NEOPLASMS Clonality

Alterations in genes regulating growth and behaviour

WHAT IS A TUMOR? occur in every cell monoclonal population
- A swelling
Inflammatory- abscess Cancer stem cells(CSC)
Neoplasm- growth Small subpopulation of cells within the tumor, retain
ability to undergo repeated cycles of proliferation &
Neoplasm migrate to distant sites to colonize-- called metastasis
 Abnormal growth of cells which persists after
initiating stimulus has been removed Express clonogenic sequences: colony forming ability
 Cell growth has escaped from normal regulatory
mechanisms Have chromosomal abnormalities reflecting genetic
 Classification accdg to morphology: instability >> progressive selection of clones that can
 Benign survive readily in the multicellular host environment
 Malignant

Alterations in growth control

Malignant neoplasm  Proliferation
 Growth of cells is uncontrolled  Cell death
 Cells can spread into surrounding tissue and spread  Factors regulating growth and response
to distant sites
 Cancer= a malignant growth Alterations in cellular interactions
 Cell to cell
 Cell to stroma
How do tumours develop?  Increased cell proliferation more cells enter cell
 There has to be a change to DNA cycle “speeded up”
 The change must cause an alteration in cell growth  Cells have changed life span
and behaviour  Alterations in cell death-decreased apoptosis
 The change must be non-lethal and be passed onto  Angiogenesis
daughter cells  Increased or decread growth factor receptors or
 Alteration is to more than one gene altered receptors
 Genes concerned are oncogenes/ tumour  Synthesis of growth factors- autocrine or paracrine
suppressor genes  Excess/modified growth control proteins e.g.
 Sequence of gene alterations from normal to benign oncoproteins
to malignant
 Intrinsic and extrinsic / inheritance and environment
key factors Differences between benign and malignant neoplasms
Benign
PIC:  Nuclear variation in size and shape minimal
Proto-Oncogenes:  Diploid
They promote the cell growth  Low mitotic count, normal mitosis
They turn the replication process possible  Retention of specialization
WHEN MUTATED -Oncogenes  Structural differentiation retained
 Organized
Oncogenes:  Functional differentiation usually
•Increase on transcription factors
•Transcription factors Malignant
receptor's activation  Nuclear variation in size and shape minimal to
•Signal molecules mutation marked, often variable
•Increase on the expression of anti apoptotic genes  Range of ploidy
CANCER  Low to high mitotic count, abnormal mitosis
 Loss of specialization
Tumor suppressing genes:  Structural differentiation shows wide range of
They can induce apoptosis or delay the cell cycle, in order changes
to have DNA reparation and to prevent uncontrolled  Not organized
cell replication  Functional differentiation often lost
WHEN MUTATED
Benign Malignant
Epithelial
Connective tisuue
Lymphoid/ haemapoietic
Germ cell

Benign
 Papilloma
 Squamous
 Transitional

 Adenoma
 glandular

Carcinomas
Squamous: skin
Transitional: bladder
Adeno: stomach, colon
Basal cell: skin

CT neoplasms
Smooth muscle: leiomyoma
Fibrous tissue: fibroma
Bone: osteoma
Cartilage: chondroma
Fat: lipoma
Nerve: neurofibroma
Nerve sheath: neurilemmona
Glial cells: glioma

Smooth muscle: Leiomyosarcoma

Bone: osteosarcoma
Fibrous tissue: fibrosarcoma
Cartilage: chondrosarcoma
Fat: liposarcoma
Nerve: neurofibrosarcoma
Nerve sheath: neurilemmosarcoma
Glial cells: malignant glioma

Malignant lymphoma (B and T)

Hogkins disease
BONE MARROW
Acute and chronic leukemia

GERM CELL TUMORS

Testis
Teratoma
Seminoma(Yolk sac tumor)

Ovary
Dermoid cyst
Mature cystic teratoma
Endodermal sinus tumor (Yolk sac tumor)