Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
Patobiologi kanker
Sel normal
Banyak
mitosis
sel
normal
Nukleus
Blood vessel
Abnormal
heterogeneous cells
sedikit
mitosis
Tumorigenesis
Normal
cell
Initial
genetic change
Secondary
genetic change
Increase in
cell proliferation
and apoptosic
cell death
Decrease
in apoptosic
cell death
Subsequent
genetic change
Further alterations
in phenotype
(eg, invasiveness
and metastasis)
Kastan MB. Cancer: Principles & Practice of Oncology. 5th ed. 1997;121-134.
Neoplasia
Carcinogens/process of carcinogenesis
The multistep
process
involves
Chemical
carcinogenesis
1. Initiation
2. Promotion
These concepts have arisen from classical experiments performed on mouse
skin.
. The researchers have shown that initiation results from the exposure of cells to
a certain doze of
a carcinogen (initiator). An initiated cell is altered making it more likely to give
rise to a tumour
(if exposed to another agent; group 2 and 3 in figure 3). Initiation alone is not
Figure 3
sufficient for
tumour formation (group 1). Initiation cause permanent DNA damage
(Mutations). Thus it is
rapid irreversible and inheritable (group 3). In this group tumours were produced
even if the
application of the promoting agent was delayed for a long period of time after a
single application of the initiator. Initiators can themselves bind and change
DNA(direct acting) or procarcinogens, which require metabolic conversion in
Neoplasia
Table 1: Carcinogenic agents and occupational cancer
Etiology environmental
Agent
Occupation
Cancer Site
bronchus
X-rays, radium
radiologists, radiographers
skin
Radium
bone
Ultraviolet radiation
skin
2-Naphthylamine; 1-naph-thylamine
rubber workers
bladder
Benzidine; 4-aminobiphenyl
chemical workers
bladder
Asbestos
Mesothelioma lung
Arsenic
Benzene
marrow (leukemia
Vinyl chloride
PVC manufacturers
liver (angio-sarcoma)
Aflatoxin B1
Liver
Benzo(a)pyrene
Smokers
Lung
neoplasia
Gaya hidup
olah raga tidak teratur
diet rendah serat
tinggi lemak
obesitas
alkohol
rokok
prevention
Pertumbuhan tumor
29 x membelah
30 x
1sel
1 cm
2 cm
3 x
x
2 x
x
x
meninggal
8 cm
32cm
34 x
EFEK LOKAL
INFILTRASI JARINGAN SEKITARNYA , ULSERASI , INFEKSI , BERDARAH .
.EFEK METASTASIS
- paru
- liver
- otak
- tulang
. Efek paraneoplastik syndrom (Gangguan endokrin , neurologi, darah , kulit , ginjal., mata , muscle rigidity, paru)
- tumor memeproduksi zat yang langsung / tdk langsung menyebabkan gejala sistemik
- respon tubuh terhadap tumor
- penurunan substansi normal
kanker
Kemoterapi
anorexia
Malabsorpsi
faktor pro-cachexia
proteolysis,lypolisis
BB
EPIDEMIOLOGI KANKER
KESAATUAN BIOLOGI KANKER
PREDIKSI, PENCEGAHAN
DETEKSI DINI
BIOINFORMASI
KLINIKAL TRIAL TERPADU
MENYATUKAN PERBEDAAN TENTANG KANKER
Terapi
Operasi
Radiasi
kemoterapi
Hormonal
Targeting
Semuanya mempengaruhi
- biologik ( gangguan fungsi , kosmetik , anatomis , ganguan jantung , second
malignansi, infertil )
- phisikologis ( fatigue , takut kambuh, ganguan bekerja /malu )
- sosial ekonomi ( kontrol teratur , biaya terapi yang mahal. )
Radiasi
Kemoterapi
Research