Risk of malignancy associated with chronic lymphocytic leukemia: A population based Canadian study

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 20020-20020
Author(s):  
M. W. Pitz ◽  
V. Banerji ◽  
A. A. Demers ◽  
Z. Nugent ◽  
J. Strutinsky-Mason ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Cancer Registry ◽  
Population Based ◽  
Lymphocytic Leukemia ◽  
Increased Risk ◽  
Risk Of Malignancy ◽  
Synchronous Malignancies ◽  
Adjusted Incidence ◽  
Mean Time

20020 Background: Patients with Chronic Lymphocytic Leukemia (CLL) may have an increased risk of other malignancies. Available literature reports on malignancies that develop after the diagnosis of CLL, but does not discuss malignancies that precede the diagnosis of CLL. Methods: All patients diagnosed with CLL between 01/1998 and 12/2003 were extracted from the provincial cancer registry and a centralized flow cytometry database. All other malignancies were obtained from the cancer registry. Dates of diagnoses were compared. A malignancy within 30 days before or after the diagnosis of CLL was considered synchronous with that diagnosis. Results were compared with the age-adjusted incidence of cancer in the province, excluding CLL. Results: Of the 713 cases of CLL, 333 invasive cancers and 38 in situ neoplasia were identified before, synchronous to, or after the diagnosis of CLL. Synchronous malignancies occurred in 4% of cases. The Standardized Incidence Ratio (SIR) for other malignancy subsequent to CLL was 1.40 (95% confidence interval [CI] 1.09–1.80) derived from 65 tumors for males, and 1.29 (95% CI 0.90–1.80) from 35 tumors for females. Mean time to diagnosis of subsequent cancer was 2.0 years (standard deviation[SD] 1.5). The SIR for other malignancy in the 5 years preceding the diagnosis of CLL was 1.36 (95% CI 0.93–1.94) from 31 tumors for males and 0.77 (95% CI 0.54–1.08) from 35 tumors for females. Mean time from diagnosis of preceding malignancy to CLL was 9.4 years (SD 8.7). Conclusions: In this population based study, patients with CLL are at increased risk of other invasive and in situ cancers. This risk is apparent after but not before the diagnosis of CLL, particularly in males. The mechanism of this increased risk may be acquired with the presence of CLL through an underlying but undetermined mechanism, as opposed to an inherent or more longstanding predisposition to malignancy. No significant financial relationships to disclose.

Overall and Cancer-Specific Survival of Patients With Breast, Colon, Kidney, and Lung Cancers With and Without Chronic Lymphocytic Leukemia: A SEER Population-Based Study

2013 ◽  
Vol 31 (7) ◽  
pp. 930-937 ◽  
Author(s):  
Benjamin M. Solomon ◽  
Kari G. Rabe ◽  
Susan L. Slager ◽  
Jerry D. Brewer ◽  
James R. Cerhan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Chronic Lymphocytic Leukemia ◽  
Population Based ◽  
Lymphocytic Leukemia ◽  
Disease Stage ◽  
Tumor Type ◽  
Cancer Specific Survival ◽  
Lung Cancers ◽  
Increased Risk ◽  
A Site

Purpose Chronic lymphocytic leukemia (CLL) is associated with an increased risk of developing second cancers. However, it is unknown whether CLL alters the disease course of these cancers once they occur. Patients and Methods All patients with cancers of the breast (n = 579,164), colorectum (n = 412,366), prostate (n = 631,616), lung (n = 489,053), kidney (n = 95,795), pancreas (n = 82,116), and ovary (n = 61,937) reported to the SEER program from 1990 to 2007 were identified. Overall survival (OS; death resulting from any cause) and cancer-specific survival were examined, comparing patients with and without pre-existing CLL. Cancer-specific survival was evaluated for each tumor type in a site-specific manner (eg, death resulting from breast cancer in a patient with breast cancer). Results Patients with cancers of the breast (hazard ratio [HR], 1.70; P < .001), colorectum (HR, 1.65; P < .001), kidney (HR, 1.54; P < .001), prostate (HR, 1.92; P < .001), or lung (HR, 1.19; P < .001) had inferior OS if they had a pre-existing diagnosis of CLL after adjusting for age, sex, race, and disease stage. These results for OS remained significant for patients with cancers of the breast, colorectum, and prostate after excluding or censoring CLL-related deaths. Cancer-specific survival was also inferior for patients with cancers of the breast (HR, 1.41; P = .005) and colorectum (HR, 1.46; P < .001) who had pre-existing CLL after adjusting for age, sex, race, and disease stage. Conclusion Inferior OS and cancer-specific survival was observed for several common cancers in patients with pre-existing CLL. Additional studies are needed to determine the optimal management of these malignancies in patients with CLL and whether more aggressive screening or alternative approaches to adjuvant therapy are needed.

Overall and cancer-specific survival of breast, colon, and lung cancer in patients with and without chronic lymphocytic leukemia: A SEER population-based study of over 1 million patients.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 6571-6571
Author(s):  
Benjamin Maurice Solomon ◽  
Kari G. Rabe ◽  
Susan L Slager ◽  
Jerry D Brewer ◽  
James R. Cerhan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Chronic Lymphocytic Leukemia ◽  
Population Based ◽  
Lymphocytic Leukemia ◽  
Cancer Site ◽  
Cancer Specific Survival ◽  
Hazard Ratios ◽  
Increased Risk ◽  
History Of ◽  
Age And Sex

6571 Background: Chronic lymphocytic leukemia (CLL) is associated with an increased risk of developing second cancers. However, it is unknown whether CLL alters the natural history of these cancers once they occur. Methods: All patients with breast (n=583,838), colon (n=412,932), prostate (n=632,922), lung (n=489,290), kidney (n=95,902), pancreas (n=82,121) and ovarian (n=61,958) cancer reported to the Surveillance, Epidemiology, and End Results (SEER) Program from 1990 to 2007 were identified. Overall survival (OS; death due to any cause) and cancer-specific survival (death due to cancer site of interest) were examined, comparing patients with or without pre-existing CLL. Age- and sex-adjusted hazard ratios (HRs) were calculated. Results: OS for patients with pre-existing CLL was inferior for patients with breast (HR=1.61; p<0.001), colon (HR=1.65; p<0.001), kidney (HR=1.41; p<0.001), prostate (HR=1.75; p<0.001), and lung (HR=1.22; p<0.001) cancer after adjusting for age and sex. After excluding CLL-related deaths, OS remained shorter among patients with breast (p<0.001), colon (p<0.001), kidney (p=0.03), prostate (p<0.001), and lung (p<0.001) cancer. Cancer-specific survival was inferior for patients with breast (HR=1.29; p=0.03), colon (HR=1.75; p<0.001), and lung cancer (HR=1.17; p<0.001) who had pre-existing CLL after adjusting for age and sex. Conclusions: Several common cancers, including breast, colon, and lung, have inferior overall and cancer-specific survival when there is coexistent CLL. [Table: see text]

scholarly journals Relationship between chromosomal aberrations and gene expressions in the p53 pathway in chronic lymphocytic leukemia

2020 ◽  
Vol 23 (1) ◽  
pp. 15-24
Author(s):  
G Öztan ◽  
M Aktan ◽  
S Palanduz ◽  
H İşsever ◽  
S Öztürk ◽  
...  
Keyword(s):  
Gene Expression ◽  
Chronic Lymphocytic Leukemia ◽  
Protective Role ◽  
Lymphocytic Leukemia ◽  
Gene Expressions ◽  
P53 Pathway ◽  
Cytogenetic Aberrations ◽  
Increased Risk ◽  
Relative Fold Change

AbstractChronic lymphocytic leukemia (CLL) is a neoplasm characterized by excessive accumulation of B lymphocytes in the peripheral blood, bone marrow and lymph nodes. We assessed the expressions of 22 genes in the p53 pathway in 30 CLL patients and 15 healthy subjects by a RT2 Profiler PCR (polymerase chain reaction) Array technique and their relation to cytogenetic aberrations detected by fluorescent in situ hybridization (FISH). Our Student’s t-test results indicated that ATM, ATR, BAX, CASP9, CDK4, CDKN2A, CHEK1, CHEK2, E2F3, MCL1, MDM2, MDM4, PCNA, RB1, P53 and BCL2 genes were statistically significant (p <0.001). For six genes (APAF1, CDKN1A, E2F1, GADD45A, PTEN and PTX3) were not statistically significant. The ATM, ATR, BAX, CASP9, CDK4, CDKN1A, CDKN2A, CHEK1, CHEK2, MDM2, MDM4, PCNA, RB1, P53, E2F1, GADD45A and BCL2 genes were found to be upregulated by the 2-ᐃᐃCt (relative fold change in gene expression) method. The highest up-regulation was detected in CDKN2A and BCL2 genes, 10.22- and 8.51-fold, respectively. On the other hand, the PTX3 gene with a fold regulation of 1.84 was found to the highest downregulation. Overall, the CDNK2A BCL2 and PTX3 genes are related to the mechanism of the disease in the p53 pathway and may be an important predictor of the prognosis of the disease. The BCL2 gene may be associated with increased risk of developing CLL. We suggest that the PTX3 gene may be considered as a marker associated with CLL disease. The CDKN2A gene expression seems to play a protective role in CLL.

scholarly journals Increased risk of second malignancies after in situ breast carcinoma in a population-based registry

2006 ◽  
Vol 95 (3) ◽  
pp. 393-397 ◽  
Author(s):  
I Soerjomataram ◽  
W J Louwman ◽  
M J C van der Sangen ◽  
R M H Roumen ◽  
J W W Coebergh
Keyword(s):  
Breast Carcinoma ◽  
Population Based ◽  
Second Malignancies ◽  
Increased Risk ◽  
Population Based Registry

scholarly journals Expression of the c-myc proto-oncogene in multiple myeloma and chronic lymphocytic leukemia: an in situ analysis

Blood ◽  
1991 ◽  
Vol 78 (1) ◽  
pp. 180-191 ◽  
Author(s):  
R Greil ◽  
B Fasching ◽  
P Loidl ◽  
H Huber
Keyword(s):  
Cell Cycle ◽  
Multiple Myeloma ◽  
Chronic Lymphocytic Leukemia ◽  
Peripheral Blood ◽  
Proliferative Activity ◽  
Plasma Cells ◽  
Lymphocytic Leukemia ◽  
Myc Gene ◽  
Gene Transcripts

Abstract The c-myc gene plays a pivotal role in mediating the competence state for cell cycle transversion. This biologic role is in contradiction to reports of elevated expression of the gene in multiple myeloma, a tumor with restricted self-renewal capacity. To more clearly define the role of this gene in plasma cells of myeloma patients, c-myc messenger RNA (mRNA) and/or oncoprotein expression were semiquantitatively analyzed on the single cell level in 19 cases of multiple myeloma, among them 1 biclonal case and 1 case with coexistent chronic lymphocytic leukemia (CLL). Performing anti-sense/mRNA in situ hybridization, mature c-myc gene transcripts were detected in 92% (12 of 13) of cases and could definitely be attributed to the plasma cells by our study. The number of Ki 67-positive plasma cells actively passing the cell cycle was less than 1% and independent of c-myc gene expression. However, because the presence of the 152-c-MYC epitope was correlated to extent of marrow plasmacytosis (r = .64; P = .043) and content of plasmablasts (P = .09), the c-myc gene might serve a function different from proliferative activity, but also associated with tumor cell mass. In CLL cells (21 of 22 cases) and their benign counterparts, ie, bone marrow and peripheral blood lymphocytes, the anti-sense/c-myc mRNA hybridization signals remained below the threshold considered as cutpoint between negative and positive. The low amounts of c-myc transcripts were correlated to neither stage of disease (P = .52) nor lymphocyte counts (P = .24). Because the numbers of peripheral blood lymphoma cells were independent of tumor mass and of c-myc gene transcripts expressed, peripheral blood lymphocytosis might more likely reflect homing processes than proliferative activity in CLL.

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