Pathophysiology

Underactivity of those genes causes tumors (thus tumor suppressor genes).
They include retinoblastoma (normally prevent cell division), TP53 (initiates apoptosis if DNA damage)

Initiation: Exposure to carcinogenic agent (physical, chemical, biological) which changes the genome. Most susceptible are those actively synthesizing DNA
Promotion: growth of cells, triggered by growth factors. reversible if promoting substance is removed
Progression: tumor gets malignant (cells no longer need stimuly)

Blood test for tumor markers, cytologic studies and tissue biopsy, endoscopic examinations, ultrasonography, x-ray, MRI, CT, PET

Antigens expressed on the surface of tumor cells, or substances released from normal cells in presence of tumors.
Some substances (like hormones) become overexpressed with cancer

Papanicolau test, cytologic method to detect cancer. Microscopyc examination to detect abnormal cells. Tissue removed via biopsy

Grading: according to cellular characteristscs (I- IV)

or

Staging: according to the spread of disease  (TNM)

T: size and local spread of primary tumor
N: involvement of regional lymph nodes
M: extent of metastatic involvement

Curative
Control
Palliative (relieving pain without dealing with the cause)

Surgery: First treatment with solid tumors (if small and well defined margins, large and intertangled tumors not really possible)
Radiation therapy: alone or adjuvant (additive to..), High energy particles destroy cancer cells (affects fast proliferating more because it destroys DNA), palliative treatment too...
Chemotherapy: Kills cells by stopping DNA, RNA and protein synthesis and preventing cell mitosis. Systemic treatment (reaches distant sites)
Hormonal therapy: Disrupt hormonal environment (disrupt signals that stimulate them, if receptors available).
Biotherapy: involves immunotherapy (stimulate own immunesystem to attack cancer)

A posterior lobe (neural component): secretes oxytocin (targets breasts, chemical messenger in brain) and antidiuretic hormone (targets kidney and blood vessle, important in conserve the fluid volume)

and the anterior glandular lobe: secretes ACTH (controls release of cortisol from adrenal gland), TSH (controls thyroid hormone), FSH (regulates fertilit), LH (regulates sex hormone) and growth hormone

Decreased secretion of pituitary hormones (congenital or a variety of abnormalities).

Occure gradually. Cronically unfit with weakness and fatigue, loss of appetita, impairement of sexual function.
ACTH (adrenocorticotropic hormone) is the most serious. GH (Growth hormone) typically first to be lost)

Growth Hormone (GH): stimulates growth, regulates metabolic functions
Luteinizing Hormone (LH): regulates sex hormones (ovaries, testes)
Follicle-stimulating hormone (FSH): regulates fertility (ovaries, testes)
Thyriod stimulating hormone (TSH): Control release of thyroid hormones
Adrenocorticotropic hormone (ACTH): Corntrols release of cortisol from adrenal gland
 

Treat and identify cause.
Cortisol replacement when ACTH deficiency is present (same for other hormones)

Necessary for growth and regulation of metabolic functions. Facilitates protein synthesis. Increases use of fatty acids for fuel, and blood glucose level. Induces insulin resistance.
Regulated by hypothalamic hormones.

Abnormalities can lead to dwarfism or gigantism (in adults only tissue grows but not bone anymore)

Acute lymphocytic leukemia (ALL): lymphocytic progenitor defect

Chronic lymphocytic leukemia (CLL): differentiated lymphocyte defect

Acute myelogenous leukemia (AML): myeloid progenitor defect

Chronic myelogenous leukemia (CML): myeloid pluripotent cell defect

Acute: Cancer in hematopoietic progenitor cells. Sudden onset, symptome related to depressed bone marrow function

Chronic: Cancer that involve the proliferation of more fully differentiated cells. Slow or fast onset, symptoms related to infiltration of bone marrow and lymphoid tissues

T-cells (thymus:  cell mediated immunity)

B-cells (bone marrow: humoral immunity (related to antibodies))

NK-cells (Natural Killer: modulate macrophages and t-cells, are cytotoxic)
 

largely unknown but riskfactors are hig levels of radiation, exposure to benzen and unknown toxins, drugs, chemicals and gases. 
May occur as secondary cancer after aggressive chemotherapy

Acute lymphocytic leukemia affects precursors of B or T-lymphocytes (also called lymphoblasts). Cause numeric and structural changes in the chromosomes and thus dysregulate expression and function of transcription factors required for normal hematopoietic (process to develop blood cells) cell development

Most frequently in children. Abrupt onset of symptoms like fatigue (resulting from anemia), fever, night sweats, weight loss (due to rapid proliferation of leukemic cells), bleeding (decreased platelets) bone pain (BM expansion), infections (low concentration of neutrophils)

Affects the myeloid precursor cells by alterations in genes that inhibit differentiation (mostly). Thus normal marrow elements are replaced by accumulations of undifferentiated blast cells. Leads to anemia, low neutrophils and thrombocytes

 (Same as ALL)

Most frequently in children. Abrupt onset of symptoms like fatigue (resulting from anemia), fever, night sweats, weight loss (due to rapid proliferation of leukemic cells), bleeding (decreased platelets) bone pain (BM expansion), infections (low concentration of neutrophils)

Proliferation of more fully differentiated lymphoid cells is disturbed. Usually high count of nonfunctional lymphocytes.

Sometimes years without therapy, other times deadly rabidly. Symptoms due to infiltration of bone marrow and lymphoid tissues and secondary immunologic defects.
Growing and newly involved lymph nodes, fever, abdominal pain, weight loss, anemia and rise of lymphocyte count

Disorder of myeloid pluripotent progenitor cells, characterised by excessife proliferation of granulocytes (fight bacterial infections), erythroid precursors and megakaryocytes (plateletes) which are often non functioning.
High WBC count (immature granulocytes), anemia and too little (functioning) plateletes
 

Three phases, 1. Chronic phase of variable length: slow onset non-specific symptoms (weakness weight loss)

2. Short accelerated phase: enlargement of spleen and more symptoms. fever, sweating, bone pain (growing BM), weight loss (rapid proliferation), bleeding and easy bruising (low functioning platelete count)

3. Terminal blast crisis phase: increased numer of myeloid precursors in blood. Spleen increases signigicantly due to high WBC count and infiltration of leukemic cells in skin, lymph nodes, bone and CNS

Cancer of the lymphatic system, can arise from B and T lymphocytes.

Hodgkin (arises in a single node/node chain) and non-Hodgkin (B-,T-, or NK-cell origin)

B-,T-, or NK cell origin (lymphocytes) of different sites. Most commonly B-cell.

The tumors resemble primary lymphoid follicles and secrete cytokines, induce T-cell exhaustion and apoptosis and interacts with T-cells to promote survival and proliferation

Believed to be environmental, genetic and other unidentified factros. May also involve virus infections

Depends on lymphoma type involved (B,T,NK) but generally rapidly fatal if untreated.

Usually painless, but can change more agressive forms (or leukemia) are developed. Leads to fever, sweat, weight loss, increased susceptibility to infections.

largely unknown. Could be carcinogens and viruses but also genetic and immune mechanism but not prooven.

Arise in a single node or a chain of nodes. Presence of large, atypical mononuclear tumor cells (reed-sternberg cells). 

Painless enlargement of lymph nodes. Chest discomfor and dyspnea (shortness of breath), fever, weight loss.
anemia and fatigue if diseas is spread. Can also affect spleen, liver, lungs and CNS.
Finally leads to immunologic defects (cell-mediated immunity) -> more infections