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Modul 2
• responses adaptation main:
• atrophy, hypertrophy, Hyperplasia and metaplasia,
• If ability adaptive excessive, cell experience lesion.
• reversible
• irreversible
• 2 basic pattern of cell death:
• - necrosis ---- after the blood supply is lost / after exposure to toxins &
Marked dith swelling cell
• apoptosis------ (Physiological: embryogenesis; pathological: damage mutation
who do not repaired)
• Oxygen deprivation
• Chemical material
• The infectious agent
• immunological reactions
• genetic defects
• nutrition
• physical Agents
• aging
Oxygen deprivation
• Hypoxia ---- fatty acid oxidation (mitochondria) releases energy

• Penghantaran ATP to various cell organelles ( "mitochondrial dance").

• Cessation of ATP synthesis
• ---- anaerobic glycolysis energy (and ATP) without oxygen, lactic acid dlm ↑
cells. mRNA synthesis stops.
• 4. Cation and water pump
• Because mRNA (-), the ribosome complex is broken single ribosome,
protein synthesis stops
Cell Adaptation
• Physiologic
• Pathologic
Cell injury
Cell injury
• Cell  maintain the environment by adapting of physiological stress or
Pathological stimuli

• The main adaptation of cells: hypertrophy, hyperplasia, atrophy, and metaplasia

• If the adaptive capability of excessive or harmful external stress, the cells undergo
The lesion is divided into two:

1. The lesion Reversible  Occurs when cells exposed to a mild injury and
cells undergoing injury can return to normal
2. Irreversible  lesion occurred when the stress is severe or prolonged and
occurs suddenly and will result in irreversible injury to Dead in cell
Death Type Cells
1. Necrosis
• Cell death associated with loss of membrane integrity and leakage of the
contents of the cell, causing cell damage.
• Dapat identified by a lysis enzymes that dissolve the various elements of cells
and the onset of inflammation.
• Leukocytes will help digesting cells die
2. Apoptosis
• Apoptosis is programmed cell death,
• Component that normally occurs in a cell growth to maintain a balance in
multicellular organisms.
• The cells that die are in response to a variety of stimuli and during apoptotic
cell death that occurs in a controlled manner in an orderly regulation
The lesion Causes Cells
1. Lack of Oxygen / Hypoxia
• hypoxia, or deficiency of oxygen, interfering with oxidative aerobic
respiration and is the leading cause of injury and cell death is important and
common yangsangat
• One of the most common causes of Hypoxia is ischemia
• ischemia a state in which reduced blood supply to the tissues as a result of
interrupting the flow of arterial or venous flow decrease.
2. Chemical Agents
• Increased substance kImia Excessive body will cause injury to cells
• For example: glucose, salt, and water, if absorbed or given in excess will
disrupt osmotic environment resulting in cell injury or cell death.
• Chemical substances are toxic will also result in damage to the cell by
disrupting membrane permeability, osmotic homeostasis and integrity of
enzymes or cofactors and then exposure to the toxin can result in death of
the entire organism
3. The causative agent of infection
• The causative agent of infection varies from size virus submicroscopic up
Tapeworm several meter long; among others are rickettsial, bacteria,
fungi, and protozoa
4. Reaksilmunologi
• Role the immune system that is protect the body against mycobacterial
pathogens, However immune reactions may also result in cell injury and
• Example reaction autoimmune against its own network and allergic
reactions against environmental substances in patients with genetic
disorders can cause injury to cells
5. Genetic Factors

• Genetic defect may lead to cell injury due to deficiency of functional

proteins such as functional protein deficiency that causes congenital
metabolic disorders, or the accumulation of several DNA damage or mis-
folding of proteins, both of which can lead to cell death if it occurs in the
repair process
6. Nutritional Deficiency
• Nutritional defficiency become the most common cause of injury to the

• Lack of protein calories and certain vitamin deficiencies can cause injury to
7. Physical Agents

• Trauma, temperature extremes, radiation, electric shock and sudden

changes in atmospheric pressure resulting in a broad effect on cells one

occurrence of injury to cells

8. Aging
• The aging of the cell will cause interference with replication and repair
capabilities in cells and tissues.
• The whole of this change could result in a decreased ability to respond to
cell damage and then could end up dead on cells and organisms.
3. Histopatology of
Benign Neoplasm
Malignant NeopLasm
• Chemical Carsinogen
• Direct-Acting Agent
• Indirect-Acting Angent
• Radiation Carsinogen
• Viral Carsinogen
• Oncogenic RNA Viruses
• Oncogenic DNA Viruses
Faktor yang Mempengaruhi
Perkembangan Tumor dan Kanker
Genetik dan Lingkungan
Akibat Kerja
Tempat Tinggal
Usia diatas 55 tahun
• Sindrom Kanker Herediter
• Kanker Familial
• Sindrom resesif autosomal gagguan
perbaikan dna
• Invasion is the spread of tumor cells to the surrounding area causing damage
to the surrounding tissue.
• Human tissue is arranged into a series of compartments separated from each
other by two types of extracellular matrices (ECM), namely the basal
membrane and interstitial connective tissue.
• Stretch of tumor cells - Basically, each cell is bound by intereleg glue, E-
cadrein. The E-cadrein part in the cytoplasm binds to beta-katenin. The
adjacent E-cadre molecules keep the cells together, whereas homotypic
attachments mediated by E-cadrein transmit anti-growth signals via beta-
katenin. However, E-cadrein function disappears in almost all epithelial cell
cancers, both due to the mutation of the E-cadrein gene inactivation as well
as by the activation of the beta-katenin gene, so that the tumor cells seem to
separate from other cells
• The attachment of tumor cells to various ECM proteins - Examples of
ECM proteins: laminin and fibronectin. Normal epithelial cells have
receptors for laminin basal membrane polarized on the basal surface. In
contrast, carcinoma cells have more receptors, and these receptors are spread
throughout the cell membrane, allowing more attachment.
• Local degradation of basal membrane and interstitial connective
tissue - Tumor cells secrete proteolytic enzymes to secrete proteases. Some
matrix destruction enzymes called metalloproteinases, including gelatinase,
collagenase, and stromelisin, play a role.
• Migration of tumor cells penetrates the basal membrane - Migration is
mediated by various cytokines originating from tumor cells, for example the
autocrine motility factor. In addition, decomposition products of matrix
components (eg collagen, laminin) and some growth factors (eg insulin-like
growth factor I and II) have chemotactic activity for tumor cells.
Metastasis is the invasion of tumor cells over a greater distance, allowing the
same tumor cells to grow in a new place / organ.
The process of blood vessel metastasis is as follows:
• Invasion: Tumor cells penetrate the basal membrane layer and enter the
extracellular matrix.
• Intravasation: From the extracellular matrix, tumor cells enter through the
vascular endothelium (intravasation) and begin to spread through the flow of
the vessels.
• Circulation: while in circulation, tumor cells are susceptible to destruction
by host immune cells. In the bloodstream, some tumor cells form an
embolus (clot) / adhesion and then attach to leukocytes and platelets. The
embolus will obtain more protection from the attack of host antitumor
effector cells. But most tumor cells enter in their own circulars.
• Extravasation: when it arrives at the location of the organ to be hosted,
tumor cells or embolus will attach to the vascular endothelium followed by
movement through the basement membrane with a mechanism similar to
that which plays a role in invasion.
• Angiogenesis: Upon arrival of the tumor cells in the host organ, these cells
will secrete PLGF growth factors to stimulate the formation of new blood
• Growth: after all the facilities are sufficient to support the life of these
tumor cells, the tumor cells begin to grow and divide to form new tumors
Tumor Antigens
Tumor Antigens

1. Products of Mutated Oncogenes and Tumor Suppressor Genes

2. Products of Other Mutated Genes
3. Overexpressed or Aberrantly Expressed Cellular Proteins
4. Tumor Antigens Produced by Oncogenic Viruses
5. Oncofetal Antigens
6. Altered Cell Surface Glycolipids and Glycoproteins
7. Cell Type–Specific Differentiation Antigens
Antitumor Effector Mechanisms
1. Antitumor Effector Mechanisms
2. Cytotoxic T Lymphocytes
3. Natural Killer Cells
4. Macrophages
5. Humoral Mechanisms
Immune Surveillance and
Immune Evasion by
Several escape mechanisms have been
1. Selective outgrowth of antigen-negative variants.
2. Loss or reduced expression of histocompatibility molecules.
3. Immunosuppression.
4. Antigen masking.
5. Downregulation of co-stimulatory molecules.
Blood test, urine, liver function, blood sugar, hemostatic physiology, serum
protein, alkaline phosphatase, electrolytes serum, LDH, uric acid,
immunoglobulin serum.


 to find out if there is complication in the patient's cancer

 and also to find out the therapeutic preparations that will be performed, both
surgical and medical.
This examination is a morphological tumor examination both
macro and micro. Material that can be obtained from biopsy.

Required to help establish a diagnosis. Many types of imaging
from easy to sophisticated, and also useful for determining
several staging stages
Consisting of proteins (enzymes, hormones, etc.) that are not
normally present, or that the body produces very little. PT can be
used for screening, establishing diagnosis, prognosis, regulating
the results of treatment and detection of recurrence.
Diagnose Breast Carcinoma
Breast ultrasound, mammography, mammary MRI, laboratory
examination, fine needle aspiration, and biopsy examination. To
determine the presence of metastasis a chest photo can be
examined,bone surveyAbdominal / hepatic ultrasound.

Ultrasound examinations can only distinguish solid or cystic

lesions / tumors, but can know the blood supply and the
surrounding tissue.
On Mammography, malignancy can provide primary and
secondary signs.

The primary sign :

 Reactive fibrosis,
 Comet sign (Stellata),
 There is a marked difference between clinical and radiological

 There are cerebral calcification,

 The presence of spicules, and
 Distortion in the structure of breast architecture.
Secondary signs

 Retraction,

 Thickening of the skin,

 Increased vascularization,

 Changes in the position of the papilla and areola,

 Presence bridge of tumor

 The state of the tumor area and irregular fibroglandular tissue,

 Infiltration in the soft tissue behind the mammary,

 The presence of glandular metastases