Mature B

Mature B
AACC uses cookies to ensure the best website experience. Continuing without changing cookie settings assumes you consent to our use of cookies on this device. You can change these settings at any time, but that may impair functionality on our websites. Review our cookie and privacy policy

About AACC

Media

Annual Meeting

Career Center

Artery

Login

Join

Renew

Artery Discussion Boards

Scientific Divisions

Local Sections

For Early Career Members

Fellows of AACC Academy

Merit Awards

Clinical Laboratory Scientists

Learn About Membership

Member Directory

Diversity, Equity, and Inclusion

Coronavirus Resources

Data Analytics in Laboratory Medicine

Clinical Chemistry Journal

The Journal of Applied Laboratory Medicine

Clinical and Forensic Toxicology News

AACC Academy Guidance

Practice Guidelines

POCT Guide for Non-Laboratorians

Scientific Shorts

Toxin Library

Universal Sample Bank

Clinical Laboratory Analyzer Archive

Research Grants

Clinical Laboratory Marketplace

All Articles

CLN Monthly

COVID-19 CLN Articles

CLN Stat

The Lab Advocate

CLN Daily

ACCENT

Subscribe

Contact Us

Find Continuing Education

Watch a Webinar

Earn a Certificate

Take an Online Course

Get Certified in Point-of-Care Testing

Accredit Your Education Program

Explore AACC Learning Lab

UNIVANTS of Healthcare Excellence Award

Annual Scientific Meeting

2022 Annual Meeting Session Recordings

Annual Meeting Session Recordings

AACC Middle East

International CPOCT Symposium

POCT Boot Camp

Preanalytical Conference

Resources from past meetings

Travel Grants

International Travelers Assistance

Advocacy Priorities

Laboratory Voice

Position Statements

Comment Letters

AACC Policy Reports

Policy Briefings

The Lab Advocate

Global Lab Quality Initiative

Guide to Lab Test Utilization

Harmonization

Laborastories

Membership Grants

Community

Science & Research

Clinical Laboratory News

Education

Meetings

Advocacy & Outreach

Join and Renew

About AACC

Media

Annual Meeting

Career Center

Artery

Join
Renew

Clinical Chemistry Trainee Council

CCTC Preview Videos

Become a CCTC Member

CCTC (English)

Webcasts

Pearls of Laboratory Medicine

Clinical Case Studies

Clinical Chemistry Podcasts

Clinical Chemistry Guide to Scientific Writing

The Journal Club

Q and A

Inspiring Minds

CCTC Coordinating Committee

Question Bank

CCTC (Español)

CCTC (中文)

CCTC (日本語)

CCTC (Français)

CCTC (Português)

Topics:

Pathophysiology and Organ Systems ,

Cancer

AACC.org
//

...
//

CCTC (English)
//

Pearls of Laboratory Medicine
//

Mature B-Cell Neoplasms

Author: Kamran Mirza

//

Date: AUG.20.2018

//

Source: Trainee Council in English

My name is Dr. Kamran Mirza and together with my AP/CP pathology resident Dr. Michael Moravek I would like to welcome you to this Pearl of Laboratory Medicine on “Mature B-cell Neoplasms”.
An understanding of mature B-cell neoplasms requires a general understanding of the outline of lymphocyte development. The main cells in this system are T-cells, B-cells and NK-cells. Similar to phases of development of all hematopoietic cells, B-cell maturation starts with immature, pro-B cells and passes through several stages before culminating at the formation of the plasma cell.
This mature B-cell, highlighted in the box represents the basis of all lesions that will be discussed in this video. Immature B-cell neoplasms such as acute lymphoblastic leukemias and terminal B-cell lesions such as plasma cell neoplasms are discussed separately. Overall, mature B-cell neoplasms account for 75% of all lymphoid neoplasms
In general, B-cell lymphomas arise as a result of genetic alterations that lead to deregulation of cell proliferation or apoptosis. Low-grade B-cell lymphomas are typically chronic diseases with a relatively indolent course. These commonly present as painless lymphadenopathy, hepatosplenomegaly or incidentally found CBC abnormalities. Higher grade, or more aggressive lesions typically present with rapidly enlarging masses or lymph nodes in addition to a spectrum of symptoms known as B-symptoms. These include fever, weight loss and night sweats
The mature B-cell undergoes exposure to antigen in lymph nodes. This diagram gives an overview of that process. Neoplastic change can occur at any point along this path and the subsequent clonal proliferation demonstrates similar morphology and phenotype as it’s cell of origin
Generally, pre-germinal center B-cells are naïve cells that have yet to encounter antigen. Such naïve cells are the cell of origin of mantle cell lymphoma. Similarly, there is a variety of germinal center derived lymphomas that can be identified on morphologic and phenotypic findings including Burkitt lymphoma, follicular lymphoma and some diffuse large B-cell lymphomas. Marginal zone B-cell derived lymphomas arise from marginal zone cells that are usually seen in the spleen and pelvic lymph nodes
Post-germinal B-cell neoplasms include the activated B-cell or ABC type diffuse large B-cell lymphoma, chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), marginal zone lymphoma of mucosa-associated lymphoid tissue, or MALT lymphoma and plasma cell neoplasms. Various stages of B-cell development can be identified by morphology as well as their changing antigen expression phenotype. Immunohistochemical analysis helps us subclassify various mature B-cell lymphomas and allows differentiation from immature B-cell lesions.
Over the past few decades, our understanding of the biology, pathophysiology, and prognosis of B-cell neoplasms has greatly improved. Putting this understanding to good use, there have been several classification schemes for lymphomas. Older classification systems defined lesions based on morphology alone. Over time, classification schemes evolved to incorporate clinical features, immunophenotype, cytogenetic, and molecular genetic data. Here is the most current list of mature B-cell neoplasms as defined by the most recent edition of the WHO classification of Tumors of hematopoietic and lymphoid tissue published in 2017.
In this video, we will be reviewing the lesions highlighted here. Our discussion will commence with the most frequently encountered lesions. Reported data shows diffuse Large B-cell lymphoma is the most common, accounting for just under 30% of all B-cell neoplasms
CLL/SLL, follicular lymphoma, marginal zone lymphoma, mantle cell lymphoma and Burkitt lymphoma follow DLBCL in decreasing frequency. The first step in determining the presence of a B-cell neoplasm is identifying the presence of a clonal population of B cells. This can be done by observing light chain restriction via flow cytometry or immunoglobulin heavy chain rearrangement studies. When a clonal population of B-cells is identified, subclassification is based on the lymphoma cell morphology and their immunophenotype. This algorithm represents an easy way to approach B-cell neoplasm by their antigen expression
The CD5 positive B-cell lymphomas include CLL/SLL and mantle cell lymphoma – These two entities are most often differentiated based on the expression of Cyclin D1 and CD23 or FMC7 and the intensity of CD20 expression. The follicular center cell origin, or CD10 positive lesions can be differentiated on size, morphology and architectural patterns. We start our discussion with CLL/SLL. A CD5 positive, CD23 positive mature B-cell neoplasm
Chronic lymphocytic leukemia and Small lymphocytic lymphoma, CLL/SLL define the same lymphoma, but are named based on whether the lymphoma is mostly in leukemic phase, which is CLL, or present as a nodal or tissue lesion, where it is called small lymphocytic lymphoma. The WHO classification collectively refers to these lesions by CLL/SLL. CLL/SLL accounts for the most frequently encountered lymphoma in western countries
This is usually a lymphoma of older patients, with a median age of 70, who usually present with unintentional weight loss, fatigue, and fever. Sometimes, CLL/SLL is discovered in patients with no definitive symptoms. To make a diagnosis of CLL, the CBC and differential should reveal an absolute lymphocytosis with greater than 5000 lymphoma cells per microliter
CLL/SLL is not defined by specific genetic alterations; however arises as a multistep process of genetic changes, and commonly demonstrates cytogenetic abnormalities
SLL can have a vaguely nodular appearance. At low power pale zones can be appreciated, as seen in the image on the left. These are pseudo proliferation growth centers. This pallor is due to a greater proportion of larger prolymphocytes with abundant cytoplasm in these regions. In the peripheral blood, CLL cells have high N:C ratio, irregular condensed chromatin that is often referred to as having a soccer ball pattern. Blood smears from CLL patients often demonstrate numerous smudge cells, or basket cells. Phenotypically, CLL/SLL is a CD5 positive B-cell lymphoma. It usually demonstrates dim expression of CD19, CD20 and CD5. CD23 positivity and Cyclin D1 negativity differentiate CLL/SLL from Mantle cell lymphoma. Large/confluent proliferation centers and proliferation centers with high mitotic activity are adverse prognostic indicators.
A series of adverse prognostic factors have been associated with CLL/SLL. These include high stage disease, high levels of beta 2 microglobulin, Unmutated immunoglobulin heavy chain and expression of CD38, ZAP70 and CD49d. Cytogenetic or FISH assessment of deletions of 11q and 17p and molecular assessment for mutations of TP53, BIRC, Notch1 and SF3B1 is important. Large cell transformation of CLL/SLL is known as Richter’s transformation. Most factors that predispose to Richter’s transformation are similar to the adverse prognostic factors of CLL/SLL
Apart from CLL/SLL the differential diagnosis of CD5 positive B-cell lymphoma includes the CD23 negative, Cyclin D1 and FMC7 positive mantle cell lymphoma. Mantle cell lymphoma is also a disease of older adults. Patients typically present with adenopathy, hepatosplenomegaly and marrow involvement. This is a disease with poor prognosis.
Two MCL subtypes recognized with different clinicopathological manifestations and molecular pathogenetic pathways: one largely with unmutated/minimally mutated IGH and mostly SOX11+ and the other largely with mutated IGHV and mostly SOX11− (indolent leukemic non- nodal MCL with PB, bone marrow (BM), ±splenic involvement, may become more aggressive). The t(11;14)(q13;q32) translocation between the IGH and CCND1 genes is found in >95% of cases and leads to overexpression of the cyclin D1 protein. This portends to a better prognosis.
Arising from the mantle zones around the germinal center, mantle cell lymphoma is comprised of mature, slightly irregular lymphocytes. Sox11 is the most sensitive monoclonal antibody and is seen in >90% of mantle cell lymphoma, including the rare CD5 negative mantle cell lymphomas
We now turn our attention to the CD5 negative, CD10 positive follicular lymphoma. FL is a germinal center origin lymphoma that is usually seen in older patients who can be asymptomatic despite widespread disease. This is generally a chronic, low grade process. However, progression to GCB type DLBCL is one of the known adverse outcomes. While usually a nodal disease, extranodal FL can involve the spleen, marrow, blood, tonsils and other tissues. The underlying genetic alteration in FL is translocation of the IgH and BCL-2 genes on chromosomes 14 and 18 leading to an inappropriately high rate of bcl-2 transcription for a mature B cell. BCL-2 overexpression leads to diminished apoptosis of abnormal B-cells within germinal centers that lead to the proliferation of a malignant clone.
As the name suggests, Follicular lymphoma demonstrates a proliferation of back-to-back follicles devoid of tingible body macrophages. Follicular centers are composed of a mixture of centrocytes and centroblasts. Follicular lymphoma is graded by counting the number of centroblasts per high power field in 10 neoplastic follicles. If this number is greater than 15, it is considered a grade 3, or high grade FL. The CD20 positive B-cells of follicular lymphoma are CD10 and BCL-6 positive cells that express BCL-2, consistent with neoplastic follicular cells.
This video has described garden variety follicular lymphoma. It should be noted that specific subtypes such as Pediatric-type follicular lymphoma, duodenal-type FL, and in situ follicular neoplasia exist; however, are outside the scope of today's discussion.
As their name suggests, diffuse large B-cell lymphomas are composed of diffuse sheets of large, clonal B-cells. Immunophenotypically, DLBCL can come in two main groups, the CD10 positive and CD10 negative. These phenotypic differences have prognostic relevance. As previously discussed, nodal and extranodal DLBCLs account for the most number of B-cell neoplasms This diagnosis is usually made in adults, with a mean age of 70 years. In general, these lesions present abruptly, are high-grade and carry a poor prognosis
From a biologic perspective, DLBCLs can arise de novo from their cell of origin, represent a large-cell transformation from a low-grade B-cell lymphoma, or arise in the setting of immune suppression or chronic inflammation. Distinction of germinal center b-cell type versus activated B cell type, which is also referred to as no
Hairy Mature Mom
Xvideos Masturbate Orgasm
Lesbian Lesbian Part 2

Mature B

Report Page