Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
Oncology
Root words
Normal cells
Cancer cells
Cell cycle
10 leading cancer sites
3 categories of cell proliferation
ONCOLOGIC NURSING
Group of many diseases of multiple causes that can arise in any cell that is able to
evade regulatory control over cell proliferation and differentiation
Disease process that begins when an abnormal cell is transformed by genetic
mutation
Study, detection, treatment, and management of cancer and neoplasia
Neo- New A- None
-plasia Growth Ana- Lack
-plasm Substance Hyper- Excessive
-trophy Size Meta- Change
-oma Tumor Dys- Bad, deranged
-stasis Location
Senescence
- Cells grow old Die
- Programmed cell death
- Normal cell has capacity to divide 50-60 times
- Chromosomal end is protect by telomere (biological clock) to protect DNA
Apoptosis
- Suicide of cell
- Cell death that happens in event of serious damage or when theres loss of
regulation
Apoptosis and senescence are defective Abnormal cells continue to divide
Malignant cell membranes contain tumor specific antigen (TSA)
(E.g. Carinoembryonic antigen [CEA], prostate specific antigen [PSA])
Malignant cell membranes contain less fibronectin (cellular cement)
Cancer cells have larger nucleoli
Cancer cells are less dependent on oxygen, glucose, and serum growth factors
Gap 0 (G
0
) Resting phase (quiescence)
Gap 1 (G
1
) Normal cell activity, increase in size, getting ready for DNA synthesis
Synthesis (S) DNA replication/synthesis
Gap 2 (G
2
) Pre-mitotic, protein synthesis for cellular division
Mitosis (M) Mitosis (cells chromosomes divide between two daughter cells) and
cytokinesis (cytoplasm divides in half forming distinct cells)
- Prophase: Spindle forms, centrioles move to opposite pols, chromosomes
become visible
- Metaphase: Chromosomes line up along equator
- Anaphase: Centromeres divide, chromatids separate and move to opposite poles
- Telophase: Nuclear membrane forms around each group of chromosomes,
chromosomes unwind, cytokinesis begins (one cell becomes two individual cells)
1. Breast
2. Lung
3. Liver
4. Colon/rectum
5. Cervix
6. Leukemia
7. Stomach
8. Prostate
9. Brain/nervous system
10. Ovary
Static tissues: Those in brain; do not retain capacity to divide
Expanding tissues: Cells in liver, kidney, endocrine glands; stops growing when
reaches adult size but can multiply in times of physiologic need
Renewing: Blood cells, epithelial cells of GI mucosa, germ cells; constantly replacing
Proliferative patterns
Benign vs. malignant
Tumor name according to
parenchyma, organ, or cell
Pattern and structure
(gross or microscopic)
Embryonic origin
Benign tumors
Malignant tumors
Names according to other tissue
types
Dysplasia Bizarre cell growth Differ in size, shape, arrangement
Hyperplasia Increase in number of cells
Metaplasia Conversion of one type of cell to another type (Ex:RoundRectangle)
Neoplasia Uncontrolled cell growth following no physiologic demand
Anaplasia Cells lack normal cell characteristics, differ in shape and organization
Benign Characteristic Malignant
Slow Speed of growth Rapid
Remains localized Mode of growth Infiltrates surrounding
tissues
Well differentiated mature
cells, poor cell function
Cell characteristic Poorly differentiated
(anaplastic)
Encapsulated Capsule Not capsulated
Extremely unusual when
surgically removed
Recurrence Common following surgery
Never occur Metastasis Common
Not harmful to host Effect of neoplasm Always harmful
Very good Prognosis Poor
Hepatoma Liver Melano Pigment cell Lipo Fat
Osteoma Bone Adeno Gland Myelo Bonemarrow
Myoma Muscle Chondro Cartilage Cysto Bladder
Lympho Lymph nodes Hemangio - Vessels
Fluid filled Cyst Finger-like Papillo
Glandular Polyp Stalk Polyp
Ectoderm Usually gives rise to epithelium (brain)
Endoderm Usually gives rise to glands (GI system)
Mesoderm Usually gives rise to connective tissue (muscles and bone)
-OMA suffix is used
LipOMA Adipose tissue AngiOMA Blood vessels
OsteOMA Bone FibrOMA Fibrous tissues
MyOMA Muscle
Named according to embryonic cell origin
1. Ectodermal, endodermal, glandular, epithelial
-CARCINOMA suffix is used
Pancreatic adenoCarcinoma
Squamous cell Carcinoma
2. Mesodermal, connective tissue
-SARCOMA suffix is used
FibroSarcoma Fibrous tissue
MyoSarcoma Muscle
AngioSarcoma Vessel
Lymphomas Cancers originating in infection-fighting organs (lymph nodes)
Leukemias Cancers originating in blood-forming organs
Germ cell tumor Tumors derived from totipotent cells (testlcle and ovary)
Blastic tumor/blastoma Tumor resembles an immature or embryonic tissue; most
common in children; usually malignant if has blast (Wilms tumor)
Exceptions to the rule
Classifications of tumors
Proposed molecular cause of
cancer
Genes in DNA
Carcinogenesis
Three phases of
carcinogenesis
Body defenses against tumor
Metastasis
Tissue of origin Benign Malignant
Connective tissue
Bone
Fibrous tissue
Adipose tissue
Cartilage
Osteoma
Fibroma
Lipoma
Chondroma
Osteosarcoma
Fibrosarcoma
Liposarcoma
Chondrosarcoma
Epithelial Tissue
Glandular
Surface
Blood vessels
Adenoma
Papilloma
Hemangioma
Adenocarcinoma
Squamous cell carcinoma
Angiosarcoma
Hematopoietic
Erythrocytes
Granulocytes
Lymphatic tissue
Erythroleukemia
Leukemia
Hodgkins disease,
malignant lymphoma
Lymphocytes Lymphocytic leukemia
Plasma cells Multiple myeloma
-OMA but malignant: HepatOMA, lymphoma, gliOMA, melanoma
Three germ layers: Teratoma
Non-neoplastic but OMA: ChoristOMA, hematOMA
Solid Associated with organs from which they develop (Ex: breast cancer)
Liquid Originate from blood-forming tissues (leukemias, lymphomas, myelomas)
Change in DNA structure Altered DNA function Cellular aberration Cell
death Neoplastic change
Proto-oncogene
Anti-oncogene (tumor suppressor gene)
Process which normal cells are damaged Cells lose normal control mechanisms
of growth Proliferate out of control
1. Initiation Conversion of normal cell to tumor cell
Must be an initiator (carcinogen) agent that permanently alters DNA structure
Example: Radiation
2. Promotion Genetic expression of cell is altered
Increasing DNA synthesis, increasing number of copies of particular gene, altering
intracellular communication
3. Progression Cells lead to morphologic changes and malignant behavior
1. T-cell system (thymus gland) / Cellular immunity
Cytotoxic T-cells kill tumor cells
2. B-cell system (bone marrow) / Humoral immunity
B-cells can produce antibodies
3. Phagocytic cells
Macrophages can engulf cancer cells
Genetic mutation of cellular DNA
Abnormal cloning and proliferation
Tissue infiltration (access to lymph nodes and blood vessels)
Cancer cells spread to other areas of body through systemic circulation
Metastasis
Mechanisms of metastasis
Four most common sites of
metastasis
Common sites of metastasis
Etiology of carcinogenesis
Lymphatic spread Via lymphatic circulation
Hematogenous spread Via blood stream
Angiogenesis Release of growth factors and enzymes such as vascular endothelial
growth factors (VEGF) Growth of new capillaries Malignant cells get nutrients
and oxygen Cancer enters circulation
Lungs
Liver
Brain
Bones
Bladder cancer Liver, lung, bone, pelvis
Brain tumors CNS
Prostate cancer Liver, lung, vone, spine, kidneys
Breast cancer Liver, lung, bone, brain
Testicular cancer Liver, lung, bone, adrenal glands, lymph nodes
Colorectal cancer Liver
Familial or genetically orient carcinomas Defective genes are inherited
Examples: Hereditary retinoblastoma, breast cancer, colorectal cancer, lymphomas
Viral carcinogenesis Viruses incorporate themselves into genetic structure
Altering future generations of that cell population
Example: Epstein-Carr virus (Burkitt lymphoma, some cases of Hodgkins)
Bacterial carcinogenesis H. pylori has been associated with increased number of
gastric malignancy
Hormonal agents DES, OCP, especially estrogen
Immune disease AIDS
Dietary carcinogenesis Fats, alcohol, salt-cured or smoked meats, nitrate
Chemical carcinogenesis Free radicals interact with cellular DNA
Examples: Tobacco, vinyl chloride, metals, benzene, 2-napthylamine
Physical carcinogenesis Exposure to sunlight or radiation