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The World Health Organization classification of lymphoma recommends the subdivision of follicular lymphoma (FL) into 3 grades (FL1-3) based on the average number of centroblasts per high-power field in the neoplastic follicles, but does not recognize a form of FL characterized by a predominance of large cleaved cells (centrocytes) without enough centroblasts to meet the World Health Organization criteria for FL3. We have classified such cases as follicular large cleaved cell lymphoma (FLC) and, herein, describe the pathologic and clinical features of 72 cases of this entity. The features of FLC include a follicular growth pattern with pale follicles at low magnification and frequent follicular and/or interfollicular fibrosis. Cytologically, the cells are predominantly large cleaved cells with moderately coarse to fine chromatin, absent or inconspicuous nucleoli, and small to moderate amounts of pale cytoplasm. The mean nuclear diameter of the large cleaved cells was 10.1μ, approximately twice that of small lymphocytes and similar to centroblasts. The t(14;18) was present in 83% of the cases, and a high proportion expressed BCL2 (84%), BCL6 (100%), and CD10 (88%) and had high Ki67 proliferation (81%). The clinical features of patients with FLC were similar to those with other types of FL, and survival was excellent with anthracycline-based chemotherapy plus rituximab. FLC is a variant of follicular lymphoma which should be recognized in future lymphoma classifications because the diagnosis of FLC may be important for the selection of therapy., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Background: Deletion of chromosome 9p has been reported in numerous tumor types. The authors demonstrated in an earlier study that spontaneous chromosome aberrations on chromosome 9 in peripheral blood lymphocytes (PBLs) were a significant risk predictor for lung carcinoma., Methods: The current study evaluated the relationship between self-reported family history of cancer and spontaneous chromosome aberrations in the PBLs of 97 previously untreated lung carcinoma patients. The authors' hypothesis was that individuals exhibiting specific chromosome aberrations might have inherited genetic instability and thus be more likely to report a family history of cancer. For each individual, a personal interview was conducted to construct a detailed family history, and 100 metaphases from PBLs were analyzed for spontaneous aberrations by G-banding., Results: The patients reported having 829 first-degree relatives, including 74 (8.9%) with cancer. A significantly elevated odds ratio (OR) of 2.7 was noted in smokers for having chromosome 9 aberrations and a first-degree relative with cancer. When the family history of cancer was dichotomized into lung carcinoma or other cancers, the OR associated with chromosomal aberrations was 8.5 for lung carcinoma but only 2.3 for other cancers. In addition to chromosome 9 aberrations, other spontaneous chromosome aberrations and family history of cancer were also evaluated, but no associations were found. There were no associations between age, gender, ethnicity, or smoking status and the chromosome 9 aberration profile., Conclusions: The findings of this study suggest that chromosome 9 aberrations may be a marker of cancer susceptibility and may be associated with familial aggregation of cancer.

Genetic predisposition to lung cancer was determined by observing nonrandom chromosomal alterations in peripheral blood lymphocytes (PBLs) of lung cancer patients. The histological distribution of the cases showed that chromosomes 7 and 9 were frequently altered in squamous cell lung carcinoma (SCLC) patients. We analyzed PBLs of 26 SCLC patients and 5 controls using fluorescent in situ hybridization (FISH) with whole chromosome painting probes of chromosomes 7 and 9 to further investigate the frequency of rearrangements in these chromosomes. Our results suggested that seeking nonrandom aberrations in larger numbers of cells using FISH strengthened our previous observation of mosaicism and involvement of specific chromosomes in lung cancer patients. On combining our previous data, aberrations in chromosome 7 (16 of 26 patients), chromosome 9 (14 of 26), and the present study, we could actually pinpoint more individuals with abnormalities of chromosome 7 (23 of 26) and chromosome 9 (21 of 26). Thus, analyzing more cells in PBLs and adding FISH analysis serve as useful adjuncts to our studies of nonrandom chromosomal aberrations and genetic mosaicicm.

Mitomycin C (MMC)-induced lymphocytic sister chromatid exchange (SCE) frequency was studied in 40 oral cancer (OC) patients, 40 normal tobacco chewers (NC) and in 40 normal healthy individuals not consuming tobacco/areca nut in any form. Significantly higher MMC-induced SCE/cell values were observed among OC patients as compared to healthy non-chewer controls as well as NC. Although the mean SCE frequency for NC was comparable to that of healthy controls, three individuals showed an SCE rate higher than the highest observed among controls. The comparable frequency of the tobacco habit in these three individuals with that of the rest of the thirty-seven individuals indicated the possible involvement of factors other than tobacco consumption for the higher susceptibility to mutagens.

Chromosomal anomalies were analyzed in the lymphocyte cultures among 96 untreated lung cancer patients and 74 clinically normal comparison subjects. The analysis revealed that >15% of the lung cancer patients showed structural or numerical rearrangements in chromosomes 1,3,5,7,9,12,14, and 21. A case control comparison showed that these aberrations were significantly higher in chromosome 7 [odds ratio (OR) = 2.32; 95% confidence interval (CI), 1.14 and 4.82], chromosome 9 (OR = 2.61; 95% CI, 1.27 and 5.48), chromosome 12 (OR = 4.10; 95% CI, 1.40 and 14.54), and chromosome 21 (OR = 7.75; 95% CI, 1.73 and 70.80) of the patients than in the controls. However, only chromosome 9 (OR = 3.57; 95% CI, 1.33 and 9.46) and chromosome 21 (OR = 6.94; 95% CI, 3.15 and 9.98) retained significance after stratifying on smoking status. Among the lung cancer patients, the breakpoints cluster in specific regions of some of these chromosomes. These regions are 1p13-q21, 3q21-q13, 7p12-q12, 7q12-q12,7q22, 7q32, 9p13-q13, 12p13, 14q11, and 14q32. The distribution of lung cancer patients, according to histological types, showed that aberrations in chromosomes 1,7, and 9 dominated the scenario of chromosomal changes in non-small cell lung carcinomas. Thus, the data on lymphocytic chromosomal rearrangements in lung cancer patients not only indicate the importance of specific genetic changes in the etiology of lung cancer but also emphasizes the putative role of such analysis in determining primary genetic abnormalities in the large heterogeneous group of lung cancers.

Smokeless tobacco consumption is causally associated with oral cavity cancers; however, extensive cytogenetic studies have not been done. In the present study, individuals consuming dry snuff or tobacco with lime have been studied for frequency of micronucleated cells (MNC) in exfoliated buccal mucosa and chromosome aberrations (CA) and sister chromatid exchanges (SCE) in lymphocytes. The significant elevation in the values of all the three cytogenetic markers among tobacco users compared to the controls reveal the extent of genomic damage on target and nontarget tissues. The findings emphasize the possible use of cytogenetic endpoints for monitoring smokeless tobacco consumers.

Thirteen healthy females and thirteen untreated patients with carcinoma of the uterine cervix were studied for spontaneous and mitomycin C (MMC)-induced rates of sister chromatid exchange (SCE) and cell cycle progression. The mean values of spontaneous as well as MMC-induced SCE rates showed no statistically significant difference between groups. For studying cell cycle progression, cells in the M1, M2, and M3 stages were scored from the same samples. The percent values of cells in these stages, identified by the nature of differential sister chromatid staining, were found to be almost identical in normal as well as MMC-treated cultures in controls and patients. It was concluded that the presence of carcinoma of the uterine cervix in human females has no bearing either on spontaneous and MMC-induced SCE rates or on cell cycle progression in PHA-stimulated cultures of peripheral blood lymphocytes.