scholarly journals NUTRITIONALLY VARIANT STREPTOCOCCI BACTEREMIA IN CANCER PATIENTS: A RETROSPECTIVE STUDY, 1999-2014

2015 ◽  
Vol 7 ◽  
pp. e2015030 ◽  
Author(s):  
Abraham Tareq Yacoub ◽  
Jayasree Krishnan ◽  
Ileana M. Acevedo ◽  
Joseph Halliday ◽  
John Norman Greene
Keyword(s):  
Cancer Patients ◽  
Clinical Characteristics ◽  
Blood Stream Infection ◽  
Hematologic Malignancies ◽  
Blood Stream ◽  
Lymphocytic Leukemia ◽  
Myelogenous Leukemia ◽  
Cancer Center ◽  
Underlying Malignancy ◽  
Acute Myelogenous

BackgoundNutritionally variant Streptococci (NVS), Abiotrophia and Granulicatella are implicated in causing endocarditis and blood stream infections more frequently than other sites of infection. Neutropenia and mucositis are the most common predisposing factors for infection with other pathogens in cancer patients. In this study we investigated the clinical characteristics of NVS bacteremia in cancer patients and identified risk factors and outcomes associated with these infections. Materials and MethodsWe retrospectively reviewed all cases of NVS bacteremia occurring from June 1999 to April 2014 at H. Lee Moffitt Cancer Center and Research Institute. The computerized epidemiology report provided by the microbiology laboratory identified thirteen cancer patients with NVS bacteremia. We collected data regarding baseline demographics and clinical characteristics such as age, sex, underlying malignancy, neutropenic status, duration of neutropenia, treatment, and outcome.ResultsThirteen patients were identified with positive NVS blood stream infection. Ten patients (77%) had hematologic malignancies, including chronic lymphocytic leukemia (CLL) (1), multiple myeloma (MM) (1), acute myelogenous leukemia (AML) (4), and non Hodgkin’s lymphoma (NHL) (4).  The non-hematologic malignancies included esophageal cancer (2) and bladder cancer (1).ConclusionNVS should be considered as a possible agent of bacteremia in cancer patients with neutropenia and a breach in oral, gastrointestinal and genitourinary mucosa (gingivitis/mucositis).

Elevated serum ras level predicts decreased survival in patients with hematologic malignancies

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 6562-6562 ◽  
Author(s):  
E. M. Nelli ◽  
K. Leitzel ◽  
S. M. Ali ◽  
H. A. Al-Mondhiry ◽  
L. Demers ◽  
...  
Keyword(s):  
Overall Survival ◽  
Patient Group ◽  
Acute Myelogenous Leukemia ◽  
Elevated Serum ◽  
Hematologic Malignancies ◽  
Lymphocytic Leukemia ◽  
Myelogenous Leukemia ◽  
Ras Signaling ◽  
Potential Biomarker ◽  
Acute Myelogenous

6562 Background: Ras is a GDP/GTP binding G protein that acts as a molecular switch converting signals from the cell membrane to the nucleus to regulate cell proliferation, differentiation, and protein synthesis. Activation of ras oncogenes has been identified in a variety of cancers, including 30% of acute myelogenous leukemia patients. The purpose of our study was to evaluate serum ras levels and correlate with survival in hematologic cancer patients. Methods: A novel ras p21 ELISA (Oncogene Science/Bayer Diagnostics, Cambridge, MA) employing two monoclonal antibodies reactive with H, K, and N ras was utilized to quantify total ras levels in serum obtained from patients with various hematologic malignancies including acute myelogenous leukemia (AML), acute lymphocytic leukemia (ALL), chronic myelogenous leukemia (CML), and chronic lymphocytic leukemia (CLL). Results: The total leukemia patient group consisted of 52 patients. At the 75th percentile serum ras cutpoint (524 pg/ml) 11/52 patients were defined as elevated for serum ras. From this patient group, 38 patients had clinical followup available and were included in the Kaplan-Meier analysis of overall survival. Patients with elevated serum ras (>524 pg/ml) had significantly shorter overall survival compared to those without (median OS 205 vs. 677 days) (p= 0.04). In a multivariate analysis including serum ras level and type of leukemia, serum ras level remained a significant independent variable for shorter overall survival (p=0.004). Within leukemia subtypes 2/18 AML, 4/9 CML, 3/7 ALL, and 0/4 CLL patients had elevated serum ras levels. Conclusions: Leukemia patients with elevated serum ras levels had a significantly shorter overall survival. Serum ras should be evaluated as a potential biomarker in larger leukemia trials, especially for response to treatment with inhibitors of the ras signaling pathway. [Table: see text]

Compound GW506U78 in refractory hematologic malignancies: relationship between cellular pharmacokinetics and clinical response.

1998 ◽  
Vol 16 (11) ◽  
pp. 3607-3615 ◽  
Author(s):  
V Gandhi ◽  
W Plunkett ◽  
C O Rodriguez ◽  
B J Nowak ◽  
M Du ◽  
...  
Keyword(s):  
T Cell ◽  
Mononuclear Cells ◽  
Peak Plasma ◽  
Lymphoblastic Leukemia ◽  
Plasma Concentrations ◽  
Hematologic Malignancies ◽  
Lymphocytic Leukemia ◽  
Myelogenous Leukemia ◽  
Cancer Center ◽  
Pharmacokinetic Studies

PURPOSE In vitro investigations with arabinosylguanine (ara-G) demonstrated potent cytotoxicity to T-lymphoblastoid cell lines. The goals of the present study were to evaluate GW506U78, a prodrug of ara-G, against human hematologic malignancies and to determine its pharmacokinetics in plasma and cells. PATIENTS AND METHODS During a phase I multicenter trial of GW506U78, 26 patients were treated at M.D. Anderson Cancer Center (MDACC). Daily doses between 20 and 60 mg/kg were administered for 5 days. Parallel plasma and cellular pharmacokinetic studies were conducted. RESULTS Complete (n=5) or partial remission (n=5) was achieved in T-cell acute lymphoblastic leukemia (T-ALL), T-lymphoid blast crisis, T-lymphoma, and B-cell chronic lymphocytic leukemia (B-CLL) (n=13). In contrast, patients with B-ALL, B-lymphoma, acute myelogenous leukemia (AMI), or T-CLL did not respond. Peak plasma concentrations of GW506U78 and ara-G were dose-dependent. The elimination of GW506U78 (half-life [t1/2]=17 minutes) was faster than the elimination of ara-G (t1/2=3.7 hours). Median peak concentrations of ara-GTP were 23, 42, 85, and 93 micromol/L at 20, 30, 40, and 60 mg/kg, respectively. T-lymphoblasts accumulated significantly (P=.0008) higher peak arabinsylguanosine triphosphate (ara-GTP) (median, 140 micromol/L; n=7) compared with other diagnoses (median, 50 micromol/L; n=9) and normal mononuclear cells (n=3). The ara-GTP elimination was slow in all diagnoses (median, > 24 hours). Responders accumulated significantly (P=.0005) higher levels of ara-GTP (median, 157 micromol/L) compared with patients who failed to respond (median, 44 micromol/L). CONCLUSION GW506U78 is an effective prodrug and a potent agent for hematologic malignancies with major efficacy in T-cell diseases. The pharmacokinetics of ara-GTP in leukemia cells are strongly correlated with clinical responses to GW506U78.

Nosocomial Infection Rates at an Oncology Center

1988 ◽  
Vol 9 (1) ◽  
pp. 13-19 ◽  
Author(s):  
Coleman Rotstein ◽  
K. Michael Cummings ◽  
Andreas L. Nicolaou ◽  
Joyce Lucey ◽  
John Fitzpatrick
Keyword(s):  
Nosocomial Infection ◽  
Nosocomial Infections ◽  
Blood Stream ◽  
Myelogenous Leukemia ◽  
Infection Rates ◽  
Coagulase Negative Staphylococci ◽  
Underlying Malignancy ◽  
Acute Myelogenous ◽  
Tract Infections ◽  
Oncology Center

AbstractNosocomial infection rates were computed for 5,031 patients at an oncology center during a 20-month period. Twelve percent of the patients developed nosocomial infections, accounting for a total of 802 infections. The overall incidence of nosocomial infections during this study period was 6.27 infections per 1,000 patient days. The highest incidence of nosocomial infections was found in patients having acute myelogenous leukemia (30.49 infections per 1,000 patient days); bone and joint cancer (27.27 infections per 1,000 patient days); and liver cancer (26.58 infections per 1,000 patient days). The respiratory tract was the most common site of infection, followed by blood-stream, surgical wound, and urinary tract infections. Staphylococcus aureus, Escherichia coli, Pseudomonas aeruginosa, Klebsiella pneumoniae, and coagulase-negative staphylococci were most frequently implicated as pathogens. The distribution of specific types of infection according to underlying malignancy was also tabulated. These data provide nosocomial infection rates, common pathogens, and sites of infection for cancer patients, thus assisting in directing appropriate therapy for these patients.

scholarly journals Elevated Expression of the Apoptotic Regulator Mcl-1 at the Time of Leukemic Relapse

Blood ◽  
1998 ◽  
Vol 91 (3) ◽  
pp. 991-1000 ◽  
Author(s):  
Scott H. Kaufmann ◽  
Judith E. Karp ◽  
Phyllis A. Svingen ◽  
Stan Krajewski ◽  
Philip J. Burke ◽  
...  
Keyword(s):  
Initial Therapy ◽  
Chemotherapeutic Agents ◽  
Lymphocytic Leukemia ◽  
Myelogenous Leukemia ◽  
Paired Samples ◽  
Elevated Expression ◽  
Leukemic Relapse ◽  
Acute Myelogenous ◽  
Weak Negative Correlation ◽  
Apoptosis Inhibitor

Abstract Bcl-2, Bcl-xL, and Mcl-1 are three related intracellular polypeptides that have been implicated as negative regulators of apoptosis. In contrast, the partner protein Bax acts as a positive regulator of apoptosis. Based on the observation that all four of these polypeptides are expressed in a variety of acute myelogenous leukemia (AML) and acute lymphocytic leukemia (ALL) cell lines, cellular levels of these polypeptides were examined by immunoblotting in bone marrow samples harvested from 123 adult AML patients and 36 adult ALL patients before initial antileukemic therapy. Levels of Bcl-2, Mcl-1, Bcl-xL, and Bax each varied over a more than 10-fold range in different pretreatment leukemia specimens. When the 54 AML and 23 ALL samples that contained greater than 80% malignant cells were examined in greater detail, it was observed that pretreatment levels of Bcl-2 and Mcl-1 correlated with each other (R = .44,P < .001 for AML and R = .79,P < .0001 for ALL). In addition, a weak negative correlation between Bax expression and age was observed in AML samples (R = −0.35, P < .02) but not ALL samples. There was no relationship between pretreatment levels of these polypeptides and response to initial therapy. However, examination of 19 paired samples (the first harvested before chemotherapy and the second harvested 23 to 290 days later at the time of leukemic recurrence) revealed a greater than or equal to twofold increase in Mcl-1 levels in 10 of 19 pairs (7 of 15 AML and 3 of 4 ALL) at recurrence. In contrast, 2 of 19 pairs contained twofold less Mcl-1 at the time of recurrence. Approximately equal numbers of samples showed twofold increases and decreases in Bcl-2 (5 increases, 3 decreases) and Bcl-xL (1 increase, 4 decreases) at recurrence. Bax levels did not show a twofold decrease in any patient. These results, coupled with recent observations that cells overexpressing Mcl-1 are resistant to a variety of chemotherapeutic agents, raise the possibility that some chemotherapeutic regimens might select for leukemia cells with elevated levels of this particular apoptosis inhibitor.

scholarly journals Blood stream infection in cancer patients—device management and epidemiology: the BSIDE study

2017 ◽  
Vol 28 ◽  
pp. vi96-vi97
Author(s):  
F. Cortiula ◽  
D. Basile ◽  
L. Gerratana ◽  
M. Bonotto ◽  
E. Ongaro ◽  
...  
Keyword(s):  
Cancer Patients ◽  
Blood Stream Infection ◽  
Blood Stream ◽  
Device Management

scholarly journals Active Mycobacterium tuberculosis infection at a comprehensive cancer center, 2006–2014

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Joumana Kmeid ◽  
Prathit A. Kulkarni ◽  
Marjorie V. Batista ◽  
Firas El Chaer ◽  
Amrita Prayag ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Cancer Patients ◽  
Hematopoietic Cell Transplantation ◽  
Average Rate ◽  
Hematologic Malignancies ◽  
Comprehensive Cancer Center ◽  
Cancer Center ◽  
Mycobacterium Tuberculosis Infection ◽  
Patients With Cancer ◽  
Disseminated Disease

Abstract Background Morbidity and mortality from Mycobacterium tuberculosis (Mtb) infection remain significant in cancer patients. We evaluated clinical characteristics, management, and outcomes in patients with active Mtb infection at our institution who had cancer or suspicion of cancer. Methods We retrospectively examined medical records of all patients with laboratory-confirmed active Mtb infection diagnosed between 2006 and 2014. Results A total of 52 patients with laboratory-confirmed active Mtb infection were identified during the study period, resulting in an average rate of 6 new cases per year. Thirty-two (62%) patients had underlying cancer, while 20 (38%) patients did not have cancer but were referred to the institution because of suspicion of underlying malignancy. Among patients with cancer, 18 (56%) had solid tumors; 8 (25%) had active hematologic malignancies; and 6 (19%) had undergone hematopoietic-cell transplantation (HCT). Patients with and without cancer were overall similar with the exception of median age (61 years in cancer patients compared to 53 years in noncancer patients). Pulmonary disease was identified in 32 (62%) patients, extrapulmonary disease in 10 (19%) patients, and disseminated disease in 10 (19%) patients. Chemotherapy was delayed in 53% of patients who were to receive such treatment. Eleven patients (all of whom had cancer) died; 3 of these deaths were attributable to Mtb infection. Conclusions Although not common, tuberculosis remains an important infection in patients with cancer. Approximately one-third of patients were referred to our institution for suspicion of cancer but were ultimately diagnosed with active Mtb infection rather than malignancy.

scholarly journals Immunolocalization of the Bcl-2 protein within hematopoietic neoplasms

Blood ◽  
1991 ◽  
Vol 78 (4) ◽  
pp. 1062-1068 ◽  
Author(s):  
M Zutter ◽  
D Hockenbery ◽  
GA Silverman ◽  
SJ Korsmeyer
Keyword(s):  
Cell Survival ◽  
Large Cell ◽  
Hematologic Malignancies ◽  
Lymphocytic Leukemia ◽  
Myelogenous Leukemia ◽  
Protein Levels ◽  
Stage Of Development ◽  
T Cell Lymphomas ◽  
A Cell ◽  
Reactive Hyperplasia

Abstract The Bcl-2 proto-oncogene was discovered at the t(14;18) breakpoint found in most follicular B-cell lymphomas and some diffuse large-cell lymphomas. Bcl-2 is unique among proto-oncogenes, being localized to mitochondria and extending cell survival by blocking programmed cell death. We examined Bcl-2 protein expression in 82 hematologic malignancies and reactive lymphoid processes. All lymphomas with Bcl-2 rearrangement demonstrated high levels of Bcl-2 protein. However, most follicular and diffuse lymphomas without Bcl-2 rearrangement also displayed intense Bcl-2 staining. In these cases, mechanisms other than classic translocation may be deregulation Bcl-2. The pattern of Bcl-2 staining in follicular lymphoma is the inverse of the pattern in reactive hyperplasia, confirming a role for Bcl-2 immunolocalization in routine diagnosis. Small lymphocytic malignancies, including small lymphocytic lymphoma, mantle zone lymphoma, and chronic lymphocytic leukemia, expressed intermediate levels of Bcl-2. Bcl-2 protein varied in plasma cell dyscrasias. Bcl-2 protein levels in T-cell lymphomas reflected their corresponding stage of development. No substantial Bcl- 2 was present in the Reed-Sternberg cells of nodular sclerosing Hodgkin's disease. Chronic myelogenous leukemia was strongly positive for Bcl-2, consistent with the presence of Bcl-2 in normal myeloid progenitors. Immunohistochemistry identified an expanded spectrum of hematopoietic neoplasms in which Bcl-2 may provide a cell survival advantage.

Hypermethylation of E-cadherin in leukemia

Blood ◽  
2000 ◽  
Vol 95 (10) ◽  
pp. 3208-3213 ◽  
Author(s):  
John R. Melki ◽  
Paul C. Vincent ◽  
Ross D. Brown ◽  
Susan J. Clark
Keyword(s):  
Messenger Rna ◽  
Cpg Island ◽  
Surface Protein ◽  
Hematologic Malignancies ◽  
Lymphocytic Leukemia ◽  
Myelogenous Leukemia ◽  
Metastasis Suppressor ◽  
Normal Donor ◽  
Sodium Bisulphite ◽  
E Cadherin

Abstract E-cadherin gene is often termed a “metastasis suppressor” gene because the E-cadherin protein can suppress tumor cell invasion and metastasis. Inactivation of the E-cadherin gene occurs in undifferentiated solid tumors by both genetic and epigenetic mechanisms; however, the role of E-cadherin in hematologic malignancies is only now being recognized. E-cadherin expression is essential for erythroblast and normoblast maturation, yet expression is reduced or absent in leukemic blast cells. This study examined the messenger RNA (mRNA) and protein expression of the E-cadherin gene in bone marrow and blood samples from normal donors and patients with leukemia. We found that all normal donor samples expressed E-cadherin mRNA, whereas both samples of acute myelogenous leukemia and chronic lymphocytic leukemia had a significant reduction or absence of expression. However, normal blast counterparts expressed only a low level of E-cadherin surface protein. Sodium bisulphite genomic sequencing was used to fully characterize the methylation patterns of the CpG island associated with the E-cadherin gene promoter in those samples with matched DNA. All of the normal control samples were essentially unmethylated; however, 14 of 18 (78%) of the leukemia samples had abnormal hypermethylation of the E-cadherin CpG island. In fact both alleles of the E-cadherin gene were often hypermethylated. We conclude the E-cadherin gene is a common target for hypermethylation in hematologic malignancies.

Incidence of second and secondary malignancies in patients with CLL: A single institution experience.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 6568-6568 ◽  
Author(s):  
Samir Dalia ◽  
Julio C. Chavez ◽  
Gelenis Domingo ◽  
Estrella M. Carballido ◽  
Paibel I. Aguayo-Hiraldo ◽  
...  
Keyword(s):  
Solid Tumor ◽  
Light Exposure ◽  
Lymphocytic Leukemia ◽  
Myelogenous Leukemia ◽  
Cancer Center ◽  
Secondary Malignancy ◽  
Cancer Type ◽  
Second Malignancy ◽  
Second Malignancies ◽  
Increased Risk

6568 Background: Patients with chronic lymphocytic leukemia (CLL) have a higher incidence of second malignancies than the general population with one study showing the risk at 2.2 times the general popualtion. The increased incidence is thought to be due to immunosupression which results in decreased cell surveillance and proliferation of malignant cells. Our study aims to present the rate of second malignancies by cancer type in patients with CLL at our institution. Methods: The Moffitt Cancer Center Total Cancer Care (TCC) database was used to identify patients who had a diagnosis of CLL between January 1993-December 2009. Individual charts were reviewed to confirm the diagnosis of CLL, collect demographic data, and to assess for the presence of a second malignancy under an IRB approved protocol. A second malignancy was defined as another malignancy or transformation of CLL reported in the medical record. Second malignancy data was placed in three categories; skin cancers, solid tumor malignancy, and hematologic malignancy. Results: 546 CLL patients were included in the study. Median age was 62.5 years. 84 (43%) were Stage 0 and 62 (32%) were Stage 1 RAI at diagnosis indicating earlier disease. 266 (49%) patients had a second or secondary malignancy. A total of 304 cancers were identified. 14% of patients had more than one malignancy. Melanoma was identified in 44 (16.5%) patients and non-melanoma skin cancer was identified in 54 (20%). Lung cancer was identified as the most frequent solid tumor malignancy with 36 (13.5%) cases, followed by prostate (35), breast (21), colorectal (15), and bladder (14). 10 patients had a Richter’s transformation of their CLL. 26 patients developed either myelodysplastic syndrome or acute myelogenous leukemia. Conclusions: Second malignancies are frequent in CLL patients. Immunosupression, increased UV light exposure, longer life expectancy in low risk CLL, and tertiary cancer center referral bias are likely reasons for these increased rates. Further research is needed to identify the precise mechanism which cause patients with CLL to have higher rates of second malignancies and to identify if there is an increased risk of a specific type of malignancy in patients with CLL.

Sign in / Sign up

Export Citation Format

Share Document