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Abramson Cancer Center
NCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of ALL - October 2002
National Cancer Institute®
Last Modified: October 1, 2002
- Serum immunoglobulins to endotoxin core glycolipid: acute leukaemia and other cancers.
- Causes of mortality in children with acute lymphocytic leukemia.
- Increased incidence of spontaneous apoptosis in the bone marrow of hyperdiploid childhood acute lymphoblastic leukemia.
- Genetic instability of adult T-cell leukemia/lymphoma by comparative genomic hybridization analysis.
- Bone marrow biopsy in adult acute lymphoblastic leukemia: morphological characteristics and contribution to the study of prognostic factors.
- Repression of IRF-4 target genes in human T cell leukemia virus-1 infection.
- [Invasive aspergillosis in the leukemic patient]
- [Detection of BCR-ABL gene sequences using RT-PCR in patients with leukemia in the IX region. Chile]
- MIC2, TdT, bcl-2, and CD34 expression in paraffin-embedded high-grade lymphoma/acute lymphoblastic leukemia distinguishes between distinct
- Racial and ethnic differences in survival of children with acute lymphoblastic leukemia.
- Involvement of the MLL gene in T-lineage acute lymphoblastic leukemia.
- Deletion of the Ink4-locus (the p16ink4a, p14ARF and p15ink4b genes) predicts relapse in children with ALL treated according to the Nordic
- Partial deletions of long arm of chromosome 6: biologic and clinical implications in adult acute lymphoblastic leukemia.
- Quantitative assessment of WT1 expression by real time quantitative PCR may be a useful tool for monitoring minimal residual disease in acute
- [Study on abnormal expression of the p73 gene in childhood acute lymphoblastic leukemia]
- [The relationship between expression of lung resistance-related protein gene or multidrug resistance-associated protein gene and prognosis in
- The genetics of childhood acute lymphoblastic leukaemia.
- Study on P16 gene in acute leukemia.
- The proliferation of human T lymphoblastic cells induced by 5-HT1B receptors activation is regulated by 5-HT-moduline.
- Parental medication use and risk of childhood acute lymphoblastic leukemia.
- [Adult T-cell leukemia/lymphoma. Clinical aspects]
- Alterations of the putative tumor suppressor gene p16/MTS1 in human hematological malignancies.
Table of Contents
1
UI - 2386384
AU - Jackson SK; Parton J; Shortland G; Stark JM; Thompson EN
TI -
Serum immunoglobulins to endotoxin core glycolipid: acute leukaemia and
other cancers.
SO - Arch Dis Child 1990 Jul;65(7):771-3
AD - University of Wales College of Medicine, Heath Park, Cardiff.
Circulating antibody to endotoxin core glycolipid and total serum
immunoglobulin concentrations were measured in 86 children with cancer
(54 with acute lymphoblastic leukaemia, four with acute myeloid
leukaemia, and 28 with various solid tumours). Measurements were made
before treatment in the group with acute lymphoblastic leukaemia as well
as when patients were both on and off chemotherapy. In the other two
groups measurements were made when patients were both on and off
treatment. Significant reductions in endotoxin antibody and serum
immunoglobulin concentrations were found only in patients with acute
lymphoblastic leukaemia. In addition, there was a significant
correlation between febrile episodes and the concentration of antibody
to core glycolipid in the children with acute lymphoblastic leukaemia.
These findings suggest that the use of prophylactic high titre endotoxin
antibody may be of benefit to children with life threatening Gram
negative infections who are receiving cytotoxic chemotherapy.
2
UI - 1500128
AU - Choudhry VP; Krishnamurthy L; Arya LS; Desai N; Pati H
TI -
Causes of mortality in children with acute lymphocytic leukemia.
SO - Indian Pediatr 1992 Jun;29(6):709-13
AD - Department of Hematology, All India Institute of Medical Sciences, New
Delhi.
Fifty five deaths between January, 1982 to September, 1989 in children
with acute lymphoblastic leukemia (ALL) were evaluated to determine the
cause of mortality. Fifty cases died during remission. Infection alone
was responsible for death in 26 of 55 (47.3%) cases while hemorrhage was
seen in 7 (12.7%) children. Infection and hemorrhage together were
responsible in another 13 cases. Gastrointestinal tract and pulmonary
system were the major sites of bleeding. Infections either alone or in
combination with other factors were responsible for death in 42 of 55
(76.5%) of children. Septicemia (n = 11), gastrointestinal (n = 15) and
pulmonary infections (n = 10) and meningitis in 2 cases were the major
sites of infections. Pseudomonas and Klebsiella in 6 cases each
accounted for 54.5% of isolates.
3
UI - 11937268
AU - Zhang Y; Lu J; van den Berghe J; Lee SH
TI -
Increased incidence of spontaneous apoptosis in the bone marrow of
hyperdiploid childhood acute lymphoblastic leukemia.
SO - Exp Hematol 2002 Apr;30(4):333-9
AD - Department of Pathology, National University Hospital, National
University of Singapore, Singapore 119074.
OBJECTIVE: Hyperdiploidy of 51-65 chromosomes is associated with a good
prognosis in childhood B-lineage acute lymphoblastic leukemia (ALL).
Blasts from childhood ALL patients with a hyperdiploid karyotype have a
tendency to apoptosis when cultured on stromal layers in vitro. In this
study, we apply a novel method to investigate the relationship between
apoptosis and hyperdiploidy in lymphoblasts of childhood ALL. MATERIALS
AND METHODS: The DNA content of individual ALL blasts in Feulgen-stained
archival bone marrow smears can be determined by static cytometry. TUNEL
(TdT-mediated dUTP-biotin nick end labeling) detects the DNA degradation
associated with apoptosis. We performed TUNEL in situ sequential to DNA
ploidy analysis in archival bone marrow smears from 12 patients with
childhood ALL. RESULTS: Five patients were diploid and seven were
hyperdiploid (51-65 chromosomes) by conventional cytogenetic analysis.
In the five diploid cases, the percentage of TUNEL-positive blasts
ranged from 1.0% to 1.3%; in the seven hyperdiploid cases, the
percentage of TUNEL-positive blasts ranged from 3.6% to 9.0%. Comparing
TUNEL and corresponding Feulgen images, we found that apoptotic blasts
were predominantly of high DNA ploidy in both diploid and hyperdiploid
cases. The mean DNA value of apoptotic blasts was larger than that of
the total blast population in each case. CONCLUSIONS: The results
demonstrate an increased incidence of spontaneous apoptosis in situ of
hyperdiploid blasts in ALL bone marrow and indicate that this phenomenon
is not restricted to in vitro cultures. The findings provide a possible
rationale for the good prognosis associated with hyperdiploid childhood
ALL.
4
UI - 11998893
AU - Tsukasaki K
TI -
Genetic instability of adult T-cell leukemia/lymphoma by comparative
genomic hybridization analysis.
SO - J Clin Immunol 2002 Mar;22(2):57-63
AD - Department of Hematology, Atomic Bomb Disease Institute, Nagasaki
University School of Medicine, Japan.
Adult T-cell leukemia/lymphoma (ATL) is a distinct clinicopathological
entity, i.e., peripheral T-lymphocytic malignancy caused by human
T-lymphotropic virus type I (HTLV-1) with diverse clinical features.
High frequency of genetic instability (GIN) in both aggressive and
indolent ATL was detected by comparative genomic hybridization (CGH).
Among GIN, chromosomal instability, i.e., ancuploidy, in indolent ATL
was as frequent but less complex and dynamic as compared to those in
aggressive ATL. Some of the CGH alterations, including gain of 14q32,
appear to be rather ATL specific. Clonal instability of HTLV-1-infected
T cells. i.e., emergence of distinct clone, was detected in about one
forth of acute crisis from indolent ATL by CGH and Southern blotting for
HTLV-1. Taking together with the previous reports of frequent subtle
mutations in several tumor suppressor genes in aggressive ATL, GIN in
multistep leukemogenesis of ATL is diverse including clonal,
chromosomal, and nucleotide levels.
5
UI - 12163052
AU - Thomas X; Le QH; Danaila C; Lheritier V; Ffrench M
TI -
Bone marrow biopsy in adult acute lymphoblastic leukemia: morphological
characteristics and contribution to the study of prognostic factors.
SO - Leuk Res 2002 Oct;26(10):909-18
AD - Service d'Hematologie Clinique, Hopital Edouard Herriot, Lyon, France.
xavier.thomas@chu-lyon.fr
Bone marrow (BM) sections were examined in 128 untreated adult patients
with newly diagnosed acute lymphoblastic leukemia (ALL), seen in our
institution over a 19-year period. BM biopsy was performed in order to
assess the incidence, degree and prognostic significance of histological
data of the disease. BM features studied were reticular fibrosis, total
cellularity, residual hematopoiesis, mitotic activity, and blastic
infiltration. T-cell lineage ALL were diagnosed in 23% of the cases,
while B-cell lineage ALL represented 70% of the cases. There were 7% of
non-T-non-B-cell lineage ALL. The percentage of BM leukemic cells was
related to cellularity (P=0.02), while it was related to the
disappearance of normal cell lines (P<0.0001). BM cellularity was
related to the percentage of circulating leukemic cells at diagnosis
(P=0.006). Residual hematopoiesis was related to a higher initial
granulocyte count (P=0.04) and lower percentage of circulating blasts
(P=0.04). The degree of fibrosis was inversely related to that of BM
cellularity (P=0.04). All patients, but four, received standard ALL
induction chemotherapy according to different successive protocols. In
this whole cohort of patients, complete remission (CR) rate was 78%.
Median disease-free survival (DFS) and median overall survival (OS) were
13.7 months and 20.2 months, respectively. In univariate analysis, CR
rate was positively affected by mitotic activity (P=0.01) and residual
hematopoiesis (P=0.008). OS was positively influenced by a higher
leukemic cell mitotic activity (P=0.03) and the persistence of more than
two residual normal cell lines in BM (P=0.04). Patients presenting with
both of those characteristics had better outcome than patients who did
not, as well as, in terms of CR (P=0.03), or DFS (P=0.002), or OS
(P=0.003). T-cell lineage ALL and L3 ALL did not significantly influence
those results. Our findings did not confirm that among marrow features,
reticular fibrosis has any prognostic value. A multivariate analysis of
both clinical and histological data was performed to test their
prognostic relevance. In a model including age, immunophenotype,
Philadelphia chromosome status, mitotic index, and level of normal
residual hematopoiesis, the only significant predictor of CR achievement
were the persistence of normal residual hematopoietic cell lines
(P=0.01) and the mitotic activity of leukemic cells (P=0.002).
Philadelphia chromosome status (P=0.03) and age (P<0.0001) were of
prognostic value, respectively for DFS and OS.We conclude that some
characteristics of BM biopsy afford not only descriptive but also
prognostic information for predicting the outcome. The persistence of
normal residual hematopoiesis and intense leukemic cells mitotic
activity were both factors of favorable outcome, while BM fibrosis did
not display any prognostic value.
6
UI - 12360402
AU - Mamane Y; Grandvaux N; Hernandez E; Sharma S; Innocente SA; Lee JM;
TI -
Azimi N; Lin R; Hiscott J
Repression of IRF-4 target genes in human T cell leukemia virus-1
infection.
SO - Oncogene 2002 Oct 3;21(44):6751-65
AD - Terry Fox Molecular Oncology Group, Lady Davis Institute for Medical
Research, and Department of Microbiology and Immunology, McGill
University, Montreal, Canada H3T 1E2.
The human T cell leukemia/lymphotropic virus-1 (HTLV-I) is the etiologic
agent of adult T cell leukemia (ATL), an aggressive and fatal leukemia
of CD4+ T lymphocytes. Interferon regulatory factor-4 (IRF-4) was shown
previously to be constitutively expressed in T cells infected with
HTLV-1. In this study, we investigated the role of IRF-4 gene regulation
in the context of HTLV-1 infection using gene array technology and IRF-4
expressing T cells. Many potential IRF-4 regulated genes were
identified, the vast majority of which were repressed by IRF-4
expression. Cyclin B1, a G2-M checkpoint protein identified as an IRF-4
repressed gene in the array, was further characterized in the context of
HTLV-1 infection. All HTLV-1 infected cell lines and ATL patient
lymphocytes demonstrated a dramatic decrease in cyclin B1 levels;
subsequent analysis of the cyclin B1 promoter identified two sites
important in IRF-4 binding and repression of cyclin B1 expression.
Furthermore, IRF-4-mediated repression of cyclin B1 led to a significant
decrease in CDC2 kinase activity in HTLV-1 infected T cells. IRF-4
expression in HTLV-1 infected T cells also downregulated other genes
implicated in the mitotic checkpoint as well as genes involved in actin
cytoskeletal rearrangement, DNA repair, apoptosis, metastasis and immune
recognition. Several of the identified genes are dysregulated in ATL and
may provide important mechanistic information concerning pathways
critical to the emergence of ATL.
7
UI - 11924181
AU - el Omri H; Mili-Fathallah A; Amara H; Ben Youssef Y; Garrouche A; Ben
TI -
Said M; Ennabli S
[Invasive aspergillosis in the leukemic patient]
SO - Rev Mal Respir 2001 Dec;18(6 Pt 1):607-14
AD - Service d'Hematologie Clinique, CHU Farhat Hached, 4000 Sousse, Tunisie.
Invasive pulmonary aspergillosis (IPA) remains a life threatening
complication in immuno-compromised and especially in neutropenic
patients. We report our experience in the diagnosis and therapeutic
management of IPA in 8 patients with acute leukemia. All patients were
neutropenic (PNN < 100/mm3, mean duration = 37 days) when IPA was
diagnosed. Clinical signs included fever above 39 degrees and cough in
all cases, chest pain in 4 cases, hemoptysis in 3 cases, rales in 5
cases. Chest x ray showed one lesion in 4 cases and multiple lesions in
4 cases. The diagnosis of IPA was established by bronchoalveolar lavage
(BAL) in 5 cases, tissue biopsy in one case, positive sputum in one case
and it was highly probable in one case. Thoracic computed tomographic
(CT) scans were preformed after diagnosis confirmation of IPA and showed
one or multiple lesions with air crescent signs. Serological tests were
positive in 4 cases late in the course of IPA. All patients were treated
with i.v. Amphotericin B. Outcome was favorable in 5 cases and three
patients died by massive hemoptysis (in two cases) and systemic
aspergillosis (in one case). Early diagnosis and appropriate treatment
are essential to improve IPA prognosis.
8
UI - 12194684
AU - Artigas CG; Melo A; Roa JC; Paez E; Vittini C; Arriagada M; Gonzalez L;
TI -
Pflaumer E; Roa I
[Detection of BCR-ABL gene sequences using RT-PCR in patients with
leukemia in the IX region. Chile]
SO - Rev Med Chil 2002 Jun;130(6):623-30
AD - Departamento Medicina Interna, Facultad de Medicina, Universidad de La
Frontera, Casilla 54-D, Temuco-Chile. cgartiga@ufro.cl
BACKGROUND: The BCR-ABL fusion gene is the molecular expression of the
Philadelphia chromosome. This cytogenetic aberration is the most
frequent alteration found in leukemias, which is produced by the
translocation t(9;22). Two different fusion proteins are produced
depending on the break point (210 kD and 190 kD). The detection of this
gene has both diagnostic and prognostic importance, associated with poor
prognosis in acute lymphoblastic leukemia (ALL). AIM: To detect BCR-ABL
gene sequences in patients with leukemia from the IX Region of Chile.
MATERIAL AND METHODS: We studied 58 patients: 5 chronic myeloid leukemia
(CML), 35 ALL, 15 acute myeloid leukemia (AML) and 3 biphenotypic
leukemia. The gene sequences were detected using reverse transcriptase
polymerase chain reaction (RT-PCR). RESULTS: BRC-ABL gene sequences were
positive in all patients with CML, 2 of 35 ALL (one child and one
adult). The remaining patients were negative. We found p210 and p190
co-expression in 2 CML and 1 ALL. CONCLUSIONS: Our results are in
agreement with other reports. The detection of these and other genetic
alterations will allow us to have invaluable diagnostic and prognostic
information from our patients with leukemia.
9
UI - 9343323
AU - Soslow RA; Bhargava V; Warnke RA
TI -
MIC2, TdT, bcl-2, and CD34 expression in paraffin-embedded high-grade
lymphoma/acute lymphoblastic leukemia distinguishes between distinct
clinicopathologic entities.
SO - Hum Pathol 1997 Oct;28(10):1158-65
AD - Department of Pathology, New York Hospital-Cornell Medical Center, New
York 10021, USA.
We propose that 12E7 (CD99) expression, along with TdT, bcl-2, and CD34
reactivity in lymphoblastic lymphoma (LyL)/acute lymphoblastic leukemia
(ALL), distinguishes this group of neoplasms from small noncleaved cell
lymphomas (SNCLs) in both pediatric and adult patients, thereby
narrowing the differential diagnosis of high-grade non-Hodgkin's
lymphomas and acute lymphoblastic leukemias in paraffin sections. 12E7
(CD99) is one of a group of available antibodies that recognizes the
product of the mic-2 gene, which was originally identified in ALL.
Despite this, most clinicopathological research has focused on the
reactivity of 12E7 in a subset of the small round cell tumors of
childhood. Although TdT is widely used in the subtyping of blastic
leukemias, its use in the distinction of high-grade lymphomas in
paraffin sections has been limited. We collected 24 cases of LyL/ALL (13
B-cell and 11 T-cell) and 15 cases of SNCL from 1984 through 1993. We
confirmed the diagnoses using morphology and analysis of immunologic
data. We performed immunohistochemistry with the 12E7 antibody, TdT,
bcl-2, and CD34 on formalin-fixed, paraffin-embedded material. The
patients' ages ranged from 4 to 81 years; nine of the study patients
were children. Sixteen of the 24 LyL/ALLs stained with 12E7. In
contrast, none of the 15 cases of SNCL reacted with this antibody
(chi-square P < .0001). A larger percentage of T-cell LyL/ALLs reacted
with 12E7 than did B-cell LyL/ALLs (82% v 54%). Sixteen of 20 LyL/ALLs
reacted with the anti-TdT antibody, as compared with none of 11 SNCLs
(chi-square P < .0001). Six LyL/ALLs were CD34 positive (of 23), and
none of the SNCLs were CD34 positive (0 of 12) (chi-square P = .0519).
Bcl-2-positive cases were found among both LyL/ ALLs and SNCLs, although
they were more prevalent among LyL/ ALLs (92% v 25%; chi-square P <
.0001). When one considers the differential diagnosis of a high-grade
lymphoma/acute lymphoblastic leukemia, positive reactions with 12E7,
TdT, bcl-2, and CD34 support the diagnosis of LyL/ALL over SNCL.
Moreover, we present data that suggests that evaluating for TdT in
formalin-fixed paraffin-embedded tissue is a more sensitive test than
using either 12E7, bcl-2 or CD34 alone.
10
UI - 12200352
AU - Bhatia S; Sather HN; Heerema NA; Trigg ME; Gaynon PS; Robison LL
TI -
Racial and ethnic differences in survival of children with acute
lymphoblastic leukemia.
SO - Blood 2002 Sep 15;100(6):1957-64
AD - Children's Oncology Group, City of Hope National Medical Center, PO Box
60012, Arcadia, CA 91006-6012, USA. sbhatia@coh.org
Black children with acute lymphoblastic leukemia (ALL) have poor
outcomes, but limited information is available for children from other
racial and ethnic backgrounds, such as Hispanic and Asian. We undertook
a retrospective cohort study of children with ALL treated on Children's
Cancer Group therapeutic protocols to determine outcomes by racial and
ethnic backgrounds of patients treated with contemporary risk-based
therapy. In total, 8447 children (white, n = 6703; Hispanic, n = 1071;
black, n = 506; and Asian, n = 167) with newly diagnosed ALL between
1983 and 1995 were observed for a median of 6.5 years. Analysis of
disease outcome was measured as overall survival (OS) and event-free
survival (EFS) and was adjusted for known predictors of outcome
including clinical features, disease biology, socioeconomic status, and
treatment era (1983-1989 vs 1989-1995). There was a statistically
significant difference in survival by ethnicity (P <.001). Five-year EFS
rates were: Asian, 75.1% +/- 3.5%; white, 72.8% +/- 0.6%; Hispanic,
65.9% +/- 1.5%; and black, 61.5% +/- 2.2%. Multivariate analysis
revealed that when compared with white children, black and Hispanic
children had worse outcomes and Asian children had better outcomes after
adjusting for known risk factors. The poorer outcomes among black
children were most apparent among patients with standard-risk features
(relative risk [RR], 2.0; 95% confidence interval [CI], 1.6-2.5),
whereas poorer outcomes in Hispanic children (RR, 1.4; 95% CI, 1.2-1.6)
were most evident among patients with high-risk features. Asian children
had better outcomes than all racial and ethnic groups among high-risk
patients, particularly in the recent era (5-year EFS, 90.9% +/- 6.1%).
Racial and ethnic differences in OS and EFS persist among children with
ALL who receive contemporary risk-based therapy. Future studies should
focus on reasons-perhaps compliance or pharmacogenetics-for those
differences.
11
UI - 12229886
AU - Moorman AV; Richards S; Harrison CJ
TI -
Involvement of the MLL gene in T-lineage acute lymphoblastic leukemia.
SO - Blood 2002 Sep 15;100(6):2273-4
12
UI - 12357355
AU - Calero Moreno TM; Gustafsson G; Garwicz S; Grander D; Jonmundsson GK;
TI -
Frost BM; Makipernaa A; Rasool O; Savolainen ER; Schmiegelow K;
Soderhall S; Vettenranta K; Wesenberg F; Einhorn S; Heyman M
Deletion of the Ink4-locus (the p16ink4a, p14ARF and p15ink4b genes)
predicts relapse in children with ALL treated according to the Nordic
protocols NOPHO-86 and NOPHO-92.
SO - Leukemia 2002 Oct;16(10):2037-45
AD - Research Laboratory of Radiumhemmet, CCK Karolinska Hospital, Stockholm,
Sweden.
Inactivation of the Ink4 gene locus locus on 9p comprising the tumour
suppressor gene p16ink4a and its neighbours p14ARF and p15ink4b is
common in childhood acute lymphoblastic leukaemia (ALL), but the
prognostic significance is controversial. DNA from 230 patients was
retrospectively analysed by Southern blotting, single strand
conformation polymorphism (SSCP) and sequencing techniques. The results
were correlated with clinical characteristics and outcome. One hundred
and ninety-four fully analysed patients, similarly treated using the
Nordic NOPHO-86 or the current NOPHO-92 protocols, were included in the
outcome analysis. Deletions approached a minimally deleted region
between the p16ink4a and p15ink4b genes, making the p14ARF gene the most
commonly deleted coding sequence. Bi-allelic deletion was associated
with high white blood cell count (WBC) (P < 0.001), T cell phenotype (P
< 0.001) and mediastinal mass (P < 0.001). Patients with Ink4 locus
bi-allelic deletions had an inferior pEFS (P < 0.01) and multivariate
analysis indicated that bi-allelic deletion of the p16ink4a and the
p14ARF genes was an independent prognostic risk factor (P < 0.05).
Sub-group analysis revealed a pronounced impact of deletion status for
high-risk patients, ie with high WBC. Deletion-status and clinical risk
criteria (WBC) could thus be combined to further differentiate risk
within the high-risk group. The analysis of the Ink4 locus adds
independent prognostic information in childhood ALL treated by Nordic
protocols and may help in selection of patients for alternative
treatment.
13
UI - 12357357
AU - Mancini M; Vegna ML; Castoldi GL; Mecucci C; Spirito F; Elia L; Tafuri
TI -
A; Annino L; Pane F; Rege-Cambrin G; Gottardi M; Leoni P; Gallo E;
Camera A; Luciano L; Specchia G; Torelli G; Sborgia M; Gabbas A;
Tedeschi A; Della Starza I; Cascavilla N; Di Raimondo F; Mandelli F; Foa
R
Partial deletions of long arm of chromosome 6: biologic and clinical
implications in adult acute lymphoblastic leukemia.
SO - Leukemia 2002 Oct;16(10):2055-61
AD - Department of Cellular Biotechnologies and Hematology, University La
Sapienza, Rome, Italy.
Within 285 adult acute lymphoblastic leukemias (ALL) included in the
multicenter GIMEMA 0496 trial and prospectively studied by conventional
cytogenetics, 18 cases (6%) with long arm deletion of chromosome 6 (6q)
were identified. These cases were divided into: (i) del(6q) only (n =
6); (ii) del(6q) plus other numerical and/or structural abnormalities (n
= 8); (iii) del(6q) and other 'specific' translocations (n = 4). The
biologic and clinical features of the patients carrying this anomaly, as
well as their outcome, were compared with those of 267 patients without
del(6q). A T cell phenotype was more frequently associated with del(6q)
cases in general (P = 0.001) and particularly with cases presenting
del(6q) as the isolated abnormality (P = 0.0027). No significant
difference with respect to multidrug resistance (MDR)/P glycoprotein
expression was observed between the two groups of patients (21% vs 28%
of MDR-positive cases, respectively). A BCR-ABL fusion transcript was
less frequently detected in cases with del(6q) (11%) compared with those
without the anomaly (29%). p15 and p16 deletions were identified by
Southern blot analysis in 21% of cases with del(6q) and in 26% of cases
without del(6q). In this latter group, a T cell phenotype was less
frequently associated with p15 and/or p16 deletion than in the group
carrying del(6q) (36% vs 100% of cases, P = 0.011). Overall, patients
with ALL and del(6q) had a high complete remission (CR) rate (83%);
however, they had a lower 18 month event-free survival (31% vs 41%) and
a higher relapse rate (70% vs 37%, P = 0.02) compared with patients
without del(6q). To date, this is the largest series of adult ALL cases
reported with del(6q) homogeneously treated, which have also been
prospectively studied for MDR expression and for the detection of known
fusion genes. This anomaly, as an isolated change, identifies a subset
of cases with hyperleukocytosis (median WBC count 52 x 10(9)/l) and a
strict correlation with a T cell phenotype. Overall, del(6q) seems to be
associated with an unfavorable clinical outcome, although this finding
will need to be confirmed by extended FISH analysis.
14
UI - 12357365
AU - Cilloni D; Gottardi E; De Micheli D; Serra A; Volpe G; Messa F;
TI -
Rege-Cambrin G; Guerrasio A; Divona M; Lo Coco F; Saglio G
Quantitative assessment of WT1 expression by real time quantitative PCR
may be a useful tool for monitoring minimal residual disease in acute
leukemia patients.
SO - Leukemia 2002 Oct;16(10):2115-21
AD - Division of Hematology and Internal Medicine, Dept of Clinical and
Biological Sciences of the University of Turin, Italy.
In order to verify if quantitative assessment of the WT1 transcript
amount by the real time quantitative PCR (RQ-PCR) can be used as a
marker for minimal residual disease detection, the WT1 transcript amount
was determined in BM and PB samples of patients with myeloid and
lymphoid acute leukemia, in normal controls, in regenerating bone marrow
samples and in purified CD34-positive cells from normal subjects. In 10
patients bearing a fusion gene transcript suitable for minimal residual
disease quantitative assessment, we performed a simultaneous analysis of
the WT1 and of the fusion-gene transcript at sequential time intervals
during follow-up. Sequential WT1 analysis was also performed in five AML
patients lacking additional molecular markers. The data obtained show
that normal and regenerating BM samples and purified CD34-positive cells
consistently express minimal amounts of WT1 transcript and that this is
extremely low and frequently undetectable in normal PB. By contrast,
high levels of WT1 expression are present in the BM and PB samples of
all acute leukemia (AL) cases at diagnosis. The WT1 levels during
follow-up were found to follow the pattern of the other molecular
markers (fusion gene transcripts) used for MRD monitoring and increased
WT1expression in the BM and/or PB during follow-up of AL patients was
always found to be predictive of an impending hematological relapse.
15
UI - 12133444
AU - Liu M; Li R; Hayashi Y; Zhu G; Guo S
TI -
[Study on abnormal expression of the p73 gene in childhood acute
lymphoblastic leukemia]
SO - Zhonghua Xue Ye Xue Za Zhi 2002 May;23(5):239-42
AD - Peking Union Medical College Hospital, Chinese Academy of Medical
Sciences, Beijing 100730, China.
OBJECTIVE: To investigate the relationship between p73 gene and the
development and progression of childhood acute lymphoblastic leukemia
(ALL). METHODS: The levels of p73 transcripts in 61 ALL cell lines and
53 childhood ALL patients were assayed using reverse
transcriptase-polymerase chain reaction (RT-PCR), and their relationship
with the clinicopathological characteristics was analyzed. Besides, the
methylation status of p73 exon 1 was analysed by restriction-enzyme
related PCR, methylation-specific PCR and bisulfite genomic sequencing
in the 61 ALL cell lines. RESULTS: Of the 61 ALL cell lines, 42 showed
expression of p73 mRNA, with a negative rate of 31.1%, and of the 53
primary childhood ALL samples, 39 showed expression of p73 mRNA, with a
negative rate of 26.4%. Loss of p73 expression was significantly
associated with the reduced disease free survival and overall survival
of the patients. 39.3% (24/61) of the ALL cell lines showed
hypermethylation of p73 exon 1, while normal lymphocytes and most cell
lines expressed p73 mRNA were not hypermethylated. CONCLUSION: There was
a higher negative expression rate of p73 mRNA in childhood ALL. The main
mechanism of the loss expression would be the hypermethylation of p73
gene. p73 gene inactivation might play an important role in the
pathogenesis of ALL. Examination of p73 mRNA might have clinical
significance in predicting prognosis of childhood ALL.
16
UI - 11940320
AU - Zhao Y; Yu L; Wang Q; Lou F; Pu J
TI -
[The relationship between expression of lung resistance-related protein
gene or multidrug resistance-associated protein gene and prognosis in
newly diagnosed acute leukemia]
SO - Zhonghua Nei Ke Za Zhi 2002 Mar;41(3):183-5
AD - Hematology Department, The General Hospital of PLA. Beijing 100853,
China.
OBJECTIVE: To evaluate the relationship between the expression of lung
resistance-related protein (lrp) gene or multidrug resistance-associated
protein (mrp) gene and prognosis in untreated acute leukemia (AL)
patients. METHODS: Reverse transcriptase-polymerase chain reaction
(RT-PCR) was used to examine the expression of lrp and mrp gene in 58
newly diagnosed AL patients. RESULTS: The positive rate of lrp and mrp
gene expression in newly diagnosed acute lymphocytic leukemia (ALL)
group was 15.0% and 40.0% and it was 15.8% and 42.1% in newly diagnosed
acute nonlymphocytic leukemia (ANLL) group. In both the ALL and ANLL
groups, the difference of the first complete remission rate in lrp
negative and in lrp positive patients was not significant (P > 0.05),
the same results were found with mrp gene. The difference of the first
complete remission rate between lrp(+)/mrp(+) and lrp(-)/mrp(-) patients
was significant (P < 0.05). There was no relationship between lrp and
mrp gene. CONCLUSION: Neither lrp nor mrp gene as a single indicator to
forecast original multidrug resistance is sensitive, but lrp combined
with mrp as one indicator will be sensitive.
17
UI - 11030043
AU - Harrison CJ
TI -
The genetics of childhood acute lymphoblastic leukaemia.
SO - Baillieres Best Pract Res Clin Haematol 2000 Sep;13(3):427-39
AD - Department of Haematology, Royal Free and University College Medical
School, London, UK.
In childhood acute lymphoblastic leukaemia (ALL) a number of genetic
changes have been identified which provide diagnostic and prognostic
information with a direct impact on patient management. The most
significant abnormalities include the translocation, t(12;21)(p13;q22),
giving rise to the ETV6/AML1 gene fusion; BCR/ABL arising from
t(9;22)(q34;q11); re-arrangements of the MLL gene; the E2A/PBX1 from the
t(1;19)(q23;p13); re-arrangements of MYC with the immunoglobulin genes
and re-arrangements of the T cell receptor genes. Chromosomal deletions,
particularly those of the short arms of chromosomes 9 and 12 and the
long arm of chromosome 6, have been postulated to be the sites of tumour
suppressor genes (TSG). Numerical chromosomal abnormalities are of
particular importance in relation to prognosis. High hyperdiploidy
(50-65 chromosomes) is associated with a good risk, whereas the outlook
for patients with near haploidy (23-29 chromosomes) is extremely poor.
In view of the introduction of risk-adjusted therapy into the UK
childhood ALL treatment trials, an interphase FISH screening programme
has been developed to reveal chromosomal abnormalities with prognostic
significance in childhood ALL.
18
UI - 11215050
AU - Chen Y; Zhang H; Yue B; Li H
TI -
Study on P16 gene in acute leukemia.
SO - J Tongji Med Univ 2000;20(3):210-1
AD - Institute of Hematology, Xiehe Hospital, Tongji Medical University,
Wuhan 430030.
To study the change of suppressing cancer gene P16 in acute leukemia,
the P16 antigen expression of leukemia cell surfaces in 61 cases were
investigated with ABC assay and gene structural defects in 51 cases of
acute leukemia were examined with multiple comparative PCR method. It
was found that antigen expression of P16 in leukemia was obviously lower
than that innormal subjects (P < 0.001). At the same time, antigen
expression in All was lower than that AML (P < 0.05). No significant
difference was found between the complete remission (CR) and
non-remission (NR) subjects from AML and ALL groups (P > 0.05). THe exon
2 of P16 gene showed homozygous deletion only inn 4 cases out of 30
cases in ALL. No structural defect was revealed in 21 cases of AML. It
was suggested that expression defect of P16 gene was a main cause in
development and progression of acute leukemia, and structural defect of
exon 2 was not a primary molecular event.
19
UI - 11386084
AU - Sibella-Arguelles C
TI -
The proliferation of human T lymphoblastic cells induced by 5-HT1B
receptors activation is regulated by 5-HT-moduline.
SO - C R Acad Sci III 2001 Apr;324(4):365-72
AD - Unite de pharmacologie neuro-immuno-endocrinienne, departement de
physiopathologie, Institut Pasteur, 28, rue du Dr-Roux, 75724 Paris,
France. mhj@pasteur.fr
Serotonin (5-hydroxytryptamine, 5-HT) is a well-known neurotransmitter
and immunomodulator, which has been reported to affect the function of
cells in the immune system. The purpose of the herein reported
experiments was to investigate whether serotonin could regulate the
proliferation of a human T lymphoblastic leukemia cell line (CCRF-CEM
cells) and to characterize the 5-HT receptor(s) involved in this
phenomenon using a pharmacological approach. The herein presented
results show that serotonin alone stimulated the proliferation of
CCRF-CEM cells and that this effect could be mimicked by two 5-HT1B/1D
receptor agonists (L-694,247 and GR 46611). Serotonin- or
L-694,247-induced increase in cell proliferation was inhibited by a
selective 5-HT1B receptor antagonist, SB-224289. A recently identified
endogenous tetrapeptide, 5-HT-moduline (Leu-Ser-Ala-Leu, LSAL), which
specifically antagonizes 5-HT1B/1D receptor activity, was also shown to
reverse the stimulating action of L-694,247 on T cell proliferation.
Taken together, these results establish the existence of a direct
serotonergic control of the T cell proliferation mediated through
h5-HT1B receptors. In addition, these results are in favour of an
immunomodulatory role of 5-HT-moduline.
20
UI - 12365028
AU - Wen W; Shu XO; Potter JD; Severson RK; Buckley JD; Reaman GH; Robison LL
TI -
Parental medication use and risk of childhood acute lymphoblastic
leukemia.
SO - Cancer 2002 Oct 15;95(8):1786-94
AD - Department of Medicine, School of Medicine, Vanderbilt University,
Nashville, Tennessee, USA.
BACKGROUND: Few studies have examined the risk of childhood acute
lymphoblastic leukemia (ALL) associated with parental medication use. As
part of a large case-control study conducted by the Children's Cancer
Group, we evaluated the association between maternal and paternal
medication use and the risk of ALL in offspring. METHODS: Information on
selected medication use in the year before and during the index
pregnancy was obtained by telephone interview. Participants included
1842 children of 14 years or younger with newly diagnosed and
immunophenotypically defined ALL and 1986 individually matched controls.
Data were analyzed using logistic regression models and stratified by
immunophenotypes of ALL and age at diagnosis of cases. RESULTS: After
adjusting for potential confounders and other medication use, we found
that maternal use of vitamins (odds ratio [OR] = 0.7, 99% confidence
interval [CI]: 0.5-1.0) and iron supplements (OR = 0.8, 99% CI: 0.7-1.0)
only during the index pregnancy was associated with a decreased risk of
ALL. Parental use of amphetamines or diet pills and mind-altering drugs
before and during the index pregnancy was related to an increased risk
of childhood ALL, particularly among children where both parents
reported using these drugs (OR = 2.8, 99% CI: 0.5-15.6 for amphetamines
or diet pills, OR = 1.8, 99% CI: 1.1-3.0 for mind-altering drugs).
Stratified analyses showed that maternal use of antihistamines or
allergic remedies and parental use of mind-altering drugs were strongly
associated with infant ALL, whereas patterns of association between
childhood ALL and parental medication use did not influence markedly the
immunophenotypic subgroup of ALL. CONCLUSIONS: The findings of this
study suggest that certain parental medication use immediately before
and during the index pregnancy may influence risk of ALL in offspring.
Copyright 2002 American Cancer Society.
21
UI - 12385062
AU - Besson C; Plumelle Y; Arnulf B; Gonin C; Panelatti G; Bazarbachi A;
TI -
Hermine O
[Adult T-cell leukemia/lymphoma. Clinical aspects]
SO - Presse Med 2001 Feb 10;30(5):239-42
AD - Service d'Hematologie clinique, Hopital Necker, 149, rue de Sevres,
F75743 Paris.
BACKGROUND DATA: Adult T-cell leukemia/lymphoma (ATL) is a malignant
proliferation of activated CD4+ T lymphocytes. The disease is almost
exclusively found in patients living in retrovirus HTLV-1 endemic areas.
VIROLOGY: In ATL, monoclonal HTLV-1 provirus is integrated into atypical
lymphocytes, called clover-leaf lymphocytes. The pathogenic mechanism
leading to HTLV-1-induced leukemogenesis remains obscure. The disease
generally occurs after a long latency period. FOUR CLINICAL SUBTYPES:
The diversity of the clinical presentation has led to the classification
of ATL into four subtypes: acute or prototype, lymphoma, chronic, and
painless. In the acute form of ATL there is a tumor syndrome associated
with paraneoplastic hypercalcemia and a high rate of opportunistic
infections due to the immunodepression predominated by cellular
immunity. CLINICAL COURSE: Prognosis is poor for the acute and
lymphomatous forms with a median survival of 6 and 10 months
respectively. Infectious episodes are frequent, often caused by
Pneumocystis carinii, and require systematic prophylaxis. Screening for
anguilulosis and prophylaxis is also necessary.
22
UI - 7882134
AU - Duro D; Flexor MA; Bernard O; d'Agay MF; Berger R; Larsen CJ
TI -
Alterations of the putative tumor suppressor gene p16/MTS1 in human
hematological malignancies.
SO - C R Acad Sci III 1994 Oct;317(10):913-9
AD - INSERM U301 et SDI n. 1954 I du CNRS, Institut de Genetique Moleculaire,
Paris, France.
The chromosome band 9p21-22 is frequently rearranged or deleted in a
variety of tumors including hematological malignancies. This supports
the notion of a tumor suppressor gene in this chromosome region. Indeed,
the p16/MTS1 gene encoding a cyclin-dependent kinase (CDK) inhibitor has
been shown to be frequently deleted and/or inactivated by nonsense
mutations in a number of tumors. We have examined 98 DNA samples from
blood, bone marrow cells and lymph node biopsies of patients with
leukemia (ALL and AML) or lymphoma (follicular lymphoma and T-cell
lymphoma), using Southern blot hybridization and a p16/MTS1-specific
probe. Molecular abnormalities, mainly homozygous deletions, were found
principally in ALL (8 out of 22 patients), much less frequently in AML
(2/32) and lymphoma (2/32). While these data argue in favor of a large
involvement of p16/MTS1 in ALL, AML and lymphomas appear to be less
frequently implicated.
The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.
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