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

Blood vessel
Abnormal
heterogeneous cells

Loss of contact inhibition

Increase in growth factor secretion
Increase in oncogene expression
Loss of tumor suppressor genes
Neovascularization

sedikit
mitosis

Oncogene expression is rare

Intermittent or coordinated
growth factor secretion
Presence of tumor suppressor
genes

Tumorigenesis
Normal
cell

Initial
genetic change

Secondary
genetic change

(eg, loss of function of pRb

or overexpression of c-myc)

(eg, dysfunction of p53

or overexpression of bcl-2)

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

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

(fungi)

Liver

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

meninggal

8 cm

32cm
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

intake makanan (-)

Malabsorpsi

faktor pro-cachexia

proteolysis,lypolisis

lean body mass, fat mass(-)

cachexia

BB

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 )