days
| Intervention | Participants (Count of Participants) |
|---|---|
| GO1 Dose Level Phase 1 | 0 |
| GO3 Dose Level Includes Phase 1 and Phase 2 | 2 |
OS was calculated for all participants and measured from initial trial therapy to death from any cause. Patients last known ot be alive were censored at date of last contact. Will be estimated using the Kaplan-Meier method. Regression models (logistic regression for binary endpoints, Cox regression for time-to-event endpoints [Cox models for the hazard of the subdistribution for events with competing risks]) will be used to compare outcomes with patients who have received GCLAM without GO at our institution, controlling for measured prognostic factors. (NCT03531918)
Timeframe: 3 years and 1 month
| Intervention | percentage of participants (Number) |
|---|---|
| GO3 Dose Level | 60 |
RFS was calculated for participants who achieved a complete remission (with or without count recovery; CR or CRi) and measured from the date remission to the first of relapse from CR/CRi or death from any cause. Patients last known to be alive in CR /CRi were censored at date of last contact. Will be estimated using the Kaplan-Meier method. Time to relapse will be estimated using non-parametric estimates of the cumulative incidence curve with death analyzed as a competing event. Regression models (logistic regression for binary endpoints, Cox regression for time-to-event endpoints [Cox models for the hazard of the subdistribution for events with competing risks]) will be used to compare outcomes with patients who have received GCLAM without GO at our institution, controlling for measured prognostic factors. (NCT03531918)
Timeframe: Up to 5 years. 2-year RFS reported.
| Intervention | percentage of participants (Number) |
|---|---|
| GO3 Dose Level Includes Phase 1 and Phase 2 | 51 |
A two-stage design will be used to evaluate the EFS. Patients treated at the maximum tolerated dose (MTD) from the phase 1 portion of the trial will be used in the phase 2 analysis. If censoring occurs, secondary analyses analyzing 6-month or 1-year EFS accounting for censoring will be done, including estimating 6-month or 1-year EFS using the Kaplan-Meier method. The first stage of the two-stage phase 2 design will evaluate 30 patients. If 20 or more of the first 30 patients are alive without event at 6-months after study registration, an additional 30 patients will be enrolled. If 46 or more of the 60 patients treated at the MTD are alive and without event at 6-months after study registration, the study will consider the regimen of interest for further investigation. Patients last known to be alive in CR were censored at date of last contact. (NCT03531918)
Timeframe: From the start of study treatment, assessed at 6 months and 1 year
| Intervention | percent of participants (Number) | |
|---|---|---|
| Event-free Survival (6 months) | Event-free survival (12 months) | |
| GO3 Dose Level Includes Phase 1 and Phase 2 | 73 | 58 |
"Will be estimated and 95% confidence intervals will be calculated. Regression models (logistic regression for binary endpoints, Cox regression for time-to-event endpoints [Cox models for the hazard of the subdistribution for events with competing risks]) will be used to compare outcomes with patients who have received GCLAM without GO at our institution, controlling for measured prognostic factors.~Complete response (CR) rate is defined as the frequency of patients achieving CR, which is defined by the European LeukemiaNet 2017 guidelines as bone marrow blasts <5%; absence of circulating blasts and blasts with Auer rods; absence of extramedullary disease; ANC ≥1.0 x 109/L (1000/mL); platelet count ≥100 x 109/L. (100 000/mL). MRD negative (MRDneg) status is defined as negative for leukemic markers by multiparameter flow cytometry.~Aplasia was defined as absence of tumoral cells but cellularity not meeting criteria for MLFS.~Statistical significance tests were not performed." (NCT03531918)
Timeframe: 90 days
| Intervention | Participants (Count of Participants) | |
|---|---|---|
| MRDneg | MRDpos | |
| GO1 Dose Level Phase 1 | 4 | 0 |
| GO3 Dose Level Includes Phase 1 and Phase 2 | 38 | 7 |
| Substance | Relationship Strength | Studies | Trials | Classes | Roles |
|---|---|---|---|---|---|
| adenine [no description available] | 2.08 | 1 | 0 | 6-aminopurines; purine nucleobase | Daphnia magna metabolite; Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite |
| cytosine [no description available] | 3.1 | 1 | 0 | aminopyrimidine; pyrimidine nucleobase; pyrimidone | Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite |
| purine 1H-purine : The 1H-tautomer of purine.. 3H-purine : The 3H-tautomer of purine.. 9H-purine : The 9H-tautomer of purine.. 7H-purine : The 7H-tautomer of purine. | 1.99 | 1 | 0 | purine | |
| verapamil Verapamil: A calcium channel blocker that is a class IV anti-arrhythmia agent.. verapamil : A racemate comprising equimolar amounts of dexverapamil and (S)-verapamil. An L-type calcium channel blocker of the phenylalkylamine class, it is used (particularly as the hydrochloride salt) in the treatment of hypertension, angina pectoris and cardiac arrhythmia, and as a preventive medication for migraine.. 2-(3,4-dimethoxyphenyl)-5-{[2-(3,4-dimethoxyphenyl)ethyl](methyl)amino}-2-(propan-2-yl)pentanenitrile : A tertiary amino compound that is 3,4-dimethoxyphenylethylamine in which the hydrogens attached to the nitrogen are replaced by a methyl group and a 4-cyano-4-(3,4-dimethoxyphenyl)-5-methylhexyl group. | 2.01 | 1 | 0 | aromatic ether; nitrile; polyether; tertiary amino compound | |
| chlorambucil Chlorambucil: A nitrogen mustard alkylating agent used as antineoplastic for chronic lymphocytic leukemia, Hodgkin's disease, and others. Although it is less toxic than most other nitrogen mustards, it has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (Merck Index, 11th ed). chlorambucil : A monocarboxylic acid that is butanoic acid substituted at position 4 by a 4-[bis(2-chloroethyl)amino]phenyl group. A chemotherapy drug that can be used in combination with the antibody obinutuzumab for the treatment of chronic lymphocytic leukemia. | 4.87 | 2 | 1 | aromatic amine; monocarboxylic acid; nitrogen mustard; organochlorine compound; tertiary amino compound | alkylating agent; antineoplastic agent; carcinogenic agent; drug allergen; immunosuppressive agent |
| mitoxantrone Mitoxantrone: An anthracenedione-derived antineoplastic agent.. mitoxantrone : A dihydroxyanthraquinone that is 1,4-dihydroxy-9,10-anthraquinone which is substituted by 6-hydroxy-1,4-diazahexyl groups at positions 5 and 8. | 2 | 1 | 0 | dihydroxyanthraquinone | analgesic; antineoplastic agent |
| prednisolone Prednisolone: A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states.. prednisolone : A glucocorticoid that is prednisone in which the oxo group at position 11 has been reduced to the corresponding beta-hydroxy group. It is a drug metabolite of prednisone. | 2.02 | 1 | 0 | 11beta-hydroxy steroid; 17alpha-hydroxy steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(1),Delta(4)-steroid; C21-steroid; glucocorticoid; primary alpha-hydroxy ketone; tertiary alpha-hydroxy ketone | adrenergic agent; anti-inflammatory drug; antineoplastic agent; drug metabolite; environmental contaminant; immunosuppressive agent; xenobiotic |
| prednisone Prednisone: A synthetic anti-inflammatory glucocorticoid derived from CORTISONE. It is biologically inert and converted to PREDNISOLONE in the liver.. prednisone : A synthetic glucocorticoid drug that is particularly effective as an immunosuppressant, and affects virtually all of the immune system. Prednisone is a prodrug that is converted by the liver into prednisolone (a beta-hydroxy group instead of the oxo group at position 11), which is the active drug and also a steroid. | 6.83 | 4 | 1 | 11-oxo steroid; 17alpha-hydroxy steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(1),Delta(4)-steroid; C21-steroid; glucocorticoid; primary alpha-hydroxy ketone; tertiary alpha-hydroxy ketone | adrenergic agent; anti-inflammatory drug; antineoplastic agent; immunosuppressive agent; prodrug |
| cytarabine [no description available] | 4.03 | 4 | 0 | beta-D-arabinoside; monosaccharide derivative; pyrimidine nucleoside | antimetabolite; antineoplastic agent; antiviral agent; immunosuppressive agent |
| cordycepin [no description available] | 2.08 | 1 | 0 | 3'-deoxyribonucleoside; adenosines | antimetabolite; nucleoside antibiotic |
| pyridostigmine bromide Pyridostigmine Bromide: A cholinesterase inhibitor with a slightly longer duration of action than NEOSTIGMINE. It is used in the treatment of myasthenia gravis and to reverse the actions of muscle relaxants. | 3.17 | 1 | 0 | pyridinium salt | |
| 2-chloroadenosine 5-chloroformycin A: structure given in first source | 11.37 | 44 | 5 | purine nucleoside | |
| 2-fluoroadenosine [no description available] | 2.08 | 1 | 0 | adenosines; organofluorine compound | |
| azacitidine Azacitidine: A pyrimidine analogue that inhibits DNA methyltransferase, impairing DNA methylation. It is also an antimetabolite of cytidine, incorporated primarily into RNA. Azacytidine has been used as an antineoplastic agent.. 5-azacytidine : An N-glycosyl-1,3,5-triazine that is 4-amino-1,3,5-triazin-2(1H)-one substituted by a beta-D-ribofuranosyl residue via an N-glycosidic linkage. An antineoplastic agent, it is used in the treatment of myeloid leukaemia. | 2.01 | 1 | 0 | N-glycosyl-1,3,5-triazine; nucleoside analogue | antineoplastic agent |
| 2-fluoroadenine 2-fluoroadenine : An organofluorine compound that is adenine in which the hydrogen at position 2 (the carbon between the two nitrogens of the pyrimidine ring) is replaced by a fluorine. | 2.08 | 1 | 0 | organofluorine compound; purines | antineoplastic agent |
| deoxycytidine [no description available] | 3.5 | 2 | 0 | pyrimidine 2'-deoxyribonucleoside | Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite |
| dideoxyadenosine Dideoxyadenosine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is an inhibitor of HIV replication, acting as a chain-terminator of viral DNA by binding to reverse transcriptase. Its principal side effect is nephrotoxicity. In vivo, dideoxyadenosine is rapidly metabolized to DIDANOSINE (ddI) by enzymatic deamination; ddI is then converted to dideoxyinosine monophosphate and ultimately to dideoxyadenosine triphosphate, the putative active metabolite. | 1.97 | 1 | 0 | adenosines; purine 2',3'-dideoxyribonucleoside | EC 3.5.4.4 (adenosine deaminase) inhibitor; EC 4.6.1.1 (adenylate cyclase) inhibitor |
| cladribine [no description available] | 3.39 | 1 | 1 | organochlorine compound; purine 2'-deoxyribonucleoside | antineoplastic agent; immunosuppressive agent |
| buthionine sulfoximine Buthionine Sulfoximine: A synthetic amino acid that depletes glutathione by irreversibly inhibiting gamma-glutamylcysteine synthetase. Inhibition of this enzyme is a critical step in glutathione biosynthesis. It has been shown to inhibit the proliferative response in human T-lymphocytes and inhibit macrophage activation. (J Biol Chem 1995;270(33):1945-7). 2-amino-4-(S-butylsulfonimidoyl)butanoic acid : A non-proteinogenic alpha-amino acid that is homocysteine in which the thiol group carries an oxo, imino and butyl groups.. S-butyl-DL-homocysteine (S,R)-sulfoximine : A sulfoximide that is the sulfoximine derivative of an analogue of DL-methionine in which the S-methyl group is replaced by S-butyl. | 2.01 | 1 | 0 | diastereoisomeric mixture; homocysteines; non-proteinogenic alpha-amino acid; sulfoximide | EC 6.3.2.2 (glutamate--cysteine ligase) inhibitor; ferroptosis inducer |
| vidarabine adenine arabinoside : A purine nucleoside in which adenine is attached to arabinofuranose via a beta-N(9)-glycosidic bond. | 6.81 | 10 | 0 | beta-D-arabinoside; purine nucleoside | antineoplastic agent; bacterial metabolite; nucleoside antibiotic |
| daunorubicin Daunorubicin: A very toxic anthracycline aminoglycoside antineoplastic isolated from Streptomyces peucetius and others, used in treatment of LEUKEMIA and other NEOPLASMS.. anthracycline : Anthracyclines are polyketides that have a tetrahydronaphthacenedione ring structure attached by a glycosidic linkage to the amino sugar daunosamine.. daunorubicin : A natural product found in Actinomadura roseola. | 2.01 | 1 | 0 | aminoglycoside antibiotic; anthracycline; p-quinones; tetracenequinones | antineoplastic agent; bacterial metabolite |
| zidovudine Zidovudine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by an azido group. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA during reverse transcription. It improves immunologic function, partially reverses the HIV-induced neurological dysfunction, and improves certain other clinical abnormalities associated with AIDS. Its principal toxic effect is dose-dependent suppression of bone marrow, resulting in anemia and leukopenia.. zidovudine : A pyrimidine 2',3'-dideoxyribonucleoside compound having a 3'-azido substituent and thymine as the nucleobase. | 2.9 | 1 | 0 | azide; pyrimidine 2',3'-dideoxyribonucleoside | antimetabolite; antiviral drug; HIV-1 reverse transcriptase inhibitor |
| etoposide [no description available] | 2.01 | 1 | 0 | beta-D-glucoside; furonaphthodioxole; organic heterotetracyclic compound | antineoplastic agent; DNA synthesis inhibitor |
| idarubicin Idarubicin: An orally administered anthracycline antineoplastic. The compound has shown activity against BREAST NEOPLASMS; LYMPHOMA; and LEUKEMIA. | 2.01 | 1 | 0 | anthracycline antibiotic; deoxy hexoside; monosaccharide derivative | |
| gemcitabine gemcitabine : A 2'-deoxycytidine having geminal fluoro substituents in the 2'-position. An inhibitor of ribonucleotide reductase, gemcitabine is used in the treatment of various carcinomas, particularly non-small cell lung cancer, pancreatic cancer, bladder cancer and breast cancer. | 3.5 | 2 | 0 | organofluorine compound; pyrimidine 2'-deoxyribonucleoside | antimetabolite; antineoplastic agent; antiviral drug; DNA synthesis inhibitor; EC 1.17.4.1 (ribonucleoside-diphosphate reductase) inhibitor; environmental contaminant; immunosuppressive agent; photosensitizing agent; prodrug; radiosensitizing agent; xenobiotic |
| nebularine nebularine: structure. nebularine : A purine ribonucleoside that is 9H-purine attached to a beta-D-ribofuranosyl residue at position 9 via a glycosidic (N-glycosyl) linkage. | 2.08 | 1 | 0 | purine ribonucleoside; purines D-ribonucleoside | fungal metabolite |
| adenosine 2',3'-ribo-epoxide adenosine 2',3'-ribo-epoxide: structure | 2.08 | 1 | 0 | ||
| 2-chloroadenine 6-amino-2-chloropurine: RN & structure given in first source | 2.08 | 1 | 0 | ||
| diosgenin [no description available] | 2.01 | 1 | 0 | 3beta-sterol; hexacyclic triterpenoid; sapogenin; spiroketal | antineoplastic agent; antiviral agent; apoptosis inducer; metabolite |
| methotrexate [no description available] | 3.32 | 2 | 0 | dicarboxylic acid; monocarboxylic acid amide; pteridines | abortifacient; antimetabolite; antineoplastic agent; antirheumatic drug; dermatologic drug; DNA synthesis inhibitor; EC 1.5.1.3 (dihydrofolate reductase) inhibitor; immunosuppressive agent |
| biotin vitamin B7 : Any member of a group of vitamers that belong to the chemical structural class called biotins that exhibit biological activity against vitamin B7 deficiency. Vitamin B7 deficiency is very rare in individuals who take a normal balanced diet. Foods rich in biotin are egg yolk, liver, cereals, vegetables (spinach, mushrooms) and rice. Symptoms associated with vitamin B7 deficiency include thinning hair, scaly skin rashes around eyes, nose and mouth, and brittle nails. The vitamers include biotin and its ionized and salt forms. | 1.99 | 1 | 0 | biotins; vitamin B7 | coenzyme; cofactor; Escherichia coli metabolite; fundamental metabolite; human metabolite; mouse metabolite; nutraceutical; prosthetic group; Saccharomyces cerevisiae metabolite |
| 2-chloro-2',3'-dideoxyadenosine [no description available] | 1.97 | 1 | 0 | ||
| glucosamine D-glucosamine : An amino sugar whose structure comprises D-glucose having an amino substituent at position 2.. 2-amino-2-deoxy-D-glucopyranose : A D-glucosamine whose structure comprises D-glucopyranose having an amino substituent at position 2. | 2.01 | 1 | 0 | D-glucosamine | Escherichia coli metabolite; geroprotector; mouse metabolite |
| pentostatin Pentostatin: A potent inhibitor of ADENOSINE DEAMINASE. The drug induces APOPTOSIS of LYMPHOCYTES, and is used in the treatment of many lymphoproliferative malignancies, particularly HAIRY CELL LEUKEMIA. It is also synergistic with some other antineoplastic agents and has immunosuppressive activity.. pentostatin : A member of the class of coformycins that is coformycin in which the hydroxy group at position 2' is replaced with a hydrogen. It is a drug used for the treatment of hairy cell leukaemia. | 5.03 | 5 | 0 | coformycins | antimetabolite; antineoplastic agent; Aspergillus metabolite; bacterial metabolite; EC 3.5.4.4 (adenosine deaminase) inhibitor |
| mycophenolic acid Mycophenolic Acid: Compound derived from Penicillium stoloniferum and related species. It blocks de novo biosynthesis of purine nucleotides by inhibition of the enzyme inosine monophosphate dehydrogenase (IMP DEHYDROGENASE). Mycophenolic acid exerts selective effects on the immune system in which it prevents the proliferation of T-CELLS, LYMPHOCYTES, and the formation of antibodies from B-CELLS. It may also inhibit recruitment of LEUKOCYTES to sites of INFLAMMATION.. mycophenolate : A monocarboxylic acid anion resulting from the removal of a proton from the carboxy group of mycophenolic acid.. mycophenolic acid : A member of the class of 2-benzofurans that is 2-benzofuran-1(3H)-one which is substituted at positions 4, 5, 6, and 7 by methyl, methoxy, (2E)-5-carboxy-3-methylpent-2-en-1-yl, and hydroxy groups, respectively. It is an antibiotic produced by Penicillium brevi-compactum, P. stoloniferum, P. echinulatum and related species. An immunosuppressant, it is widely used (partiularly as its sodium salt and as the 2-(morpholin-4-yl)ethyl ester prodrug, mycophenolate mofetil) to prevent tissue rejection following organ transplants and for the treatment of certain autoimmune diseases. | 1.99 | 1 | 0 | 2-benzofurans; gamma-lactone; monocarboxylic acid; phenols | anticoronaviral agent; antimicrobial agent; antineoplastic agent; EC 1.1.1.205 (IMP dehydrogenase) inhibitor; environmental contaminant; immunosuppressive agent; mycotoxin; Penicillium metabolite; xenobiotic |
| decitabine [no description available] | 2.01 | 1 | 0 | 2'-deoxyribonucleoside | |
| troxacitabine troxacitabine: shows good anti-HIV activity without cytotoxicity | 3.1 | 1 | 0 | carbohydrate derivative; nucleobase-containing molecular entity | |
| fludarabine [no description available] | 6.71 | 9 | 0 | purine nucleoside | |
| beta-escin [no description available] | 2.01 | 1 | 0 | ||
| adenosine kinase Adenosine Kinase: An enzyme that catalyzes the formation of ADP plus AMP from adenosine plus ATP. It can serve as a salvage mechanism for returning adenosine to nucleic acids. EC 2.7.1.20. | 1.97 | 1 | 0 | ||
| bryostatin 1 bryostatin 1: a protein kinase C activator; macrocyclic lactone from marine Bryozoan Bugula neritina; RN given refers to (1S*-(1R*,3R*,5Z,7S*,8E,11R*,12R*(2E,4E),13E,15R*,17S*(S*),21S*,23S*,25R*))-isomer; structure given in first source; activates protein kinase c. bryostatin 1 : A member of the class of bryostatins that is (17E)-2-oxooxacyclohexacos-17-ene which is substituted by hydroxy groups at positions 4, 10, and 20; an acetoxy group at position 8; methyl groups at positions 9, 9, 18, and 19; 2-methoxy-2-oxoethylidene groups at positions 14 and 24; an (E,E)-octa-2,4-dienoyloxy group at position 21; and with oxygen bridges linking positions 6 to 10, 12 to 16, and 20 to 24. It is one of the most abundant member of the class of bryostatins. | 2.42 | 2 | 0 | ||
| cyclosporine Cyclosporine: A cyclic undecapeptide from an extract of soil fungi. It is a powerful immunosupressant with a specific action on T-lymphocytes. It is used for the prophylaxis of graft rejection in organ and tissue transplantation. (From Martindale, The Extra Pharmacopoeia, 30th ed). | 3.17 | 1 | 0 | ||
| 9-arabinofuranosylguanine 9-arabinofuranosylguanine: RN given refers to (beta)-isomer. 9-beta-D-arabinofuranosylguanine : A purine nucleoside in which guanine is attached to arabinofuranose via a beta-N(9)-glycosidic bond. It inhibits DNA synthesis and causes cell death. | 3.1 | 1 | 0 | beta-D-arabinoside; purine nucleoside | antineoplastic agent; DNA synthesis inhibitor |
| Condition | Indicated | Relationship Strength | Studies | Trials |
|---|---|---|---|---|
| African Sleeping Sickness [description not available] | 0 | 2.08 | 1 | 0 |
| Trypanosomiasis, African A disease endemic among people and animals in Central Africa. It is caused by various species of trypanosomes, particularly T. gambiense and T. rhodesiense. Its second host is the TSETSE FLY. Involvement of the central nervous system produces African sleeping sickness. Nagana is a rapidly fatal trypanosomiasis of horses and other animals. | 0 | 2.08 | 1 | 0 |
| Lymphatic Diseases Diseases of LYMPH; LYMPH NODES; or LYMPHATIC VESSELS. | 0 | 2.05 | 1 | 0 |
| Diffuse Mixed Small and Large Cell Lymphoma [description not available] | 0 | 5.77 | 4 | 2 |
| Conus Medullaris Syndrome [description not available] | 0 | 2.05 | 1 | 0 |
| Destombes-Rosai-Dorfman Syndrome [description not available] | 0 | 2.05 | 1 | 0 |
| Lymphoma, Non-Hodgkin Any of a group of malignant tumors of lymphoid tissue that differ from HODGKIN DISEASE, being more heterogeneous with respect to malignant cell lineage, clinical course, prognosis, and therapy. The only common feature among these tumors is the absence of giant REED-STERNBERG CELLS, a characteristic of Hodgkin's disease. | 0 | 5.77 | 4 | 2 |
| Histiocytosis, Sinus Benign, non-Langerhans-cell, histiocytic proliferative disorder that primarily affects the lymph nodes. It is often referred to as sinus histiocytosis with massive lymphadenopathy. | 0 | 2.05 | 1 | 0 |
| Lymphoma of Mucosa-Associated Lymphoid Tissue [description not available] | 0 | 2.05 | 1 | 0 |
| Cancer of Spleen [description not available] | 0 | 2.71 | 3 | 0 |
| Lymphoma, B-Cell, Marginal Zone Extranodal lymphoma of lymphoid tissue associated with mucosa that is in contact with exogenous antigens. Many of the sites of these lymphomas, such as the stomach, salivary gland, and thyroid, are normally devoid of lymphoid tissue. They acquire mucosa-associated lymphoid tissue (MALT) type as a result of an immunologically mediated disorder. | 0 | 2.05 | 1 | 0 |
| Hand-Schu00FCller-Christian Disease [description not available] | 0 | 2.05 | 1 | 0 |
| Histiocytosis, Langerhans-Cell A group of disorders resulting from the abnormal proliferation of and tissue infiltration by LANGERHANS CELLS which can be detected by their characteristic Birbeck granules (X bodies), or by monoclonal antibody staining for their surface CD1 ANTIGENS. Langerhans-cell granulomatosis can involve a single organ, or can be a systemic disorder. | 0 | 2.05 | 1 | 0 |
| Hairy Cell Leukemia [description not available] | 0 | 7.41 | 15 | 2 |
| Leukemia, Hairy Cell A neoplastic disease of the lymphoreticular cells which is considered to be a rare type of chronic leukemia; it is characterized by an insidious onset, splenomegaly, anemia, granulocytopenia, thrombocytopenia, little or no lymphadenopathy, and the presence of hairy or flagellated cells in the blood and bone marrow. | 0 | 7.41 | 15 | 2 |
| Recrudescence [description not available] | 0 | 3.64 | 3 | 0 |
| Germinoblastoma [description not available] | 0 | 4.02 | 5 | 0 |
| Brill-Symmers Disease [description not available] | 0 | 2.99 | 1 | 0 |
| Duncan Disease [description not available] | 0 | 4.31 | 4 | 0 |
| Familial Waldenstrom's Macroglobulinaemia [description not available] | 0 | 2.99 | 1 | 0 |
| Anti-MuSK Myasthenia Gravis [description not available] | 0 | 2.99 | 1 | 0 |
| Autonomic Dysfunction, Paraneoplastic [description not available] | 0 | 2.99 | 1 | 0 |
| Lymphoma A general term for various neoplastic diseases of the lymphoid tissue. | 0 | 4.02 | 5 | 0 |
| Lymphoma, Follicular Malignant lymphoma in which the lymphomatous cells are clustered into identifiable nodules within the LYMPH NODES. The nodules resemble to some extent the GERMINAL CENTER of lymph node follicles and most likely represent neoplastic proliferation of lymph node-derived follicular center B-LYMPHOCYTES. | 0 | 2.99 | 1 | 0 |
| Lymphoproliferative Disorders Disorders characterized by proliferation of lymphoid tissue, general or unspecified. | 0 | 4.31 | 4 | 0 |
| Waldenstrom Macroglobulinemia A lymphoproliferative disorder characterized by pleomorphic B-LYMPHOCYTES including PLASMA CELLS, with increased levels of monoclonal serum IMMUNOGLOBULIN M. There is lymphoplasmacytic cells infiltration into bone marrow and often other tissues, also known as lymphoplasmacytic lymphoma. Clinical features include ANEMIA; HEMORRHAGES; and hyperviscosity. | 0 | 2.99 | 1 | 0 |
| Myasthenia Gravis A disorder of neuromuscular transmission characterized by fatigable weakness of cranial and skeletal muscles with elevated titers of ACETYLCHOLINE RECEPTORS or muscle-specific receptor tyrosine kinase (MuSK) autoantibodies. Clinical manifestations may include ocular muscle weakness (fluctuating, asymmetric, external ophthalmoplegia; diplopia; ptosis; and weakness of eye closure) and extraocular fatigable weakness of facial, bulbar, respiratory, and proximal limb muscles. The disease may remain limited to the ocular muscles (ocular myasthenia). THYMOMA is commonly associated with this condition. | 0 | 2.99 | 1 | 0 |
| B-Cell Chronic Lymphocytic Leukemia [description not available] | 0 | 6.36 | 8 | 2 |
| Leukemia, Lymphocytic, Chronic, B-Cell A chronic leukemia characterized by abnormal B-lymphocytes and often generalized lymphadenopathy. In patients presenting predominately with blood and bone marrow involvement it is called chronic lymphocytic leukemia (CLL); in those predominately with enlarged lymph nodes it is called small lymphocytic lymphoma. These terms represent spectrums of the same disease. | 0 | 6.36 | 8 | 2 |
| Leucocythaemia [description not available] | 0 | 2.01 | 1 | 0 |
| Leukemia A progressive, malignant disease of the blood-forming organs, characterized by distorted proliferation and development of leukocytes and their precursors in the blood and bone marrow. Leukemias were originally termed acute or chronic based on life expectancy but now are classified according to cellular maturity. Acute leukemias consist of predominately immature cells; chronic leukemias are composed of more mature cells. (From The Merck Manual, 2006) | 0 | 2.01 | 1 | 0 |
| Mast-Cell Leukemia [description not available] | 0 | 2.01 | 1 | 0 |
| Leukemia, Mast-Cell A form of systemic mastocytosis (MASTOCYTOSIS, SYSTEMIC) characterized by the presence of large numbers of tissue MAST CELLS in the peripheral blood without skin lesions. It is a high-grade LEUKEMIA disease with bone marrow smear of | 0 | 2.01 | 1 | 0 |
| Apoplexy [description not available] | 0 | 2.02 | 1 | 0 |
| Diplopia A visual symptom in which a single object is perceived by the visual cortex as two objects rather than one. Disorders associated with this condition include REFRACTIVE ERRORS; STRABISMUS; OCULOMOTOR NERVE DISEASES; TROCHLEAR NERVE DISEASES; ABDUCENS NERVE DISEASES; and diseases of the BRAIN STEM and OCCIPITAL LOBE. | 0 | 2.02 | 1 | 0 |
| Facial Palsy [description not available] | 0 | 2.02 | 1 | 0 |
| Hypesthesia Absent or reduced sensitivity to cutaneous stimulation. | 0 | 2.02 | 1 | 0 |
| Stroke A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810) | 0 | 2.02 | 1 | 0 |
| Disease Exacerbation [description not available] | 0 | 2.02 | 1 | 0 |
| Bladder Cancer [description not available] | 0 | 2.02 | 1 | 0 |
| Aplasia Pure Red Cell [description not available] | 0 | 2.02 | 1 | 0 |
| Cancer, Second Primary [description not available] | 0 | 5 | 3 | 1 |
| Urinary Bladder Neoplasms Tumors or cancer of the URINARY BLADDER. | 0 | 2.02 | 1 | 0 |
| Red-Cell Aplasia, Pure Suppression of erythropoiesis with little or no abnormality of leukocyte or platelet production. | 0 | 2.02 | 1 | 0 |
| Acquired Autoimmune Hemolytic Anemia [description not available] | 0 | 2.42 | 2 | 0 |
| Anemia, Hemolytic, Autoimmune Acquired hemolytic anemia due to the presence of AUTOANTIBODIES which agglutinate or lyse the patient's own RED BLOOD CELLS. | 0 | 2.42 | 2 | 0 |
| Prolymphocytic Leukemia [description not available] | 0 | 2.9 | 1 | 0 |
| Leukemia, Lymphocytic, Chronic, T Cell [description not available] | 0 | 2.9 | 1 | 0 |
| Anemia A reduction in the number of circulating ERYTHROCYTES or in the quantity of HEMOGLOBIN. | 0 | 2.9 | 1 | 0 |
| Leukemia, Prolymphocytic, T-Cell A lymphoid leukemia characterized by a profound LYMPHOCYTOSIS with or without LYMPHADENOPATHY, hepatosplenomegaly, frequently rapid progression, and short survival. It was formerly called T-cell chronic lymphocytic leukemia. | 0 | 2.9 | 1 | 0 |
| Leukemia, Prolymphocytic A chronic leukemia characterized by a large number of circulating prolymphocytes. It can arise spontaneously or as a consequence of transformation of CHRONIC LYMPHOCYTIC LEUKEMIA. | 0 | 2.9 | 1 | 0 |
| Acute Lymphoid Leukemia [description not available] | 0 | 1.99 | 1 | 0 |
| Kahler Disease [description not available] | 0 | 1.99 | 1 | 0 |
| Multiple Myeloma A malignancy of mature PLASMA CELLS engaging in monoclonal immunoglobulin production. It is characterized by hyperglobulinemia, excess Bence-Jones proteins (free monoclonal IMMUNOGLOBULIN LIGHT CHAINS) in the urine, skeletal destruction, bone pain, and fractures. Other features include ANEMIA; HYPERCALCEMIA; and RENAL INSUFFICIENCY. | 0 | 1.99 | 1 | 0 |
| Sensitivity and Specificity Binary classification measures to assess test results. Sensitivity or recall rate is the proportion of true positives. Specificity is the probability of correctly determining the absence of a condition. (From Last, Dictionary of Epidemiology, 2d ed) | 0 | 1.99 | 1 | 0 |
| Precursor Cell Lymphoblastic Leukemia-Lymphoma A neoplasm characterized by abnormalities of the lymphoid cell precursors leading to excessive lymphoblasts in the marrow and other organs. It is the most common cancer in children and accounts for the vast majority of all childhood leukemias. | 0 | 1.99 | 1 | 0 |
| Cryoglobulinemia A condition characterized by the presence of abnormal quantities of CRYOGLOBULINS in the blood. Upon cold exposure, these abnormal proteins precipitate into the microvasculature leading to restricted blood flow in the exposed areas. | 0 | 1.99 | 1 | 0 |
| Enlarged Spleen [description not available] | 0 | 3.38 | 1 | 1 |
| Eosinophilia, Tropical [description not available] | 0 | 1.99 | 1 | 0 |
| Eosinophilia Abnormal increase of EOSINOPHILS in the blood, tissues or organs. | 0 | 1.99 | 1 | 0 |
| Dysmyelopoietic Syndromes [description not available] | 0 | 1.99 | 1 | 0 |
| Myelodysplastic Syndromes Clonal hematopoietic stem cell disorders characterized by dysplasia in one or more hematopoietic cell lineages. They predominantly affect patients over 60, are considered preleukemic conditions, and have high probability of transformation into ACUTE MYELOID LEUKEMIA. | 0 | 1.99 | 1 | 0 |
| Minimal Disease, Residual [description not available] | 0 | 2 | 1 | 0 |
| Peliosis Hepatis A vascular disease of the LIVER characterized by the occurrence of multiple blood-filled CYSTS or cavities. The cysts are lined with ENDOTHELIAL CELLS; the cavities lined with hepatic parenchymal cells (HEPATOCYTES). Peliosis hepatis has been associated with use of anabolic steroids (ANABOLIC AGENTS) and certain drugs. | 0 | 7 | 1 | 0 |
| Granulocytic Leukemia [description not available] | 0 | 2.92 | 1 | 0 |
| Acute Disease Disease having a short and relatively severe course. | 0 | 2.92 | 1 | 0 |
| Leukemia, Myeloid Form of leukemia characterized by an uncontrolled proliferation of the myeloid lineage and their precursors (MYELOID PROGENITOR CELLS) in the bone marrow and other sites. | 0 | 2.92 | 1 | 0 |
| Neutropenia A decrease in the number of NEUTROPHILS found in the blood. | 0 | 3.39 | 1 | 1 |
| HIV Human immunodeficiency virus. A non-taxonomic and historical term referring to any of two species, specifically HIV-1 and/or HIV-2. Prior to 1986, this was called human T-lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV). From 1986-1990, it was an official species called HIV. Since 1991, HIV was no longer considered an official species name; the two species were designated HIV-1 and HIV-2. | 0 | 1.97 | 1 | 0 |