Cancer

General concepts of cancerGeneral concepts of cancer

Relevance of oncology:One-third of all individuals in the U.S.A.

Will develop some type of cancer during their lives.

Is the second cause of death in U.S.A.

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CANCERCANCER

NEOPLASM: SIR RUPERT WILLIS

ABNORMAL MASS OF TISSUE, THE GROWTH OF WHICH EXCEEDS AND IS UNCOORDINATED WITH THAT OF THE NORMAL TISSUES AND PERSISTS IN THE SAME MANNER AFTER CESSATION OF THE STIMULUS WHICH EVOKED THE CHANGE.

CANCER IN U.S.A.CANCER IN U.S.A.

YEAR 20001.22 MILLION NEW CASES OF

INVASIVE CANCER WERE DIAGNOSED

552,000 PEOPLE DIED FOR CANCERCAUSE 23% OF ALL DEATHS (only cardiovascular disease cause more

deaths)

CANCERCANCER

Gains in the treatment of nonresectable cancer have been gradual and have beeen focused on those malignancies characterized by unusual sensitivity to radiation and chemotherapy.

Survival rate at 5 years have been increased close to 50% as a result of progress in the early diagnosis and the therapy.

CANCERCANCER

The three most common cancers are:

LUNGBREASTCOLON/RECTUM

CANCERCANCER

ECONOMIC BURDEN: More than 10 billion dlls./year

SOCIAL IMPACT: The number of cases are increasing and are affecting young people every year.

THE NORMAL CELL CYCLETHE NORMAL CELL CYCLE

MITOSIS:Chromatin aligns itself and formed two identical daugther cells

G1:DNA synthesis ceases (rest period)

S phase:Unknown signal/ increase of DNA and RNA synthesis

G2: DNA synthesis stop

GO: Aditional resting period

CANCERCANCER

The relevance of knowing the “cell Cycle” is for a better understanding

of the mechanism of action of cancer chemotherapy drugs.

CANCERCANCER

Is a Disorder of cellular homeostasis in which there is lost of the normal growth controlling mechanisms.

The characteristics of cancer The characteristics of cancer cells are:cells are:

Clonality: Originates from a SINGLE STEM CELL that change in it`s behavior

Autonomy: The growth rate is unrestrictedAnaplasia: Lack of normal, coordinated

cellular differentiation.Metastasis: Dissemination to other parts of

the body.

Abnormalities of cancer cellsAbnormalities of cancer cells

– Abnormal DNA synthesis– Membrane cells alterations– Cytoplasmic alterations– Increase ATP asa activity (Anaerobic shift)– Increase levels of proteolytic enzymes– Angiogenesis factor synthesis

ONCOLOGY DEFINITIONSONCOLOGY DEFINITIONS

DIFFERENTIATION: Degree of morphologic and functional resemblance to comparable normal cell.

ANAPLASIA: Lack of “differentiation”, is a cancer marker.

ENCAPSULATION: Induction of peripheral fibrosis, characteristic of

“benign” neoplasm www.freelivedoctor.com

ONCOLOGY DEFINITIONSONCOLOGY DEFINITIONS

INVASION/INFILTRATION: Unrestricted permeation into contiguous structures, characteristic of “malignant” neoplasms.

METASTASES: Remote distant tumor implants from the primary neoplasm.

LOSS OF GROWTH CONTACT INHIBITION RATE.

DOUBLING TIME: Time required by the tumor to double in size.

CANCERCANCER

Oncogenesis:Are those changes induced by oncogenic

factors in the normal cellular behavior which lead to the development of malignant/ cancer behavior of cells

CANCERCANCER

ETIOLOGY: Cancer incidence vay with age, sex, race and geographic location. Hereditary traits have been obseved, also variations in diet and exposure to chemical and physical agents in the external environment contribute to the development of neoplasia.

Differences between benign Differences between benign and malignant tumor cellsand malignant tumor cells

Characteristics Benign Malignant

Growth Expansile(Capsule)

Infiltrative (notencapsulated)

Vascularity Slight Increased(Angiogenesisfactor?)

Metastases None Present (loss ofcohesiveness)

Differences between benign and Differences between benign and malignant tumor cellsmalignant tumor cells

Characteristics Benign MalignantUlceration Unusual CommonCytologic

Ultrastructure

Normalnuclear tocytoplasmicratio. Fewmitoses.Normal

Increasednuclear tocytoplasmicratio.>Mitoses.<Mitocondriaand <endoplasmicreticulum

ETIOLOGIC MECHANISMETIOLOGIC MECHANISM

GENETIC FACTORS

VIRUS DNA -RNA

CHEMICAL CARCINOGENS

PHYSICAL CARCINOGENS

OTHERS

GENETIC FACTORSGENETIC FACTORS

Proposed mechanism are: I-Genes which are deregulated and excessively

expressed, displaying dominant genetic activity. II-Genes which are supressors of tumorigenic

genetic activities and are recessive in that both alleles must be lacking for malignacy occur.

The inheritane patterns are generally autosomal dominant, with varying penetrance.

CHEMICAL CARCINOGENSCHEMICAL CARCINOGENS

Tobacco smoke: (Tar)Polycyclic hydrocarbonsNitrosamines

DiethylstilbestrolEstrogensAlkylating agentsAzathyoprineMethrotexateMany others

DIRECT-ACTING

ALKYLATINGAGENTS (H2N)SODIUMARSENITE

SKINCANCERSGICANCERS

ACTIVATEDMETABOLITES

*AROMATICHYDROCARBONS*DYES*COAL TARPRODUCTS

LUNGBLADDERSKINGI Ca.

METALS

MOLDPRODUCTS

CHROMIUMNICKELASBESTOS

AFLATOXINBRACKENFERN,CYCAD NUT

LUNG Ca.

MESOTHELIOMAGI Ca.

PHYSICAL CARCINOGENSPHYSICAL CARCINOGENS

ULTRAVIOLET LIGHT

IONIZING RADIATION

ONCOGENIC VIRUSESONCOGENIC VIRUSES

Viruses have been implicated as the direct cause of only one human cancer.

The HTLV-I (human T-lymphotrophic virus can lead to adult T-cell leukemia.

Several others are closely associated but have to be taken only as cofactors in oncogenesis.

ONCOGENIC VIRUSESONCOGENIC VIRUSES DNA VIRUS: PAPILOMA VIRUS (WARTS, C.U. Ca.,

Anogenital cancer)

HERPES SIMPLEX (C.U. Carcinoma)

EPSTEIN-BARR (Burkitt`s Lymphoma, Nasopharyngeal carcinoma)

Hepatitis B (Hepatocellular carcinoma)

ONCOGENIC VIRUSESONCOGENIC VIRUSES

RNA virus: Mainly transcriptase reverse virus

AIDS virus (Kaposy`s sarcoma, primary C.N.S. Lymphoma)

HTLV-I and II (T leukemia)

GENERAL AND LOCAL GENERAL AND LOCAL EFFECTS OF CANCEREFFECTS OF CANCER

Cancer can kill the patien by:

Local effectsSystemic effects

LOCAL EFFECTS OF LOCAL EFFECTS OF CANCER ON HOSTCANCER ON HOST

OcclusionDestruction of critical structuresUlcerationTumor infarctionAbscess formation

LOCAL EFFECTSLOCAL EFFECTS

Occlusion at the level of: Airways Gastrointestinal tract Blood vessels Lymphatic channels Urinary tract Biliary tract Heart (valves/pericardium) Cerebro-spinal fluid system

LOCAL EFFECTSLOCAL EFFECTS

DESTRUCTION OF CRITICAL STRUCTURES:

Large blood vessels (aorta, carotid, etc.)Pituitary glandC.N.S.SkullBones

SYSTEMIC EFFECTS OF SYSTEMIC EFFECTS OF CANCER ON HOSTCANCER ON HOST

Cachexia

Hormone and hormone-like production

Paraneoplastic syndromes

PARANEOPLASTIC PARANEOPLASTIC SYNDROMESSYNDROMES

Paraneoplastic syndromes are related to “remote” effects of cancer cells on the host, whic are not attributable to functions of the original normal tissue

Paraneoplastic syndromes resembles other clinical endocrine, neurologic and coagulation clinical syndromes, but, by definition the clinical abnormalities are due to systemic effects produced by the cancer cells.

Relevance of paraneoplastic syndromes remains on two facts:

1.- As explained before, these syndromes have a different etiology and sometimes different mechanisms of production, by then, treatment of the clinical abnormalities have to be different also.

2.- Some paraneoplastic syndromes dissapear completely after removal of the cancer, while some of the resembled clinical syndromes have not cure. This fact, makes more important the differential diagnosis between them.

PATHOPHYSIOLOGYPATHOPHYSIOLOGY

The pathophysiology of paraneoplastic syndromes remains unclear, but some proposed mechanisms are:

1.- Hormone & hormone “like” synthesis 2.- Synthesis of identifiable chemical mediators 3.- Production of auto-inmune responses 4.- Activation of factors of the coagulation system

1.- HORMONE & HORMONE 1.- HORMONE & HORMONE “LIKE” SYNTHESIS( ectopic “LIKE” SYNTHESIS( ectopic

hormone secretion)hormone secretion)

Gene derepression

Cellular dedifferentiation

Cellular arrested differentiation

2.- SYNTHESIS OF 2.- SYNTHESIS OF IDENTIFIABLE CHEMICAL IDENTIFIABLE CHEMICAL

MEDIATORSMEDIATORS

ProstaglandinsInterleukinsTumor necrosis factorNeurotransmitters / Neurohormones

3.-PRODUCTION OF 3.-PRODUCTION OF AUTOIMMUNE RESPONSESAUTOIMMUNE RESPONSES

Auto-antibodies

Cross reactions

4.- ACTIVATION OF 4.- ACTIVATION OF COAGULATION SYSTEM COAGULATION SYSTEM

FACTORSFACTORS

Increased Coagulation

Increased Fibrinolysis

ECTOPIC HORMONE ECTOPIC HORMONE SYNDROMES IN NON-SYNDROMES IN NON-ENDOCRINE TUMORSENDOCRINE TUMORS

Hypercortisolism (Cushing`s sd.) A.C.T.H. Synthesis C.R.H. Synthesis Etiology: Lung cancer (small cell type) 50%

Carcinoid tumorThymomaBronchial adenoma (Benign neoplasia)Medullary thyroid carcinoma

HypercalcemiaHypercalcemia

Without bone metastasis:

Prostaglandin synthesis (PGE2)

Interleukin 2-Osteoclast activating factor

P.T.H. secretion

HYPERCALCEMIA HYPERCALCEMIA ETIOLOGYETIOLOGY

Multiple myelomaSolitary plasmocytomaLung cancerLeukemiaLymphoma (Hodgkin and Non-hodgkin)Breast cancerRenal carcinoma

INAPPROPIATE SECRETION OF INAPPROPIATE SECRETION OF ANTIDIURETIC HORMONEANTIDIURETIC HORMONE

This particular syndrome “could be”associated with neoplasias and some pulmonary infections.

Etiology:Small cell carcinoma of the lungCarcinoid tumorPulmonary tuberculosisPneumonia ( Bacterial and viral)

HypoglicemiaHypoglicemia

Ectopic insulin production Insulin “like” hormone production

(somatomedins). Etiology: Gastric carcinoma Uterine fibroma Uterine fibrosarcoma Retroperitoneal fibrosarcoma Neuroma

SECRETION OF CHORIONIC SECRETION OF CHORIONIC GONADOTROPINGONADOTROPIN

Clinical features:Male: Female:

– Gynecomastia *Amenorrhea– Infertility *Menstrual disorders– Impotence (hyper-hypo)– False (+) pregnancy test *Infertility

*False (+)

pregnancy test

SECRETION OF CHORIONIC SECRETION OF CHORIONIC GONADOTROPINGONADOTROPIN

Etiology:Lung carcinomaGastric carcinomaOvarian carcinomaPancreatic carcinomaHepatoma

OTHER HORMONE OTHER HORMONE RELATED SYNDROMESRELATED SYNDROMES

T.S.H. Production Prolactin Growth hormone V.I.P. (Vasoactive intestinal polipeptide) Gastrin Bombesin Glucagon Erythropoietin

NEUROMUSCULAR NEUROMUSCULAR PARANEOPLASTIC SYNDROMESPARANEOPLASTIC SYNDROMES

Myasthenia gravis: Thymoma

Mechanism: Auto-antibodies against the acetilcholine receptor at the “motor end” plate.

Myasthenic syndrome (Lambert eaton syndrome) Etiology: Small cell carcinoma of the lung Mechanism: Auto-antibodies against the calcium

channels on the motor nerve terminals, which interfere with the Ach release.

CANCER ASSOCIATED CANCER ASSOCIATED RETINOPATHYRETINOPATHY

Etiology: Small cell carcinoma of the lung

Mechanism: Immunoglobulins against several polypeptide or protein antigens in the retinal and tumor cells. (Cross reaction)

Clinical picture: Proggressive loss of visual acuity

CEREBELLAR CEREBELLAR DEGENERATIONDEGENERATION

Etiology: Small cell carcinoma of the lung• Ovarian cancer

• Mechanism: • 1.-Immunoglobulins that react

selectively with cerebellar purkinje cells.• 2.-Associated viral c.n.s. Infections• 3.-Side effects of chemotherapy

PERIPHERAL NEUROPATHYPERIPHERAL NEUROPATHY

( 15% of all cancer patients) Sensory neuropathy

Motor neuropathy

MECHANISM:

*Unknown

*Auto-antibodies against axonal components

*Side effects of chemotherapy

HEMATOLOGIC PARANEOPLASTIC HEMATOLOGIC PARANEOPLASTIC SYNDROMESSYNDROMES

PolycytemiaHemolytic anemiaThrombocytopenic purpuraCoagulopathy

POLYCYTEMIA POLYCYTEMIA ( ERYTHROCYTOSIS)( ERYTHROCYTOSIS)

Etiology: Cerebellar hemangioblastoma Uterine benign fibroma Pheochromocytoma Adrenocortical carcinoma Hepatoma / carcinoma Ovarian cancer Mechanism: Ectopic production of erythropoietin

HEMOLYTIC ANEMIAHEMOLYTIC ANEMIA

Etiology:Lymphoid malignanciesLung carcinomaBreast cancerG.I. CarcinomaMechanism: Immune mediated hemolysis

(cross-reaction)

PARANEOPLASTIC PARANEOPLASTIC COAGULOPATHIESCOAGULOPATHIES

Hypercoagulability (thrombosis Prone)

Etiology: Pancreatic carcinoma

DISSEMINATED INTRAVASCULAR DISSEMINATED INTRAVASCULAR COAGULATION (D.I.C.)COAGULATION (D.I.C.)

Mucin producing adenocarcinomas (G.I. Tract)

Prostatic carcinomaAcute myeloblastic leukemia type IV

BLEEDING TENDENCY (CLOTTING BLEEDING TENDENCY (CLOTTING FACTOR DEFFICIENCIES)FACTOR DEFFICIENCIES)

Lymphomas : Antibodies against clotting factors

Amiloid deposit: Factor “X” defficiency

Hepatic carcinoma : Deffective fibrinogen

CAQUEXIA / MALNUTRITIONCAQUEXIA / MALNUTRITION

There are several mechanism proposed to explain the severe emaciation of patients with cancer.

Direct effect at G.I. Tract Obstruction of the lumen (dysphagia) <Gastric emptying with a fullness sensation <Gastric secretion /digestion <Small intestine digestion /absorption Increase Motility / secretion (GIP-VIP) Parasitic effect of the tumor

ANOREXIA OF CANCER PATIENTSANOREXIA OF CANCER PATIENTS

Proposed mechanism are alterations in:Smell and taste, by altered glucose & A.A.

MetabolismSecretion of inhibitory peptidesCachectin substanceCancer treatment: Chemotherapy-

Radiotherapy-Surgery-Morphine

FUNCTIONAL BEHAVIOR OF FUNCTIONAL BEHAVIOR OF NEOPLASMNEOPLASM

Functional tumors

Ectopic hormone syndromes

Paraneoplastic syndromes

HORMONE AND HORMONE-LIKE HORMONE AND HORMONE-LIKE PRODUCTIONPRODUCTION

Thyroid Ca. Hypo /hyperthyroidismAdrenal Ca. Hypo/HypercortisolismPituitary tumors Prolactin, growth h.Pancreatic Ca. Insulinoma,

Gastrinoma VIPomaOvarian Ca. Hypo/Hyperestrogen. Testicular cancer Hyperandrogenism,

Precocious puberty

Cancer

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