Download Free Medical Haematological Malignancies PowerPoint Presentation

Haematological Malignancies PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Haematological malignancies” by Otto Visser.

This medical PowerPoint presentation is about haematological malignancies, also known as blood cancers. Haematological malignancies are cancers that affect the blood, bone marrow, and lymphatic system. They are a diverse group of diseases that can affect people of all ages.

Three main types of haematological malignancies are Leukaemia, Lymphoma and Myeloma.

Tags : Haematological malignancies, blood cancers, Leukaemia, Lymphoma, Myeloma, Hematology, Hematology PowerPoint presentation

Published on : May 29, 2023 | Views : 1359 | Downloads : 1

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Introduction & haematological malignancies Otto Visser June 2019 Coding issues
Slide 2-

Introduction For most (solid) cancers, the primary site of the most important factor for the prognosis and the choice of treatment For other cancers, especially haematological malignancies, but also for an increasing number of solid cancers, the morphological classification is the most important factor
Slide 3-

How is a cancer diagnosis made? Clinical features Microscopy Large cells / small cells Specific characteristics (colour, amount of cytoplasm, type of cell nucleus, etc) Specific tests for proteins in the cytoplasm/cell nucleus/on the surface (immunohistochemistry) Immunophenotyping Cytogenetics
Slide 4-

1. Clinical diagnosis melanoma breast cancer Burkitt lymphoma
Slide 5-

2. Microscopy Small, mature cells with little cytoplasm, no mitoses (CLL) Large cells (cytoplasm ++), prominent nucleoli, mitoses (DLBCL)
Slide 6-

Expression of the estrogen receptor (ER) by using an immunostain for ER. The immunostain binds to the ER protein in the nucleus of the cancer cells and is detected by a positive brown colour 3. Immunohistochemistry
Slide 7-

Expression of HER2 by using an immunostain for HER2. The immunostain binds to the HER2 protein on the surface of the cancer cells and is detected by a positive brown colour 3. Immunohistochemistry
Slide 8-

4. Immunophenotyping Technique for the detection of proteins in the cell membrane of cancer cells Tissue Blood Bone marrow If a certain protein is absent of present this gives an indication for the type of cell
Slide 9-

4. Immunophenotyping
Slide 10-

5. Cytogenetics & molecular diagnostics Most cancer cells have ‘errors’ in the DNA (cytogenetic aberrations) With cytogenetics & molecular diagnostics these aberrations can be detected Many aberrations are not clinically relevant, but others are, because specific drugs can target specific cytogenetic aberrations, e.g. imatinib for BCR-ABL+ chronic myeloid leukaemia (‘targeted therapy’) Often, aberrations can be detected with different techniques
Slide 11-

5. Cytogenetics & molecular diagnostics Cell nucleus Chromosome Gene Protein
Slide 12-

Photo of the chromosomes Each (normal) cell has 46 chromosomes In cancer cells a (part of a) chromosome can be missing, duplicated or displaced 5. Cytogenetics: karyotyping
Slide 13-

Patient with MDS A part the long arm (q) of chromosome 5 is missing (=deletion) Diagnosis: MDS with 5q- Morphology code: 9986 5. Karyotyping: example
Slide 14-

5. Aberrations visible with karyotyping Deletion MDS with 5q- = M9986 Translocation  t(9;22) in CML =M9875 Inversion  AML with inv(3) = M9869 Trisomy (3 chromosomes in stead of 2)  Down syndrome (trisomy 21) Monosomy (1 chromosome in stead of 2) Hypodiploidy (<46 chromosomes)  hypodiploid ALL = M9816 Hyperdiploidy (>46 chromosomes)  hyperdiploid ALL = M9815
Slide 15-

5. Cytogenetics: Fluorescence in situ hybridisation (FISH) A fragment of RNA (‘probe’) is labelled with a fluorescent dye The probe binds to specific parts of the DNA (a gene or a larger part of the DNA) If the probe binds to a gene or part of DNA you see a fluorescent dot
Slide 16-

In CML there is a translocation of chromosomes 9 and 22 = t(9;22) Chromosome 9 is labelled red and chromosome 22 green. The normal situation is that you see 2 pairs of dots of the same colour (4 dots in total of each colour). If there is a combination red/green, the translocation is present. 5. FISH: example
Slide 17-

If a gene (or combination of genes = ‘fusion genes’) codes for a specific protein. The fusion gene in CML produces the protein BCR-ABL. The presence of the fusion gene BCR-ABL can be measured by detecting BCR-ABL RNA in the blood. 5. Molecular diagnostics
Slide 18-

Haematological malignancies
Slide 19-

Haematopoiesis (overview)
Slide 20-

ppt slide no 20 content not found
Slide 21-

Aim: To determine the cell type and ‘the normal counterpart’ To determine subtypes which are relevant for the prognosis and/or the treatment Classification of haematological malignancies
Slide 22-

Examples
Slide 23-

B-lymphocyte development with the malignant counterpart
Slide 24-

Classify to the most specific (WHO) diagnosis Use all information from the different diagnostics Take into account that indolent haematological malignancies can transform to aggressive haematological malignancies For lymphoid malignancies the site of the tumour (lymph node, bone marrow) can also give an indication for the tumour type Rules for classification
Slide 25-

Hodgkin lymphoma  lymph nodes Follicular lymphoma  mostly lymph nodes Lymphoplasmocytic lymphoma  bone marrow DLBCL  any site (including extranodal sites) T-ALL/LBL  bone marrow, thymus/mediastinal nodes Site of lymphoma
Slide 26-

New morphology codes in 2nd revision of ICD-O-3
Slide 27-

Changes in behaviour code in 2nd rev. of ICD-O-3 A non-malignant variant of the disease was recognized A malignant variant of the disease was recognized The disease was reclassified
Slide 28-

Langerhans histiocytosis: changes over time
Slide 29-

Hodgkin lymphoma: NLPHL versus classical HL NLPHL (~8% of all cases) higher survival, less aggressive treatment In the long run: risk of transformation to DLBCL NLPHL classical Reed-Sternberg cell (1900)
Slide 30-

CML: BCR-ABL+ versus atypical Atypical CML (~10% of all ‘CML’) Absence of t(9;22) No treatment with TKI (imatinib)  poor survival atypical BCR-ABL+
Slide 31-

De novo or as transformation of MDS or MPN In case of multiple diagnoses, code to the most specific category (1 > 2 > 3 > 4) With cytogenetic aberrations (9865, 9866, 9869, 9871, 9896, 9897, 9912) Myelodysplasia related (9895) Therapy related (9920) Other, not specified Acute myeloid leukaemia
Slide 32-

Examples Acute megakaryoblastic leukaemia (9910), therapy related (9920)  9920 Acute myeloid leukaemia, t(8;21) (9896), therapy related (9920)  9896 Acute myelomonocytic leukaemia (9867), t(8;21) (9896)  9896 Acute myeloid leukaemia
Slide 33-

EXERCISES
Slide 34-

ppt slide no 34 content not found