Disease relevance of Neoplasm, Residual

• CONCLUSION: Levels of post-treatment plasma EBV DNA in patients with NPC appear to strongly predict progression-free and overall survival and to accurately reflect the post-treatment residual tumor load [1].
• Furthermore, the determined patient-specific fusion sequences are useful for minimal residual disease monitoring of MLL associated acute leukemias [2].
• Use of polymerase chain reactions to monitor minimal residual disease in acute lymphoblastic leukemia patients [3].
• Detection of minimal residual disease by polymerase chain reaction in Philadelphia chromosome-positive chronic myelogenous leukemia following interferon therapy [4].
• Detection of minimal residual disease by immunostaining of bone marrow biopsies after 2-chlorodeoxyadenosine for hairy cell leukemia [5].

Psychiatry related information on Neoplasm, Residual

• Clinical decision making in chronic myeloid leukemia based on polymerase chain reaction analysis of minimal residual disease [6].

High impact information on Neoplasm, Residual

• These results suggest that rIL-2-activated NK cells may be used to purge peripheral blood HP cell preparations of residual tumor cells before hematopoietic reconstitution [7].
• Elevated levels of the 100K MAA were associated with evidence of residual tumor (P less than .008): Only 3 of 13 patients with no evidence of tumor had abnormal values, whereas 9 of 16 patients with evident tumor had increased serum levels [8].
• In addition, weekly injections of 25 micrograms MCA-F TSTA decreased the tumor recurrence rate and increased the survival times of hosts with recurrent neoplastic disease by virtue of residual tumor cells following resection of 2-cm masses [9].
• The amount of glucan injected and the quantity of residual tumor appeared to be related [10].
• To date, studies of VEGF antagonists have primarily focused on halting progression in models of minimal residual cancer [11].

Chemical compound and disease context of Neoplasm, Residual

• Reverse transcription polymerase chain reaction for the rearranged retinoic acid receptor alpha clarifies diagnosis and detects minimal residual disease in acute promyelocytic leukemia [12].
• The absence of detectable minimal residual disease by bone marrow biopsy, dual-color flow cytometry, and lg gene rearrangement analysis is achieveable in CLL with fludarabine and is predictive of the response duration [13].
• In B-cell non-Hodgkin's lymphoma (NHL), as in other B-cell malignancies, clonal rearrangement of the third complementarity determining region (CDR III) of the immunoglobulin heavy chain gene (IgH) provides a useful marker for the detection of minimal residual disease (MRD) after treatment [14].
• The fifth patient has residual tumor after cisplatin, etoposide, and bleomycin treatment requiring further therapy [15].
• The present investigations using a murine mammary tumor were carried out to determine how a variation in the time interval between primary tumor removal and administration of a single dose of cyclophosphamide (CY) affected labeling indices of residual tumor cells, their growth, and animal survival [16].

Biological context of Neoplasm, Residual

• Thermostable DNA polymerase chain amplification of t(14;18) chromosome breakpoints and detection of minimal residual disease [17].
• Exposure to neutralizing antibodies against IL-4 and IL-10 resulted in down-modulation of Bcl-2 and Bcl-xL, death of a considerable percentage of thyroid cancer cells, and sensitization of the residual tumor population to cytotoxic drug-induced apoptosis [18].
• Real-time analysis of tyrosine hydroxylase gene expression: a sensitive and semiquantitative marker for minimal residual disease detection of neuroblastoma [19].
• Negative immunoreactivity of 14-3-3 sigma was significantly correlated with high age and serous histology, high-grade, advanced-stage residual tumor of >2 cm, high serum CA125, high Ki-67 labeling index, and positive p53 immunoreactivity [20].
• The actual level of minimal residual disease in complete cytogenetic responders to IFN correlates with the probability of relapse [21].

Anatomical context of Neoplasm, Residual

• Trifunctional bispecific antibodies (TbsAbs) capable of cross-linking T lymphocytes, natural killer, and other FcgammaR-positive effector cells, via their Fc region, to the tumor cells may be applied together with adoptive allogeneic-cell therapy to maximize antitumor responses while acting on GVHD in patients with minimal residual disease [22].
• The presence of typical and atypical BCR-ABL fusion genes in leukocytes of normal individuals: biologic significance and implications for the assessment of minimal residual disease [23].
• Axillary lymph node examination revealed residual tumor in 33% of patients who received 8 x CVAP and 38% of patients who received further DOC [24].
• High stem cell frequency in acute myeloid leukemia at diagnosis predicts high minimal residual disease and poor survival [25].
• Our objective was to evaluate the effect of a diagnostic tracer dose of 131I on the uptake of the therapeutic dose of 1311 in the ablation of a thyroid remnant or residual tumor in patients with differentiated thyroid cancer [26].

Gene context of Neoplasm, Residual

• These results indicate that qrtPCR monitoring of PML-RAR alpha NQ can identify patients at high risk of relapse and suggest that clinically practical PB NQ monitoring at more frequent FUP intervals may improve predictive accuracy for relapse or continuing CR in patients with persistent, fluctuating minimal residual disease levels [27].
• Interleukin-2 (IL-2) therapy may improve immune reconstitution and reduce the risk of leukemic relapse in the setting of minimal residual disease by augmenting cytotoxic effector mechanisms directed at residual malignant cells [28].
• These results indicate that FLT3 mutations are secondary events in leukemogenesis, are unstable, and thus should be used cautiously for the detection of minimal residual disease [29].
• Thus, the NPM1 mutation is a frequent abnormality in AML patients without known genetic marker; the mutation may represent a new target to monitor minimal residual disease in AML and a potential candidate for alternative and targeted treatments [30].
• Finally, our data show that HOX11L2 expression was a suitable marker for minimal residual disease follow-up and was significantly associated with relapse (P =.02) [31].

Analytical, diagnostic and therapeutic context of Neoplasm, Residual

• Because the PCR detection of the AML1/MTG8(ETO) fusion at the RNA level is highly sensitive, it can be used as a sensitive method for diagnosis and detection of minimal residual disease in t(8;21) leukemia [32].
• Detection of Philadelphia chromosome-positive acute lymphoblastic leukemia by polymerase chain reaction: possible eradication of minimal residual disease by marrow transplantation [33].
• Similarly, when 10(4) BCL1 cells were given 1 day after syngeneic BMT to simulate minimal residual disease after syngeneic BMT, rIL-2 therapy administered at 14 days post-BMT seemed effective in prolonging disease-free survival in contrast to the same regimen given at 1 day after BMT [34].
• We used a nested PCR assay, which reproducibly detected a 10(4)- to 10(5)-fold dilution of t(1;19)+ into t(1;19)- cells, to evaluate minimal residual disease (MRD) in 48 children with t(1;19)+ ALL enrolled in POG clinical trials for lower (POG 9005) and higher (POG 9006) risk ALL [35].
• Competitive CBFbeta/MYH11 reverse-transcriptase polymerase chain reaction for quantitative assessment of minimal residual disease during postremission therapy in acute myeloid leukemia with inversion(16): a pilot study [36].

References