scholarly journals Del (7)(q32) is associated with a subset of small lymphocytic lymphoma with plasmacytoid features

Blood ◽  
1995 ◽  
Vol 86 (6) ◽  
pp. 2365-2370 ◽  
Author(s):  
K Offit ◽  
DC Louie ◽  
NZ Parsa ◽  
A Noy ◽  
RS Chaganti
Keyword(s):  
Early Event ◽  
Low Grade ◽  
Small Lymphocytic Lymphoma ◽  
Extranodal Involvement ◽  
Tumor Supressor ◽  
Lymphoid Malignancies ◽  
Karyotypic Abnormality ◽  
Circulating Cells ◽  
Myeloid Leukemias ◽  
Tumor Supressor Gene

Deletions of the long arm of chromosome 7, previously documented in myelodysplasias and myeloid leukemias, have also been noted in lymphoid malignancies. Of 558 karyotypically abnormal specimens of non-Hodgkin's lymphoma (NHL) serially ascertained over an 8-year period, del(7q) was identified in 24 cases, 10 of which were of the small lymphocytic (sm lym) subtype. Del(7q) was the third most common karyotypic abnormality among the cohort of 61 sm lym cases in this ascertainment. Mapping of the deletions identified a region of common deletion affecting 7q32, which was the sole karyotypic abnormality in 2 cases. Eight of the ten sm lym cases were characterized by plasmacytoid features in histologic sections of lymphoma tumors or circulating cells in the peripheral blood. The del(7)(q32) was accompanied by 14q32-associated translocations in 11 of the 14 cases with histologies other than sm lym, compared with 2 of the sm lym cases. Extranodal involvement was more frequent in the del(7)(q32) sm lym NHLs, although median survival was typical of other low-grade lymphomas. These results suggest that loss or inactivation of a putative tumor-supressor gene at 7q32 may play a role the progression of lymphomas as well as constitute an early event in the pathogenesis of lymphoplasmacytoid tumors.

CD133/CD166/Ki-67 Triple Immunouorescence Assessment for Putative Cancer Stem Cells in Colon Carcinoma*

2014 ◽  
Vol 23 (2) ◽  
pp. 161-170 ◽  
Author(s):  
Claudiu Margaritescu ◽  
Daniel Pirici ◽  
Irina Cherciu ◽  
Alexandru Barbalan ◽  
Tatiana Cârtâna ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Stem Cells ◽  
Colon Cancer ◽  
Cancer Stem Cells ◽  
Colon Carcinoma ◽  
Sodium Dodecyl ◽  
High Grade Dysplasia ◽  
Early Event ◽  
Low Grade ◽  
High Grade

Background & Aims: Colorectal cancer represents the third most common malignancy and the fourth most common cause of cancer death worldwide. The existence of drug-resistant colon cancer stem cells is thought to be one of the most important reasons behind treatment failure in colon cancer, their existence putatively leading to metastasis and recurrences. The aim of our study was to investigate the immunoexpression patterns of CD133 and CD166 in colon carcinoma, both individually and in combination, assessing their significance as prognostic markers.Methods. A total of 45 retrospective colon adenocarcinoma cases were investigated by enzymatic and multiple fluorescence immunohistochemistry for their CD133 and CD166 expression and colocalization.Results. Both CD133 and CD166 were expressed to different extents in all cancer specimens, with apredominant cytoplasmic pattern for CD133 and a more obvious membranous-like pattern for CD166.Overall, when comparing their reactivity for the tumoral tissue, CD166 expression areas seemed to be smaller than those of CD133. However, there was a direct correlation between CD133 and CD166 expression levels throughout the entire spectrum of lesions, with higher values for dysplastic lesions. Colocalization of CD133/ CD166 was obvious at the level of cells membranes, with higher coeficients in high grade dysplasia, followed by well and moderate differentiated tumours.Conclusions. CD133/CD166 colocalization is an early event occurring in colon tumorigenesis, with thehighest coeficients recorded for patients with high grade dysplasia, followed by well differentiated tumours. Thus, we consider that the coexpression of these two markers could be useful for further prognostic andtherapeutically stratification of patients with colon cancer.Abbreviations: AJCC - American Joint Committee on Cancer; CCD - charge-coupled device camera sensor; CD133 - prominin-1 (PROM1); CD166 - Activated Leukocyte Cell Adhesion Molecule (ALCAM); CRC - colorectal cancer; CSC - cancer stem cells; DAB - 3,3'-diaminobenzidine chromogen; DAPI - 4',6-diamidino- 2-phenylindole; HE - Hematoxylin and eosin staining; HGD - high grade dysplasia; HRP - horseradish peroxidase; LGD - low grade dysplasia; SDS - sodium dodecyl sulfate*Part of this work has been accepted as a poster presentation at the Digestive Disease Week (DDW) meeting, Chicago, IL, USA May 3-6, 2014

Atypical Presentation of Low-Grade Small Lymphocytic Lymphoma of the Lacrimal Sac

2015 ◽  
Vol 31 (6) ◽  
pp. e163-e165 ◽  
Author(s):  
Vasilios P. Papastefanou ◽  
Cornelius René ◽  
Dominic G. O’Donovan ◽  
Andrew F. Dean ◽  
Penny A. Wright
Keyword(s):  
Low Grade ◽  
Atypical Presentation ◽  
Lacrimal Sac ◽  
Small Lymphocytic Lymphoma

P16 Methylation Is an Early Event in Cervical Carcinogenesis

2011 ◽  
Vol 21 (3) ◽  
pp. 452-456 ◽  
Author(s):  
Lee-Wen Huang ◽  
Hun-Shan Pan ◽  
Yu-Hung Lin ◽  
Kok-Min Seow ◽  
Heng-Ju Chen ◽  
...  
Keyword(s):  
Cervical Intraepithelial Neoplasia ◽  
Promoter Methylation ◽  
Intraepithelial Neoplasia ◽  
Promoter Hypermethylation ◽  
Early Event ◽  
Low Grade ◽  
Neoplastic Progression ◽  
Frequent Event ◽  
Significant Difference ◽  
Low Grade Dysplasia

BackgroundAberrant gene promoter methylation is a critical event in tumorigenesis. The aim of this study was to explore the promoter hypermethylation of p16 and DAPK1 during the progression of cervical precancerous lesions.MethodsA series of 98 cervical neoplasms (72 cervical intraepithelial neoplasia and 26 cervical carcinomas) were evaluated. The promoter methylation status of p16 and DAPK1 was assessed from cervical scrapings by methylation-specific polymerase chain reaction.ResultsFor p16, the frequency of promoter hypermethylation showed an increasing trend from normal to dysplastic to invasive squamous cancer specimens, and this increase reached statistical significance (P < 0.0001). However, there was no significant difference in the promoter methylation state of DAPK1 with regard to the various grades of cervical lesions (P = 0.077). Specifically, methylation of p16 was a frequent event in the cervical carcinoma samples, and these figures were statistically significant compared with the normal and cervical intraepithelial neoplasia I cases (P = 0.015 and P = 0.021, respectively).ConclusionsThese results imply that promoter hypermethylation of p16 occurs at an early stage of cervical neoplastic progression. This early event may play an initiating role in the malignant transformation of low-grade dysplasia into high-grade dysplasia and invasive carcinoma. We suggest that aberrant promoter methylation of p16 may serve as a useful biomarker during the follow-up of low-grade dysplasia.

Expression of the Wilms’ Tumor Supressor Gene (WT1) in Renal Cell Carcinoma

1995 ◽  
pp. 56-62
Author(s):  
Brian P. Butler ◽  
Nishi P. Kuriyan ◽  
Raymond Rackley ◽  
Christine Campbell ◽  
Bryan R. G. Williams
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Wilms Tumor ◽  
Tumor Supressor ◽  
Tumor Supressor Gene

Two for One: B-Cell Lymphomas with Features of Marginal and Follicular Lymphomas

2018 ◽  
Vol 139 (2) ◽  
pp. 84-88 ◽  
Author(s):  
Alexey Glazyrin ◽  
Chirag Patel ◽  
Lara Kujtan ◽  
Sheshadri Madhusudhana
Keyword(s):  
Bone Marrow ◽  
Follicular Lymphoma ◽  
Tumor Cells ◽  
Marginal Zone ◽  
Lymph Node Biopsy ◽  
Low Grade ◽  
Circulating Cells ◽  
Diagnosis And Classification ◽  
Follicular Lymphomas ◽  
Normal Architecture

Low-grade follicular lymphomas are genetically characterized by the translocation t(14; 18)(q32;q21) with BCL2 gene rearrangements. Marginal zone lymphomas are often associated with translocations or transcriptional deregulations of the MALT gene. We report 2 cases of lymphomas which harbor both the t(14;18)(q32;q21) translocation and MALT gene upregulation. Patients presented with numerous circulating atypical lymphocytes. Lymph node biopsy in both cases on HE staining demonstrated vague nodularity readily highlighted by CD10, CD23, or BCL6. Staining with CD20 and BCL2 demonstrated monotonous diffuse effacement of normal architecture with tumor cells without obvious follicular structures. Morphologically, tumor cells were consistent with centrocytes. Bone marrow biopsy demonstrated a combined peritrabecular and interstitial distribution of the tumor cells. These cases present substantial difficulties for diagnosis and classification. Clinical and morphological features were mostly consistent with follicular lymphoma, with a few features more often seen in marginal zone lymphomas (leukemic presentation, no CD10 in circulating cells, interstitial location of tumor cells in bone marrow); therefore, these cases were finally classified as follicular lymphoma grade I. Both patients were treated with standard chemotherapy regimens for follicular and nongastric MALT lymphomas with a good response to date.

P53 and bcl-2 assessment in serous ovarian carcinoma

2008 ◽  
Vol 18 (2) ◽  
pp. 241-248 ◽  
Author(s):  
J. E. Palmer ◽  
L. J. Sant Cassia ◽  
C. J. Irwin ◽  
A. G. Morris ◽  
T. P. Rollason
Keyword(s):  
Prognostic Value ◽  
Disease Free Survival ◽  
Ovarian Tumors ◽  
Early Event ◽  
Low Grade ◽  
Ovarian Carcinomas ◽  
Study Objective ◽  
P53 Expression ◽  
Response To Chemotherapy ◽  
Clinicopathologic Parameters

The study objective was to determine the prognostic value of assessment of staining of p53 and bcl-2 in a well-selected group of serous ovarian carcinomas. Immunohistochemical detection was used to identify both p53 and bcl-2 positive tumors. One hundred thirty-two tumors were analyzed for positivity of staining, grade of staining intensity, and for p53 alone, percent expression rates. These were analyzed alongside traditional clinicopathologic parameters for their ability to predict overall survival (OS), disease-free survival (DFS), and response to chemotherapy (CR). Univariate COX analysis revealed percent p53 expression (P= 0.012) and p53 grade (P= 0.01) to be significant predictors of DFS. Neither the p53 nor bcl-2 measurement parameters were found significant for OS or prediction of CR. On multivariate analysis, incorporating clinicopathologic parameters, p53 parameters did not retain independent significance for any outcome measure. As in primary reported studies, bcl-2 was not found to be of clear independent prognostic value in this group of ovarian tumors. If mutation of p53 and its consequent overexpression is an early event in ovarian tumorigenesis, then p53 assessment may prove useful prognostically in the assessment of either low-grade ovarian carcinomas, as a possible indicator for progression, or in early-stage ovarian tumors, as a marker of tumor aggression or likelihood of recurrence. p53 analysis of a larger group of stage I ovarian tumors would be desirable to further explain the potential association with DFS.

scholarly journals Peritoneal Serous Borderline Tumour with Ultra-Mutated NGS Profile Including POLE E, BRAF, RB1, HER2 and P53 Mutations : A Case Report.

2020 ◽  
Author(s):  
Jean-Christophe Noel ◽  
Antonio Buonomo ◽  
Sarah Bouri ◽  
Nicky D’Haene ◽  
Xavier Catteau
Keyword(s):  
Case Report ◽  
Early Event ◽  
Low Grade ◽  
P53 Mutations ◽  
Epithelial Proliferation ◽  
Case Presentation ◽  
Mutation Status ◽  
Borderline Tumors ◽  
Borderline Tumour ◽  
Tissue Invasion

Abstract Background: Serous borderline tumors of the peritoneum are rare low-grade epithelial proliferation with a tubal-type differentiation occurring in the pelvis or abdomen without underlying tissue invasion that resemble to ovarian serous borderline tumors but by definition without ovrian or tubal involvement. To date, the mutation status in molecular biology of these tumours remains largely unknown.Case presentation: Here we describe the case of a borderline peritoneal serous tumour which occurred in a 48 year old patient in whom an analysis of the mutation status by NGS technique identified a ultra-mutated profile including POLE E, BRAF, RB1, HER2 and p53 mutations.Conclusions: To the best of our knowledge, this particular mutation status has never been described in this type of tumour. It could represent an early event with transient mutations, most of them will not fixate on the genome.

scholarly journals Single Cell Transcriptomics of Pancreatic Cancer Precursors Demonstrates Epithelial and Microenvironmental Heterogeneity as an Early Event in Neoplastic Progression

2018 ◽  
Author(s):  
Vincent Bernard ◽  
Alexander Semaan ◽  
Jonathan Huang ◽  
F. Anthony San Lucas ◽  
Feven C Mulu ◽  
...  
Keyword(s):  
Single Cell ◽  
Single Cells ◽  
Suppressor Cells ◽  
Invasive Cancer ◽  
Ductal Adenocarcinoma ◽  
Early Event ◽  
Low Grade ◽  
Neoplastic Progression ◽  
Non Invasive ◽  
Cancer Pathogenesis

AbstractBackgroundEarly detection of pancreatic ductal adenocarcinoma (PDAC) remains elusive. Precursor lesions of PDAC, specifically, intraductal papillary mucinous neoplasms (IPMNs) represent abona fidepathway to invasive neoplasia, although the molecular correlates of progression remain to be fully elucidated. Single cell transcriptomics provides a unique avenue for dissecting both the epithelial and microenvironmental heterogeneity that accompany multistep progression from non-invasive IPMNs to PDAC.MethodsSingle cell RNA-sequencing was performed through droplet-based sequencing on 5,403 cells from two low-grade IPMNs (LGD-IPMN), two high-grade IPMNs (HGD-IPMN), and two PDACs (all surgically resected).ResultsAnalysis of single cell transcriptomes revealed heterogeneous alterations within the epithelium and the tumor microenvironment during the progression of non-invasive dysplasia to invasive cancer. While HGD-IPMNs expressed many core-signaling pathways described in PDAC, LGD-IPMNs harbored subsets of single cells with a transcriptomic profile that overlapped with invasive cancer. Notably, a pro-inflammatory immune component was readily seen in low-grade IPMNs, comprised of cytotoxic T-cells, activated T-helper cells, and dendritic cells, which was progressively depleted during neoplastic progression, accompanied by infiltration of myeloid-derived suppressor cells. Finally, stromal myofibroblast populations were heterogeneous, and acquired a previously described tumor-promoting and immune-evading phenotype during invasive carcinogenesis.ConclusionsThis study demonstrates the ability to perform high resolution profiling of the transcriptomic changes that occur during multistep progression of cystic PDAC precursors to cancer. Notably, single cell analysis provides an unparalleled insight into both the epithelial and microenvironmental heterogeneity that accompany early cancer pathogenesis, and might be a useful substrate to identify targets for cancer interception.

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