Patobiologi kanker

Patobiologi kanker
Kanker adalah petumbuhan sel
yang abnormal tak terkendali dan
terus menerus serta dapat
merusak jaringan setempat serta
dapat menjalar ke tempat yang
jauh dari asalnya
Dapat tumbuh/berasal dari setiap
jenis sel di tubuh manusia
Perbedaan sel kanker dan normal
Sel Kanker Sel normal

Banyak
mitosis
sel
normal
Nukleus

sedikit
Blood vessel mitosis

Abnormal
heterogeneous cells
Loss of contact inhibition
Increase in growth factor secretion
Increase in oncogene expression
Loss of tumor suppressor genes
Neovascularization
Oncogene expression is rare
Intermittent or coordinated
growth factor secretion
Presence of tumor suppressor
genes
Tumorigenesis

Normal Initial Secondary Subsequent

cell genetic change genetic change genetic change
(eg, loss of function of pRb (eg, dysfunction of p53
or overexpression of c-myc) or overexpression of bcl-2)

Increase in Decrease Further alterations

cell proliferation in apoptosic in phenotype
and apoptosic cell death (eg, invasiveness
and metastasis)
cell death

Kastan MB. Cancer: Principles & Practice of Oncology. 5th ed. 1997;121-134.
 Neoplasia
Carcinogens/process of carcinogenesis
Chemical
The multistep carcinogenesis
process involves
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
sufficient for Figure 3
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
Etiology environmental
Table 1: Carcinogenic agents and occupational cancer
Agent Occupation Cancer Site
Ionizing radiations radon certain underground miners bronchus

X-rays, radium radiologists, radiographers skin

Radium luminous dial painters bone

Ultraviolet radiation farmers, sailors, etc. skin
Polycyclic hydrocarbons in soot chimney sweepers,oil workers scrotum, skin, bronchus

2-Naphthylamine; 1-naph-thylamine rubber workers bladder

Benzidine; 4-aminobiphenyl chemical workers bladder

Asbestos shipyard and insulation workers Mesothelioma lung

Arsenic sheep dip manufacturers, gold miners skin and bronchus

Benzene workers with glues, varnishes, etc. marrow (leukemia

Vinyl chloride PVC manufacturers liver (angio-sarcoma)

Aflatoxin B1 Food storage. Due to growth of Aspergillus flavus Liver

(fungi)

Benzo(a)pyrene Smokers Lung

Dont forget the role of viruses and bacteria in Cancer

neoplasia
Gaya hidup
olah raga tidak teratur
diet rendah serat
tinggi lemak
obesitas
alkohol
rokok
prevention

Olah raga teratur

Menghindarkan berat badan berlebih
Menghindarkan alkohol & rokok
Konsumsi sayuran dan buah secara teratur
Diet tinggi serat , rendah lemak dan karbohidrat
secukupnya
Ikan , kacang & legumes
Pertumbuhan tumor
29 x membelah
30 x

1sel
1 cm 2 cm
3 x
x
2 x
x
x

8 cm
32cm
meninggal
34 x
 Gambaran klinis kanker
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

Efek CRF ( defresi, sakit , gangguan tidur , menopouse )

- energy balance
- respon stress
- neuroendokrin

Cancer cachecia. ( intake kurang , gangguan metabolisme)

- perbaikan status nutrisi, anti inflamasi untuk terapi dan kualitas hidup.
( HYPERKALORI 30 35 k cal / kg bb , BCAA 10 15 gr /hari ( leucine ) , EPA 2 3 gr /hari )
Patogenesis cachexia syndrom

kanker

Kemoterapi anorexia faktor pro-cachexia

intake makanan (-) proteolysis,lypolisis

Malabsorpsi lean body mass, fat mass(-) BB

cachexia
Program NCCN 2015
EPIDEMIOLOGI KANKER
KESAATUAN BIOLOGI KANKER
PREDIKSI, PENCEGAHAN
DETEKSI DINI
BIOINFORMASI
KLINIKAL TRIAL TERPADU
MENYATUKAN PERBEDAAN TENTANG KANKER
Complementary alternative medicine
(folkloric,holistik,traditional,non-Western,unproven)

Kualitas hidup buruk ,efek samping berat,komplikasi perioperatip

Menghambat efek kemoterapidan radiasi
Resiko perdarahan
Hepatotoksik
Contoh : Maitake-saitake Hoxsey formula
Laetrile Shark cartilage
Mistletoe Gerson formula
Banyak digunakan untuk supportive (cachexia,nause, konstipasi )
Prevention ( lycopene, selenium, teh hijau, vitamin A,C,E )
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

Radiasi fibrosis syndrom

- akut ( selama atau setelah radiasi )
- early delay ( - 3 bulan )
- late delay (> 3 bulan )

Gejala yang timbul

tergantung dari daerah yang disinar , bisa merusak kulit, otot , ligament,
tendon , syaraf , viscera , tulang , mukosa
Kemoterapi

Diare dan konstipasi

Nause dan muntah
Hilang rambut
Cardiac toxicity
Pulmonary toxicity
Stomatitis , xerostomia
Trombosis
Beberapa komponen penting

Edukasi ( keluarga, pasien, donatur kesehatan )

Surveillance ( kekambuhan lokal , jauh , second cancer, psycososial, sosial

ekonomi

Intervensi ( pencegahan , deteksi dini, terapi)

Communication (antara dokter , pasien , dan donatur )

Research

Patient advocacy. ( pekerjaan , insuran , ketidak mampuan )