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NCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of All - October 2001
National Cancer Institute®
Last Modified: November 21, 2001
Table of Contents
1
UI - 21240475
AU - Pagano L; Pulsoni A; Mele L; Leone G
TI -
Clinical and epidemiological features of acute lymphoblastic leukemia
following a previous malignancy.
SO - Leuk Lymphoma 2000 Nov;39(5-6):465-75
AD - Cattedra di Ematologia, Universita Cattolica S. Cuore, Roma, Italia.
lpagano@rm.unicatt.it
Secondary malignancies represent a relevant complication of chemotherapy
employed for a previous cancer. Acute leukemias represent the most
frequent secondary malignancy in the first decade following primary
neoplasms; secondary leukemias are generally myeloid and can be
preceeded by a myelodysplastic syndrome. The biological and
epidemiological characteristics of secondary acute myeloid are well
known and have been the subject of numerous reports and reviews in the
last few years. The observation of a secondary acute lymphoblastic
leukemia is considered rare, and the correlation with antecedent
therapies is not definitive. Most of reported cases are single reports,
and no large study has been performed to investigate the real importance
of this problem. In this review we report data of the current literature
on secondary acute lymphoblastic leukemia, both in adults and children,
in order to analyze its incidence and clinical and laboratory features.
2
UI - 21240483
AU - Sahin G; Ertem U; Duru F; Birgen D; Yuksek N
TI -
High prevelance of chronic magnesium deficiency in T cell lymphoblastic
leukemia and chronic zinc deficiency in children with acute
lymphoblastic leukemia and malignant lymphoma.
SO - Leuk Lymphoma 2000 Nov;39(5-6):555-62
AD - Dr. Sami Ulus Children's Hospital Department of Pediatric Oncology,
Ankara, Turkey.
Magnesium and zinc are the elements having essential roles in regulation
of cell growth, division and differentiation. There have been some
studies in the literature suggesting an association between the
deficiency of these elements and the development of malignant disorders.
In this study hair and serum zinc and magnesium levels were investigated
in children with acute lymphoblastic leukemia (ALL) and malignant
lymphoma (ML) at the time of initial diagnosis. Ten children with T-cell
ALL, 10 children with B-precursor ALL, 5 children with Burkitt's
Lymphoma (BL), 11 children with Hodgkin's lymphoma (HL), 10 children
with non-Burkitt non-Hodgkin's lymphoma (NBNHL) and 12 age and sex
matched healthy children as a control group were included in the study.
Mean hair magnesium levels in all of the groups of the patients were
lower than the levels in the control group but the difference was
statistically significant only in the children with T cell ALL
comparable to the controls (28.9+/-3.9 microg/g and 87.6+/-18.5 microg/g
respectiveley, p<0,05). Mean serum magnesium levels in all the cohorts
were not significantly different than those in controls (p>0.05 in each
comparison). Mean hair zinc levels in the patients with T-cell,
B-precursor ALL, BL, HL, NBNHL were 103.4+/-14.6 microg/g, 100.9+/-7.8
microg/g, 91.1+/-19 microg/g, 72.5+/-9.1 microg/g, 103.2+/-12.2 microg/g
respectively. Each of these levels were significantly lower than the
mean hair zinc levels of the control group (141.2+/-9.6 microg/g, p<0.05
in each comparison). Although mean serum zinc levels in all of the
groups were also decreased, the differences were statistically
significant only in the groups with B-precursor ALL, HL and NBNHL
(75.9+/-5.29 microg/dl, 68.6+/-7.3 microg/dl, 85.7+/-5.5 microg/dl
respectively) when compared with controls (105.1+/-9.9 microg/dl, p<0.05
in each comparison). Hair magnesium and zinc levels showed a positive
correlation with each other in all the groups (r congruent with 0.5). No
significant difference was found in the mean hair/serum magnesium and
zinc levels between malnourished and nonmalnourished patients. In
conclusion, regarding the results of our study and previous data in the
literature chronic magnesium and zinc deficiency seems to be associated
with the development of ALL and malignant lymphoma in a group of
patients.
3
UI - 21402012
AU - Cabrera ME; Campbell M; Quintana J; Undurraga MS; Ford AA; Greaves MF
TI -
[Clinical significance and frequency of the 11q23/MLL genetic molecular
alteration in Chilean infants with acute leukemia]
SO - Rev Med Chil 2001 Jun;129(6):634-42
AD - Departamento de Medicina, Campus Oriente, Facultad de Medicina
Universidad de Chile. mcabrera@mi-mail.cl
BACKGROUND: Acute leukemia (AL) in infants generally shows distinctive
biologic features and has a poor prognosis. AIM: To study the frequency
of the cytogenetic alteration of 11q23 chromosome or the recombination
of MLL gene in infants less than 18 months old, with acute leukemia.
PATIENTS AND METHODS: We analyzed 37 cases of AL in infants less than 18
months of age diagnosed in Chile from 1989 to 1999. The clinical
features and cytogenetic/molecular defects of 11q23MLL gene
rearrangement and their influence in prognosis were determined. RESULTS:
There were 18 cases of acute Lymphoblastic leukemia (ALL) characterized
by female sex (67%) high presenting leukocyte count (median 99 x 109/L),
blast cells with a CD10 negative phenotype (50%) and 11q23/MLL
rearrangement (39%). Molecular abnormalities of 11q23 were significantly
associated with adverse prognosis, with an event free survival (EFS) of
only 14 +/- 12%. Interestingly, infants with germ line 11q23 had a very
good outcome with an EFS of 73 +/- 11% (p < 0.025). There were 19 cases
of acute myeloblastic leukemia (AML) characterized by male sex (63%)
high leukocyte count (median 93 x 109/L), FAB-MS morphology (53%) and
11q23/MLL rearrangement (53%). EFS was very poor, 20 +/- 9% and 33 +/-
4% for rearranged and germinal group respectively (p = NS), due to a
high mortality rate during the first month of diagnosis. CONCLUSIONS:
These findings demonstrate that Chilean ALL infants with 11q23
abnormalities have a very poor prognosis. However those with germinal
state can enjoy a prolonged disease free survival with the current
treatment protocols.
4
UI - 21411470
AU - Barata JT; Cardoso AA; Nadler LM; Boussiotis VA
TI -
Interleukin-7 promotes survival and cell cycle progression of T-cell
acute lymphoblastic leukemia cells by down-regulating the
cyclin-dependent kinase inhibitor p27(kip1).
SO - Blood 2001 Sep 1;98(5):1524-31
AD - Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, MA
02115, USA.
In normal T-cell development interleukin-7 (IL-7) functions as an
antiapoptotic factor by regulating bcl-2 expression in immature
thymocytes and mature T cells. Similar to what occurs in normal immature
thymocytes, prevention of spontaneous apoptosis by IL-7 in precursor
T-cell acute lymphoblastic leukemia (T-ALL) cells correlates with
up-regulation of bcl-2. IL-7 is also implicated in leukemogenesis
because IL-7 transgenic mice develop lymphoid malignancies, suggesting
that IL-7 may regulate the generation and expansion of malignant cells.
This study shows that in the presence of IL-7, T-ALL cells not only
up-regulated bcl-2 expression and escaped apoptosis but also progressed
in the cell cycle, resulting in sequential induction of cyclin D2 and
cyclin A. Down-regulation of p27kip1 was mandatory for IL-7-mediated
cell cycle progression and temporally coincided with activation of
cyclin-dependent kinase (cdk)4 and cdk2 and hyperphosphorylation of Rb.
Strikingly, forced expression of p27kip1 in T-ALL cells not only
prevented cell cycle progression but also reversed IL-7-mediated
up-regulation of bcl-2 and promotion of viability. These results show
for the first time that a causative link between IL-7-mediated
proliferation and p27kip1 down-regulation exists in malignant T cells.
Moreover, these results suggest that p27kip1 may function as a tumor
suppressor gene not only because it is a negative regulator of cell
cycle progression but also because it is associated with induction of
apoptosis of primary malignant cells.
5
UI - 21450469
AU - Smith A; Robson L; Heaps LS; Sharma P; Dunlop L; Bhave A; Bradstock K
TI -
Routine fluorescence in situ hybridization with the MLL probe does not
reliably detect two separate signals on one chromosome 11 in patients
with trisomy 11.
SO - Cancer Genet Cytogenet 2001 Sep;129(2):173-6
AD - Department of Cytogenetics, Royal Alexandra Hospital for Children,
Locked Bag 4001, NSW 2145, Westmead, Australia. ellies@nch.edu.au
Trisomy 11 is considered to be a rare cytogenetic abnormality in
myelodysplastic syndromes (MDS) and acute myelogenous leukemia (AML).
Duplication of the MLL gene (localized to 11q23) has been found on one
chromosome 11 in patients with trisomy 11, detected by DNA techniques.
We investigated copy number of MLL in seven patients with trisomy 11 to
see if duplication could be assessed by the detection of two separate
signals on fluorescence in situ hybridization (FISH). If so, FISH could
provide a quick easy screen of MLL status in routine referrals. The
diagnostic bone marrow aspirate showed trisomy 11 in five adult patients
with MDS/AML as part of a complex karyotype and in two children with
acute lymphoblastic leukemia (ALL) as part of a hyperdiploid karyotype.
Fluorescence in situ hybridization utilized the suspensions remaining
after the cytogenetic harvest. Two FISH probes were used on the adult
patients (MLL - Oncor and Vysis), and one (Vysis) for the two children
with ALL. Analysis showed that the proximity of the two putative
hybridization signals made it very difficult to unambiguously see two
separate signals. The hybridisations (Oncor probe) were convincing of
MLL duplication (namely two distinct signals) in only one patient, but
this was not borne out with the other MLL probe (Vysis). We conclude
that conventional FISH with MLL probe is not suited to act as a screen
for MLL duplication in patients with trisomy 11.
6
UI - 21452377
AU - Chessells JM; Harrison G; Richards SM; Bailey CC; Hill FG; Gibson BE;
TI -
Hann IM
Down's syndrome and acute lymphoblastic leukaemia: clinical features and
response to treatment.
SO - Arch Dis Child 2001 Oct;85(4):321-5
AD - Molecular Haematology Unit, Camelia Botnar Laboratories, Institute of
Child Health, 30 Guilford Street, London WCIN 1EH, UK.
j.chessells@ich.ucl.ac.uk
AIMS: To examine the clinical and biological features of acute
lymphoblastic leukaemia in children with Down's syndrome (DS), to
compare their survival with other children, and to determine if entry to
trials and survival has improved. METHODS: Examination of presenting
features and response to treatment in patients treated in two
consecutive national trials, MRC UKALL X and XI. RESULTS: The proportion
of children with DS was significantly higher in UKALL XI (1.9%) than
UKALL X (0.9%). Children with DS tended to be under 10 years and to have
the common ALL subtype. Cytogenetic analysis showed that favourable
features, such as high hyperdiploidy and t(12;21) were less frequent but
also that there was a lack of translocations associated with a poor
prognosis. Children with DS showed no increase in risk of relapse at any
site but their survival and event free survival were inferior to other
children. These results were caused by an increased number of infective
deaths during remission (11% compared to 2%). At five years overall
survival was 73% in DS children compared with 82% in other children;
event free survival was 53% compared to 63% in non-DS children.
CONCLUSIONS: Entry of children with DS to national trials has increased
and survival has improved. However they remain at risk of relapse and
also of treatment related mortality. These findings emphasise the need
for both intensive chemotherapy and optimal supportive care.
7
UI - 21262968
AU - Miglino M; Grasso R; Pietrasanta D; Palmisano GL; Berisso G; Clavio M;
TI -
Pierri I; Santini G; Canepa L; Gobbi M
Detection of minimal residual disease in B-lymphoproliferative
disorders: a three step SSCP-PCR method.
SO - J Exp Clin Cancer Res 2001 Mar;20(1):95-101
AD - Dept. of Internal Medicine, Azienda Ospedale S. Martino e Cliniche
Universitarie convenzionate, Genova, Italy.
The most recent therapeutic approaches can improve the outcome of B-cell
neoplasia. By PCR analysis we amplify tumor specific DNA sequences of
clonal IgH rearrangement from a limited number of malignant cells
against a background of normal B cells. Recently described PCR based
techniques for tracking minimal residual disease (MRD) in B
lymphoproliferative disorders have given promising but discordant
results, with significant variations in the sensitivity and specificity
of the procedures. We have developed a three step single strand
conformational polymorphism polymerase chain reaction (SSCP-PCR)
strategy which is able to detect clonal malignant cells in B
lymphoproliferative disorders at a frequency as low as 1 in 10(6) cells.
Since this method is simple, rapid, reliable and as specific as ASO-PCR,
it could be especially useful in monitoring patients affected by B
lymphoproliferative disorders in complete haematological and
immunophenotypic remission.
8
UI - 21305413
AU - Martin Ramos M; Fernandez Martinez F; Barreiro Miranda E
TI -
[Cytogenetic abnormalities in acute lymphoblastic leukemia]
SO - An Esp Pediatr 2001 Jul;55(1):45-52
AD - Servicio de Genetica, Hospital 12 de Octubre, Madrid, Spain.
mlmartin@tdi.es
Cytogenetic analysis of blast cells in childhood acute lymphoblastic
leukemia has led to the recognition of specific non-random chromosomal
abnormalities with prognostic value. Most patients with ALL show
karyotype abnormalities, either in chromosome number (ploidy) or as
structural changes such as translocations, inversions, or deletions.
Many of these chromosomal alterations are associated with specific
cytomorphological and immunological types. The greatest impact on
patient management has been the finding that the cytogenetic result is
an independent prognostic indicator. Certain karyotypes are associated
with a favorable prognosis while others indicate a poor outcome. This
has led to the administration of alternative therapies according to
risk. For instance, hyperdiploidy with a modal chromosome number of 51
or greater, which represents 25-30 % of all cases of ALL, has proved to
have the most favorable prognosis among established ploidy groups,
whilst translocations such as the Philadelphia translocation t(9;22) and
t(4;11) are associated with a poor prognosis. This study focuses on the
most important chromosomal abnormalities found in childhood ALL and
their prognostic and therapeutic implications.
9
UI - 21390873
AU - Wang J; Wang Q; Chen X
TI -
[Study on the sensitization of acute myeloid leukemia cell to
daunorubicin by recombinant human interleukin-3]
SO - Zhonghua Xue Ye Xue Za Zhi 1999 Jan;20(1):30-2
AD - Department of Hematology, Xin Qiao Hospital, Third Military Medical
University, Chongqing 630038.
OBJECTIVE: To evaluate the effect of recombinant human
interleukin-3(rhIL-3) on the sensitization of acute myeloid
leukemia(AML) cells to daunorubicin(DNR). METHODS: AML cells were
cultured in a DNR-containing medium supplemented or not with rhIL-3.
CFU-AML was assayed by semi-solid culture, proliferation and
differentiation of AML cells were assayed by flow cytometry,
cytomorphology and benzidine staining. Intracellular DNR concentration
was measured by spectrophotofluorometry. RESULTS: rhIL-3 could enhance
the proliferation but not differentiation of AML cells in vitro, and had
no effect on DNR intake and exclusion of AML cells while enhancing their
sensitivity to DNR. CONCLUSION: rhIL-3 combined with DNR might improve
the therapeutic effect of AML.
10
UI - 21390866
AU - Zheng H; Zhao X; Geng L
TI -
[Relationship between the bone marrow cell proliferation and the
prognosis in childhood acute lymphoblastic leukemia]
SO - Zhonghua Xue Ye Xue Za Zhi 1999 Jan;20(1):7-9
AD - Beijing Children's Hospital, Beijing 100045.
OBJECTIVE: To study the expression of proliferative antigens in leukemic
cells and the relationship between the cell proliferation activity and
the prognosis. METHODS: The labeling index (LI) of CD71, Ki-67 and PCNA
in normal and leukemic cells were measured by flow cytometry. RESULTS:
In normal children, the LI of CD71, Ki-67 and PCNA was (32.18 +/-
16.66)%, (4.82 +/- 9.27)% and (19.69 +/- 25.11)%, respectively, while in
ALL children, which was (33.66 +/- 21.52)%, (32.14 +/- 23.59)% and
(47.46 +/- 30.96)%, respectively. The PCNA LI of leukemia cells was
(47.46 +/- 30.96)% and (27.28 +/- 12.51)% when patients was at
presentation and remitted for 3 years, respectively, and was (52.59 +/-
32.00)% and at presentation in 28 CCR children and and (26.94 +/-
14.48)% in 7 high-risk group ALL children (F = 8.877, P < 0.01),
respectively. CONCLUSIONS: The proliferation, LI of leukemic cells was
higher than that of normal cells, and reduced to normal level after
treatment. The higher PCNA proliferation of untreated cells was a
favourable marker for prognosis.
11
UI - 21169678
AU - Fujiwara H; Eizuru Y; Matsumoto T; Kukita T; Imaizumi R; Kawada H;
TI -
Ohtsubo H; Matsushita K; Arima N; Tei C
The significance of cytomegalovirus infection over the clinical course
of adult T-cell leukemia/lymphoma.
SO - Microbiol Immunol 2001;45(1):97-100
AD - First Department of Internal Medicine, Center for Chronic Viral
Diseases, Faculty of Medicine, Kagoshima University, Kagoshima, Japan.
The significance of cytomegalovirus (CMV) infections developed over the
clinical course of adult T-cell leukemia/lymphoma (ATLL) were evaluated
in relation to the patient survival rate, ATL activity and
immunocompetent cells. ATLL patients with CMV infections on admission
exhibited a poor survival rate, while patients with CMV infections at
any time after admission survived longer than those not infected with
this virus. ATLL patients who exhibited a numbers of CMV infection on
admission showed higher ATL activity and had lower numbers of
CD8-positive and CD56-positive cells than those who developed CMV
infections at any time after admission. Therefore, it appears likely
that patients with CMV infections on admission were in an
immunosuppressive state due to aggressive ATL activity.
12
UI - 21377985
AU - Yashiki S; Fujiyoshi T; Arima N; Osame M; Yoshinaga M; Nagata Y; Tara M;
TI -
Nomura K; Utsunomiya A; Hanada S; Tajima K; Sonoda S
HLA-A*26, HLA-B*4002, HLA-B*4006, and HLA-B*4801 alleles predispose to
adult T cell leukemia: the limited recognition of HTLV type 1 tax
peptide anchor motifs and epitopes to generate anti-HTLV type 1 tax
CD8(+) cytotoxic T lymphocytes.
SO - AIDS Res Hum Retroviruses 2001 Jul 20;17(11):1047-61
AD - Department of Virology, Faculty of Medicine, Kagoshima University,
Kagoshima 890-8520, Japan.
Genetic risk for adult T cell leukemia (ATL) has been implicated by
ethnic and familial segregation of ATL patients from HTLV-1-associated
myelopathy/tropical spastic paraparesis (HAM/TSP). To clarify the
genetic risk for ATL, we characterized HLA class I alleles of ATL
patients and analyzed the anchor motifs of HTLV-1 peptides binding to
HLA class I molecules, using 291 lines of anti-HTLV-1 CD8(+) cytotoxic T
lymphocytes (CTLs) generated in vitro with a total of 165 synthetic
peptides for HTLV-1 Tax and Env proteins. Allele frequencies of
HLA-A*26, B*4002, B*4006, and B*4801 were significantly higher in ATL
patients than in HAM/TSP patients and asymptomatic HTLV-1 carriers in
southern Japan. CD8(+) CTL analysis revealed the HTLV-1 Tax peptide
sequence to completely lack anchor motifs of peptides binding to
HLA-A*26,B*4002, and B*4006 molecules but to possess one anchor for
HLA-B*4801, while the HTLV-1 Env peptide sequence had many anchor motifs
for HLA-A*26, B*4002, B*4006, and B*4801 molecules. Most ATL patients
featured heterozygous HLA class I alleles composed of HLA-A*26, B*4002,
B*4006, and B*4801, with a lower number of HTLV-1 Tax peptide anchor
motifs and epitopes generating anti-HTLV-1 Tax CD8(+) CTLs than
individuals possessing other HLA alleles. The relationship between Tax
epitope and ATL incidence was verified by the significantly decreased
number of HTLV-1 Tax epitopes in ATL patients compared with asymptomatic
HTLV-1 carriers (p < 0.01) as well as late onset ATL patients (p <
0.001). These results indicate that HLA-A*26, B*4002, B*4006, and B*4801
alleles predispose to ATL because of the limited recognition of HTLV-1
Tax peptide anchor motifs and epitopes capable of generating anti-HTLV-1
Tax CD8(+) CTLs.
13
UI - 21443185
AU - Tsang KS; Li CK; Chik KW; Shing MM; Tsoi WC; Ng MH; Lau TT; Leung Y;
TI -
Yuen PM
TEL/AML1 rearrangement and the prognostic significance in childhood
acute lymphoblastic leukemia in Hong Kong.
SO - Am J Hematol 2001 Oct;68(2):91-8
AD - Hematology and Bone Marrow Transplantation Division, Department of
Anatomical and Cellular Pathology, Chinese University of Hong Kong,
Prince of Wales Hospital, Hong Kong, China.
The TEL/AML1 rearrangement has been implicated as an independent good
prognostic factor in pediatric acute lymphoblastic leukemia (ALL). We
examined TEL/AML1 using nested reverse-transcription polymerase chain
reaction (RT-PCR) and correlated TEL/AML1 with cytogenetics and
immunophenotypes in 75 consecutively analyzed Chinese children with ALL
in Hong Kong. TEL/AML1 was detected in 17.9% (12/67) B-lineage ALL at
diagnosis but not in 8 T-ALL children or in 34 adults with ALL.
E2A/PBX1, MLL/AF4, and BCR/ABL were not found in TEL/AML1+ patients.
Coexpression of cross-lineage antigens was associated with TEL/AML1 gene
fusion (p = 0.032), with CD13 in 80% (4/5) TEL/AML1+ cohort. Chromosomal
abnormalities were demonstrated in 50% of the TEL/AML1+ ALL; however, a
cryptic t(12;21) was not detected in these cases. Hyperdiploidy of 47-48
chromosomes was encountered in 25%. Deletion of 12p resulting in the
loss of the normal allele of TEL and nonspecific del(6q) were noted in
8% (1/12) and 25% (3/12) of the TEL/AML1+ children, respectively. Rapid
clearance of TEL/AML1 was noted in 50% of the patients on completion of
the induction therapy; however, 16.7% (2/12) TEL/AML1+ ALL relapsed at a
mean of 48.6 months from diagnosis (25 months off-therapy). The
incidence of relapses of TEL/AML1+ ALL was comparable to that at
diagnosis in B-lineage ALL (14.3% [2/14] vs. 17.9% [12/67], p > 0.05).
The relapse rate in TEL/AML1+ ALL was similar to that of TEL/AML1- ALL
(16.7% [2/12] vs. 20.6% [13/63], p > 0.05). The duration of first
complete remission in TEL/AML1+ ALL was significantly longer as compared
to TEL/AML1- ALL (mean [range] in month: 48.6 [47.2 - 50] vs 14.6 [2.9 -
42.3], p < 0.0001). Irrespective of TEL/AML1 rearrangement, the
probabilities of the five-year overall survival and the event-free
survival of patients were comparable (overall survival: 100% vs. 72.3%,
p = 0.166 and event-free survival: 60% vs. 56.2%, p = 0.343). Our data
would not suggest a less aggressive treatment regimen for TEL/AML1+ ALL.
Copyright 2001 Wiley-Liss, Inc.
14
UI - 21466974
AU - Tomova A; Babusikova O
TI -
Shifts in expression of immunological cell markers in relapsed acute
leukemia.
SO - Neoplasma 2001;48(3):164-8
AD - Cancer Research Institute, Slovak Academy of Sciences, Bratislava,
Slovak Republic. exontoma@savba.sk
The immunophenotypic features of leukemia blast cells were analyzed in a
group of 156 patients with different immunological subtypes of acute
leukemia, both lymphoblastic and myeloblastic. Of the 58 patients for
whom immunologic studies were performed at relapse, 42 (72%) showed
changes in the expression of immunologic markers. The minor shifts in
B-ALL were observed most frequently and concerned of the loss of CD34
antigen in 17 cases and the loss of cALLA (CD10) in 7 cases of B-ALL at
the first relapse. The acquisition of cell markers was not frequently
observed, only in four cases could be seen. HLA-DR molecules remained
relatively constant from diagnosis to relapse. In 2 from 3 T-ALL cases
the loss of CD1 and CD2 markers, respectively, was noticed at relapse.
CD5 and CD7 markers were relatively stable. In AML cases at relapse the
acquisition of CD13 marker (in 4 from 7 cases) was often observed. It
was interesting that comparing to the B-ALL cases, the loss of CD34
marker in AML cases was stray. In one case the acquisition of this
antigen at relapse was actually observed. The major interlineage shift
was detected in one case of B-ALL, that was newly diagnosed at relapse
as AML M4 and presented different cytogenetic features. This case
provides strong connection with the treatment, as more recently
epipodophyllotoxins (vumon in our patient) have been linked to the
development of secondary AML associated with a shorter latency period.
The immunophenotypic changes frequently occur at relapse in all acute
leukemia types. The shifts (loss or acquisition) in expression of
individual markers at relapse are bound with the first diagnosis and may
have a relationship to the treatment and are important for correct
assessment of minimal residual disease.
15
UI - 21466977
AU - Pituch-Noworolska A; Hajto B; Mazur B; Sonta-Jakimczyk D; Balwierz W;
TI -
Janota-Krawczyk E; Kowalska H; Malinowska I; Modzelewska M; Wasik M
Expression of CD20 on acute lymphoblastic leukemia cells in children.
SO - Neoplasma 2001;48(3):182-7
AD - Department of Clinical Immunology, Polish-American Children Hospital,
Medical College, Jagiellonian University, Cracow. mipituch@cyf-kr.edu.pl
CD20 determinant expressed on B precursors is associated with regulation
of proliferation, apoptosis and maturation of these cells. The acute
lymphoblastic leukemia "common" type (cALL) based on expression of CD20
is subdivided in type I and II. However, the clinical significance of
CD20 expression on cALL and significance of cALL type I and II
discernment are not fully elucidated. The association of CD20 expression
with the expression of multidrug resistance molecule (MDR), CD34,
atypical immunophenotypes of leukemia cells and response to induction
therapy were determined in the group of 147 patients with acute
lymphoblastic leukemia (ALL) B progenitor type (ALL-proB -14 patients)
and common type (cALL-133 patients). The expression of CD20 on leukemia
cells was studied routinely at diagnosis before the therapy. This
expression was noted on leukemia cells of 6 ALL-proB patients (42.8%)
and 66 cALL patients (49.6%). The expression of CD20 showed no
association with the expression of CD34, CD22 and MDR. The reverse
association was observed between CD20 expression and the presence of
co-expression of myeloid (CD13, CD33, CD65, CD15) and T lymphoid
determinants (CD2, CD5, CD7) on leukemia cells. The effect of induction
therapy analyzed as time of blast cells cytoreduction in peripheral
blood and time of reaching the complete remission showed the slower
clearance of peripheral blood from blast cells associated with
expression of CD20. There was no association of CD20 expression with the
time of reaching the hematological remission. The above results
suggested a "protective" role of CD20 against co-expression of other
determinants (myeloid and lymphoid) and no association with the results
of induction therapy.
16
UI - 21341701
AU - Goto Y; Yue L; Yokoi A; Nishimura R; Uehara T; Koizumi S; Saikawa Y
TI -
A novel single-nucleotide polymorphism in the 3'-untranslated region of
the human dihydrofolate reductase gene with enhanced expression.
SO - Clin Cancer Res 2001 Jul;7(7):1952-6
AD - Department of Pediatrics, Kanazawa University School of Medicine,
Kanazawa, Ishikawa 920-8641, Japan.
A novel single-nucleotide polymorphism (SNP), 829C-->T in the
3'-untranslated region of the human dihydrofolate reductase (DHFR) gene
transcript, was identified in the study population of 37 patients with
childhood leukemias/lymphomas and 83 healthy Japanese children.
Frequencies of the DHFR 829C/C, 829C/T, and 829T/T genotypes were 83.8,
10.8, and 5.4%, respectively, in the cases and 74.7, 19.3, and 6.0% in
the controls, showing no significant difference in genotype frequencies
between the cases and controls. When determined by real-time
quantitative reverse transcription-PCR analysis, the highest expression
of the DHFR transcript was demonstrated in the samples with a DHFR
829T/T polymorphism (P < 0.001). Direct association of the presence of
the SNP with methotrexate-related adverse events in each patient was not
demonstrated in this limited analysis. These data suggest that the novel
DHFR 829 polymorphism is associated with a positive role in gene
expression and provide evidence of a functional SNP in the 3' regulatory
region of the gene.
17
UI - 21396248
AU - Walz CM; Nakamura M; Fukunaga T; Jasiewicz Y; Edler L; Schlehofer JR;
TI -
Tanaka Y
Reduced prevalence of serum antibodies against adeno-associated virus
type 2 in patients with adult T-cell leukaemia lymphoma.
SO - J Med Virol 2001 Sep;65(1):185-9
AD - Angewandte Tumorvirologie F0100, Deutsches Krebsforschungszentrum, Im
Neuenheimer Feld, Heidelberg, Germany.
Seroepidemiological studies have shown previously that cancer patients
are less likely to have antibodies against the tumour suppressive
adeno-associated virus (AAV) than control groups. To examine the
influence of AAV infection on the development of adult T-cell leukaemia
lymphoma (ATLL), an endemic disease in Southern Japan that is caused by
infection with the human T-cell leukaemia virus type 1 (HTLV-I), the
prevalence of serum antibodies to AAV type 2 (AAV-2) was tested in
healthy HTLV-I carriers (n = 39) and patients with ATLL (n = 31). The
results showed a significant difference in AAV-2 seropositivity between
the two groups: Only 29% of the ATLL patients had IgG antibodies against
AAV-2, whereas 84.6% of the healthy HTLV-I carriers were seropositive.
Analysis of total serum IgG and antibodies against the Epstein-Barr
virus (EBV) EBNA1 antigen showed that the lack of AAV antibodies in
patients was not due to an ATLL-associated immune deficiency. The lower
level of AAV-2 seropositivity in ATLL-patients may indicate that AAV-2
antibody-positive HTLV-I carriers might be less likely to develop ATLL
or that loss of AAV-2 antibodies may parallel the development of
disease. Copyright 2001 Wiley-Liss, Inc.
18
UI - 21456602
AU - Hokland P; Pallisgaard N
TI -
[Molecular biology in acute lymphoblastic leukemia]
SO - Ugeskr Laeger 2001 Aug 27;163(35):4721-4
AD - Arhus Amtssygehus, Arhus Universitetshospital, haematologisk afdeling,
immunhaematologisk laboratorium. hokland@gjallar.daimi.aau.dk
19
UI - 21281051
AU - Nysom K; Holm K; Hertz H; Muller J; Fleischer Michaelsen K; Molgaard C
TI -
Bone mass after treatment for acute lymphoblastic leukemia in childhood.
SO - J Clin Oncol 2001 Jun 1;19(11):2970-1
20
UI - 21277020
AU - Benko I; Kovacs P; Szegedi I; Megyeri A; Kiss A; Balogh E; Olah E;
TI -
Kappelmayer J; Kiss C
Effect of myelopoietic and pleiotropic cytokines on colony formation by
blast cells of children with acute lymphoblastic leukemia.
SO - Naunyn Schmiedebergs Arch Pharmacol 2001 May;363(5):499-508
AD - Department of Pharmacology, Medical School, Medical and Health Science
Center, University of Debrecen, Hungary. benko@king.pharmacol.dote.hu
The aim of this study was to see whether pleiotropic or myeloid
hematopoietic growth factors, which do not stimulate normal lymphoid
cells, can induce proliferation of blast cells of the acute lymphoid
leukemia (ALL) of childhood. Bone marrow cells of 13 children with
untreated ALL (nine common ALL, two myeloid antigen positive ALL and two
early T-cell ALL) formed colonies of leukemic blast cells in primary
methylcellulose cultures. Spontaneous growth was observed in three of 13
cases, whereas phytohemagglutinin-stimulated leukocyte conditioned
medium (PHA-LCM), a conventional source of various natural human
cytokines, induced colony formation in ten of 13 cases. A similar rate
of responsiveness was seen with recombinant human granulocyte
colony-stimulating factor (G-CSF), granulocyte-macrophage
colony-stimulating factor (GM-CSF) and stem cell factor (SCF); a
combination of these three cytokines induced colony formation in all
cases studied. The effect of these growth factors on colony formation
seemed to be dose-dependent in some cases. Of the stimuli studied,
GM-CSF induced the smallest number of colonies, whereas the effects of
G-CSF, SCF and PHA-LCM were similar in this respect. Combination of
cytokines proved to be even more efficient in inducing clonal
proliferation of leukemic lymphoblasts. In double combinations, G-CSF
and GM-CSF as well as G-CSF and SCF were able to potentiate each other's
effects. Triple combination of these cytokines mediated the most potent
growth stimulus. Our results demonstrate that myeloid and pleiotropic
cytokines are able to stimulate clonal proliferation of pediatric
leukemic lymphoblasts. This may present a potential hazard to children
with ALL while on adjuvant therapy with hematopoietic growth factors. In
vitro colony assays performed prior to or in parallel with the
administration of hematopoietic growth factors to ALL patients may help
to forecast their possible effects on leukemic cells in vivo.
21
UI - 21314728
AU - Landier W
TI -
Childhood acute lymphoblastic leukemia: current perspectives.
SO - Oncol Nurs Forum 2001 Jun;28(5):823-33; quiz 834-5
AD - City of Hope National Medical Center, Duarte, CA, USA. wlandier@coh.org
PURPOSE/OBJECTIVES: To provide an overview of childhood acute
lymphoblastic leukemia (ALL), including epidemiology, clinical
presentation, diagnostic classification, prognostic factors, current
treatment, long-term sequelae, and nursing management. DATA SOURCES:
Journal articles, books, and clinical experience. DATA SYNTHESIS:
Childhood ALL is a heterogeneous disorder, and current treatment is
tailored to risk factors (e.g., initial white blood count, cytogenetic
properties of the leukemic blasts). Risk-directed therapy ensures that
children with a higher risk of relapse receive more intensive treatment,
whereas those with lower risk disease receive less toxic therapy with
decreased potential for treatment-related morbidity. Quality of life in
long-term survivors is a significant issue. Late sequelae of treatment
can include neurocognitive difficulties, endocrine dysfunction,
secondary malignancies, and cardiomyopathy. CONCLUSIONS: With
risk-directed therapy, cure rates for childhood ALL continue to improve.
At least 80% of children diagnosed with ALL today are expected to
survive their disease. IMPLICATIONS FOR NURSING PRACTICE: Nurses caring
for children with ALL can have a significant impact on the children's
overall health, from diagnosis through long-term follow-up. Nursing
interventions encompass the domains of physical and psychosocial care,
as well as patient and family education. Assisting the child and family
to maintain normalcy in the face of chronic illness, as well as
fostering the family's hope for the future and their belief in the
child's potential for survival, are key nursing strategies that promote
the child's growth, development, and psychological health.
22
UI - 21477933
AU - Wang C; Yao Z; Liao J; Luo Y; Ma Y; Chen G; Zhu W
TI -
Clinicopathologic, immunophenotypic and ultrastructrual analyses of ATLL
patients with cutaneous involvement.
SO - Chin Med J (Engl) 1999 May;112(5):461-5
AD - Department of Dermatology, China-Japan Friendship Hospital, Beijing
100029, China.
OBJECTIVE: To study 4 cases of adult T-cell leukemia/lymphoma (ATLL)
associated with cutaneous lesions for clinicopathology, immunophenotype,
human T-cell leukemia/lymphoma virus type I (HTLV-I) provirus DNA and
their ultrastructure. At the same time, HTLV-I provirus DNA of ATLL
patients were also compared with 18 cases of cutaneous lymphoma (CL),
two cases of actinic reticuloid as well as two cases of lymphocytic
infiltration. METHODS: Immunohistochemistry studies were carried out on
the infiltrating cells using monoclonal antibodies against CD45-RO,
CD20, CD68 on paraffin-embedded sections by ABC method and using
monoclonal antibodies against CD3, CD4 and CD8 with indirect
immunofluorescence (IIF) on frozen sections. Skin biopsies were examined
by electron microscope. Serum and bone marrow cells were tested for
antibodies against HTLV-I-associated antigen by IIF, and HTLV-I provirus
DNA was examined by PCR method. RESULTS: The research showed four
patients with ATLL manifesting cutaneous lesions, were subsequently
found with additional systemic symptoms, as extensively enlarged
superficial lymph node, abnormal increased IL-2 receptor, flower-like
cells in their peripheral blood and marrow. The HTLV-I provirus DNA was
positive in the peripheral blood, bone marrow, cutaneous lesions and
lymph node biopsy specimens by using PCR amplification of specific
HTLV-I fragment while 18 cases of the CL were negative for HTLV-I. The
special ultrastructure of skin lesions was also found in ATLL patients.
CONCLUSIONS: The cutaneous involvement in ATLL is a type of cutaneous T
cell lymphoma (CTCL) but shows some differential immunological markers
for differential diagnosis. The examination of HTLV-I antibodies or
HTLV-I provirus DNA is necessary for diagnosis of ATLL. The
ultrastructural characteristics in skin lesions of ATLL were of atypical
lymphocytes and mononuclear cells invading the epidermis, and the
mononuclear cells are possessing the phagocytic function and
phagocytizing the degenerated epidermic cells or lymphocytes.
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