Fundamental differences from leukemias
Although both conditions belong to tumors of the hematopoietic and immune systems, there is a strict boundary between them. The main criterion is the localization of the primary malignant transformation.
In lymphomas, lymphocyte transformation never occurs in the bone marrow. The pathological process starts in peripheral structures:
- In the tissue of lymph nodes.
- In the lymphoid tissue of various internal organs.
- In other tissues and organs (a characteristic example is plasmacytoma, where the tumor substrate is located in the bones).
The second major difference lies in the nature of blood circulation: initially, tumor cells do not circulate in the peripheral blood. A solid, dense tissue node is formed.
Nevertheless, as the disease progresses, practically all lymphomas acquire the ability to disseminate. This process is called leukemization — malignant cells break through barriers, enter the systemic circulation, and secondarily seed the bone marrow. An important postulate of pathological anatomy: lymphoma can acquire the features of leukemia (leukemize), but the reverse transformation of leukemia into lymphoma is fundamentally impossible.
Pathogenesis and clinical manifestations
The development of lymphoma is accompanied by the uncontrolled proliferation of lymphoid tissue, which forms a mass lesion. This directly determines the leading clinical sign — compression syndrome.
Expanding conglomerates of lymph nodes compress neighboring anatomical structures. A typical and dangerous manifestation of such growth is the compression of major vessels, such as the development of superior or inferior vena cava syndrome, leading to severe hemodynamic disorders.
Since the source of the tumor is the immune system, its normal function suffers critically. Severe systemic failures occur:
- Immunodeficiency — the body's inability to respond adequately to infections.
- Autoimmunity — the paradoxical aggression of surviving or altered immune cells against the body's own healthy tissues.
Etiology and classification approaches
A significant role in the occurrence of lymphomas is played by background conditions. It has been proven that against the background of both congenital and acquired immunodeficiency states, the risk of developing lymphomas associated with the Epstein–Barr virus (EBV) increases manifold.
Globally, all lymphomas are traditionally divided into two major branches:
- Hodgkin's disease (also known as lymphogranulomatosis).
- Non-Hodgkin lymphomas.
The modern classification of tumors of the hematopoietic and lymphoid tissues proposed by the World Health Organization (WHO) is based on the histogenetic principle. To accurately determine the type of neoplasm, pathomorphologists require a comprehensive assessment. A combination of four parameters is taken into account simultaneously:
- Cytomorphological features (the structure of the cells themselves).
- Immunophenotypic markers (proteins on the surface and inside cells).
- Genetic abnormalities (chromosomal mutations).
- Clinical picture of the disease.
According to this approach, all hemoblastoses are divided into main types depending on the progenitor cell: myeloid, lymphoid, histiocytic, and tumors arising from mast cells.
Briefly: answers to topical questions
What cells are the specific morphological substrate of Hodgkin's lymphoma?
The specific morphological substrate of Hodgkin's lymphoma is Reed–Sternberg cells. The following names for these marker diagnostic elements are used in the literature:
- Reed–Sternberg cells (D.M. Reed) — international name.
- Berezovsky–Sternberg cells — name used in the RF.
By origin, they most likely represent transformed B cells of the germinal center of lymphoid follicles. In 70% of cases, the Epstein–Barr virus genome is detected in these cells.
What immunophenotypic markers are used to verify B-cell lymphomas?
For individual B-cell tumors, the sources indicate the following markers:
- Follicular lymphoma, Burkitt lymphoma, and diffuse lymphomas: CD19, CD20.
- Multiple myeloma: CD138 as a marker of plasma cells.
- B-cell chronic lymphocytic leukemia: CD19, CD20, CD23, SigIgM, IgD, and immunoglobulin light chains.
- Waldenström macroglobulinemia: prominent expression of CD19, CD20, CD22, and CD79a.
What chromosomal translocations are characteristic of Burkitt lymphoma?
Burkitt lymphoma is characterized by reciprocal translocations involving chromosome 8, which contains the proto-oncogene c-myc. The following variants of chromosomal rearrangements are distinguished:
- Translocation between chromosomes 8 and 14 — region 8q24 is transferred to 14q32 into the region of immunoglobulin heavy chain genes (IGH).
- Translocation to chromosome 2 — a fragment is transferred to the IGK gene locus (encodes the κ chain). Found in 10% of cases.
- Translocation to chromosome 22 — a fragment is transferred to the IGL gene locus (encodes the λ chain).
As a result, active immunoglobulin genes act as enhancers, causing overexpression of c-myc.
What stages are distinguished in the Ann Arbor clinical classification of lymphomas?
The cited sources describe the following Ann Arbor stage designations for extranodal lesions:
- IE — involvement is limited to the gastrointestinal tract: mucosa and submucosa, muscular layer, or serosa.
- IIE — involvement of nearest or distant regional lymph nodes; this category also includes serosal penetration and extension to adjacent organs and tissues.
- IIIE — lymph node involvement on both sides of the diaphragm in the specified classification scheme.
- IV — disseminated extranodal disease, distant metastases, including bone marrow involvement.
Remember the vector of transformation: "Lymphoma can become liquid (leukemization into the blood), but liquid leukemia will never become a solid lymphoma node."
Class and exam questions
Where does initial cell transformation occur in lymphomas?
The process is triggered strictly outside the bone marrow: in the lymph nodes, lymphoid tissue of various organs, or in the organs themselves (for example, in bones in plasmacytoma).
Can leukemia eventually transform into lymphoma?
No, this is pathogenetically impossible. The transition of leukemia into lymphoma is excluded.
Why do autoimmune reactions develop in lymphoma?
Since the tumor originates from tissue normally responsible for immunity, its malignant transformation disrupts the mechanisms of recognizing "self" from "nonself," causing autoimmunity and immunodeficiency.
What else to study on this topic
- Hodgkin's disease (lymphogranulomatosis): diagnostic criteria
- Group of non-Hodgkin lymphomas
- Superior and inferior vena cava syndrome
- Epstein-Barr virus as an oncogenic factor
- Principles of immunophenotyping according to WHO standards
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