kuliah dasar molekuler kanker, karsinogenesis, dan interaksi seluler - prof dr ambar mudigdo.ppt

BLOK NEOPLASMA

Prof.Dr.Ambar Mudigdo, dr, Sp.PA(K)

Basic science clinical practice

PromotifPreventifCuratif manageRehabilitatif

Cause of disease : 1.Enviromental factors2.Genetic factor’s

Diagnostik1.Curatif Manage Perawatan

Theraphy

Etiologi : CausaPredisposisiFaktor berperan

2. Patogenesis : proses /mekanisme, step by step “Pathway & mechanism”

3. Morphologi changes :Sub sel:protein,DNA/RNA,gen,Sitokin

Micros SelJaringan

OrganMacrosSistem

4. Functional changes : Hipo function Hiper function Others

Clinical signal simptoms

1.Labil cells rapid prolif gut lining

and turn over apitelial cells2.Stable cells slow-prolif

hepatocyt and turn over

3.Permanent cells not able to prolif neurones

1. Reduced oxygen supply2. Physical agents3. Chemical agents4. Micro organism5. Abnormal immunologic rx6. Nutritional deficiency7. Genetic abnormalities

To explain : - Why - How

Patologi : general pathsystem path

General path - Basic reactionSistem path- Spesific resp/organ

4 major aspecs : 1. Etiologi 2. Pathogenese 3. Morphologic changes 4. Functional changes (clinical sign &

symp)

Physiological proliferation : 1. In somatic growth during fetal

development2.Regeneration : blood cells, mucosa

cells, skin cells (rapid cell turn over)3.Slower cell turn over : liver tissue,

kidney, etc.

1. Increase in size of individual cellshypertrophy

2. Increase in the number of cellshyperplasia

3. More common : combination 1&2

A. Physiological enlargement : muscle, uterus, breast

B. Pathological enlargement :result of disease processeg: increased myocardial cell

Hipertropi : myocardium (enlargement of the heart)

Hiperplasia : - chronic iritation : skin in chronic inflamation- imbalance of hormonal activity : prostat in old age

Hipertropi : myocardium (enlargement of the heart)

Hiperplasia : - chronic iritation : skin in chronic inflamation- imbalance of hormonal activity : prostat in old age

Metaplasia : change from one type to another (frequently associated with hiperplasia) in lining epithelia or in conective tissue.

Displasia :disordered growth (frequently precursor of malignancy)e.g : uterine cervic

1. Progressive : from few cells large tumor

2. Purposeless : irregular, unstructured3. Effects on surrounding tissue : compreses4. Not related to needs of the body : distruction5. Parasitic : blood supply

1. Intrinsik : - Lesi genetik- Metabolism- Hormonal - dll

2. Ekstrinsik :- Mikrobiologi- Chemical- Physical- Nutritional- dll

1.Non neoplasma2.Neoplasma

Klinik : BENIGNA MALIGNA

Histol : MESENCHYM EPITEL

-hemopoetic -neuroectoderm

LEVEL : TUBUH

SYSTEM

ORGAN

JARINGAN

SEL

SUB SEL = CHROMOSOM GEN DNA-RNA /PROTEIN

BENIGN : + OMA → ADENOMA FIBROMA LIPOMA OSTEOMA

MALIGNA : EPITEL : + CARCINOMA →ADENO CA

MESENCHYM : + SARCOMA → FIBRO SA

1. Proliferasi tak terkendali2. Progresive3. Purpuseless4. Efek Θ jaringan sekitar/distructive5. Tak bermanfaat6. Parasitik7. Tak tergantung growth factor8. Less adhesive9. metastatic

BENIGNA MALIGNA

DEFERENSIASI Mature/baik immature / jelek Morfologi sel seperti normal abnormal Pertimbuhan lambat cepat Invasi Θ + Kapsul + Θ Efek yang ditimbulkan kompresi invasi destruksi Gerakan mobil fixedResidif Θ +Klinis desakan destroysOperasi → baik →kombinasi Metastase Θ +Prognose baik buruk

1. MULTI FAKTOR1. MULTI FAKTOR 2. MULTI HIT2. MULTI HIT 3. MULTI STEP3. MULTI STEP

1.Faktor external : Lingkungan polusi Budaya Karsinogen Mikro organisme

Radiasi Kimia

2.Faktor internal : Genetik Hormonal Immunologi

Metabolisme

HIT Beruntun , terus - menerus

Akumulasi lesi gen

Gangguan homeostatis

Onkogen dominant

1. Inisiasi 2. Promosi 3. Progresi

N

IN

TC.

PROM

PM EX.

PROG

M

MASS-COMP : - LUMEN-DISTR - VASA. N-INFIL T. OR

META

MIKRO ORGANISME : VIRUS

BACTERIKARSINOGEN BAHAN KIMIA JAMUR

PHISIK RADIOACTIVE

VIRUS : HPV : Ca Cervic EBV : Ca

NASOPHARYNX HEPATITIS Ca HEPAR HTLV : LEUKEMIA LIMFOMA

PROTO ONKOGEN - ONKOGEN TUMOR SUP GEN PROG CELL DEATH / APOPTOSIS

HOMEOSTATIS BALANCE

IMBALANCE : - MUTATION - MULTIPLICATION - DEGRADATION

PROMOTING INHIBITING

ONKOGEN TUM.SUP .GAPOP/PCD.G

DNA REPAIR G.

INDIVIDUAL SEL DEFERENSIASI :

- Baik , jelek, - tak berdeferensiasi ANAPLASI : atipik PLEOMORPHISM ANISOSITOSIS DISPLASIA

3 S :Size, shape , stainning

KELOMPOK SEL Arsitektur Loss of polarity

FIBROMA : SUB CUTAN, OVARIUM FIB MOLLE FIB DURUM

KELLOIDMYXOMA : LUNAK , JERNIHLIPOMA : SUB CUTAN PUNGGUNG , PUNDAK, EXTCHONDROMA : JARI

BATAS TEGAS , MELEKAT KERASOSTEOMA : LONG BONE , SKULLMYOMA : LEIO

RHABDO

Fibro sarcoma Myoma sarcoma : rhabdo

leio Lipo sarcoma Osteo sarcoma Angio sarcoma

Planocelulare carcinoma Adeno carsinoma Transisional cell carsinoma Undifferentiated cell Ca