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Atienza, Austria, Balbin (09272265029), Bandoma, Baez, Banico

Dr. Hipolito | March 6, 2014
SURGERY
3.4 Principles of Surgical Oncology
2013-2014 2nd

OUTLINE
I. Carcinogenesis VI. Postoperative Management
II. Cancer Metastasis VII. Principles of Chemotherapy
III. Preoperative Planning VIII. Cancer Treatment Strategies
IV. Intraoperative Conduct IX. Principles of Radiation Therapy
of Operation
V. Types of Cancer Operations X. On-going Trials in Cancer Therapy
References:
Powerpoint, recording

I. CARCINOGENESIS
Single cell (clonogenic origin) undergoes complex molecular
and biochemical interactions resulting in malignant
transformation. This means, a normal cell acquires potential to
grow and replicate due to several factors (smoking, drinking,
genetics/hereditary). Environmental and hereditary factors
cause underexpression or overexpression of genes. Balance
between the tumor suppressor genes and thos genes which
causes cancer, oncogenes.
Interaction of cancer promoting genes (oncogenes) and cancer
protecting genes (suppressor genes)
o Overexpression of oncogenes + the effects of
environmental factors
o Deletion/underexpression of suppressor genes (ex. P
53
)
Figure 1. Loss of normal growth control

HALLMARKS OF CANCER
o Sustained proliferative signaling (growth factors-tyrosine
kinase)
o Evades growth suppressors (Rb and TP53)
o Resist cell death (loss of Apoptotic potential)
o Replicative immortality (expression of Telomerase)
Telomerase, the specialized DNA polymerase that adds
telo- mere repeat segments to the ends of telomeric
DNA
o Induces angiogenesis (VEGF and Thrombospondin)- target
these factors to block growth
o Evades immune response
o Creates tumor microenvironment- target not only the
cancer cells but also the surrounding tissue (Hedgehog
Hypothesis)
o Invasion and Metastasis (MAIN HALLMARK): Loss of contact
inhibition
Normal cell can grow. A benign tumor can grow but it
has less or no ability to invade other structure.
Cancer has propensity to go to other places in the
body and grow there and cause invasion. Basically, a
cancer is a space occupying lesion. It does not produce
any toxin that will kill you. It will just grow and invade
leading to death.
Down regulation of E-Cadherin
Macrophages (activated by IL4 produced by cancer
cells)
- Macrophages at the tumor periphery can foster local
invasion by supplying matrix-degrading enzymes such
as metalloproteinases (MMP) and cysteine cathepsin
proteases













Figure 2. To illustrate what is meant by normal growth control, consider the
skin. The thin outermost layer of normal skin, called the epidermis, is roughly
a dozen cells thick. Cells in the bottom row of this layer, called the basal layer,
divide just fast enough to replenish cells that are continually being shed from
the surface of the skin. Each time one of these basal cells divides, it produces
two cells. One remains in the basal layer and retains the capacity to divide.
The other migrates out of the basal layer and loses the capacity to divide. The
number of dividing cells in the basal layer, therefore, stays the same.
Figure 3. The beginning of Cancerous Growth. Cancer cells replicate until it
invade the basement membrane.

--------------------------------------------
6
th
LE Schedule
Pathology
Psychiatry
Mar 17, Mon
Mar 17, Mon
10am-12nn
3pm-5pm
Surgery Mar 18, Tue 8am-11am
Pediatrics
Parasitology
Mar 19, Wed
Mar 19,Wed
8am-10am
3pm-5pm
Medicine Mar 20, Thurs 2pm-4pm
Pharmacology Mar 21, Fri 2pm-4pm





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SURGERY 3.4
Figure 4. This gradual increase in the number of dividing cells creates a
growing mass of tissue called a "tumor" or "neoplasm". If the rate of cell
division is relatively rapid, and no "suicide" signals are in place to trigger cell
death, the tumor will grow quickly in size; if the cells divide more slowly,
tumor growth will be slower. But regardless of the growth rate, tumors
ultimately increase in size because new cells are being produced in greater
numbers than needed. As more and more of these dividing cells accumulate,
the normal organization of the tissue gradually becomes disrupted.


Figure 5.Invasion and Metastasis. When cancer cells reach the vascular
supply and drainage, they are transported by the circulatory system to
distant sites






Figure 6.
Distant
Metastasis
Example:
o Thyroid Cancer (Papillary carcinoma of the thyroid) most
common region of metastasis is the lymph node. Eventually,
it will go to the lungs, and then bones
o Squamous Cell Carcinoma of the skin doesnt readily
metastasize
FACTORS
o Oncogenic viruses (ex. HSV/HPV & cerv CA)
o Chemicals (ex. Smoking & lung CA)
o Chronic irritation (ex. hyperkeratosis & oral cavity cancer)
o Genetic factors (ex. BRCA1/BRCA2 & breast CA)
Note: Interplay of the factors will lead to cancer. Example, if
you dont have any gene that predisposes you to lung
cancer, even if you smoke everyday, you will not have
cancer. But if you have a gene for lung cancer caused by
smoking, even one stick of smoke will trigger development
of cancer.

CELL KINETICS this tells the aggressiveness of the tumor, kind
of treatment you want to initiate.
o G
0
phase State of cells not in the active cell cycle but
capable of entering G
1
upon stimulation.
o Gap 1 phase (G
1
) period from mitosis to start of DNA
synthesis.
o DNA Synthesis (S)
o Gap 2 phase (G
2
) period between DNA synthesis to next
mitotic phase.
o Mitotic phase (M) cell division seen morphologically.

A. Cell Cycle












Figure 7. The
Cell Cycle. In
cancer cells, the stage of terminal differentiation is deleted. Most cancer cells
undergo G0 phase or the actively replicating phase (2014B trans).
Gap 1 phase (G1) Period from mitosis to start of DNA
synthesis
DNA synthesis (S)
Gap 2 phase (G2) period between DNA synthesis to next
mitotic phase
Mitotic phase (M) cell division seen morphologically
Factors that prevent cells to go into G0 or latent phase
(smoking, viruses, chronic irritation, etc)
Gap 1 phase (G1) Period from mitosis to start of DNA
synthesis

B. Cell kinetic
Intermitotic Time
Duration of 1 cell cycle to another cell cycle (ave. 8 24 hrs)
S phase (ave. 6 10 hrs)
Cells rapidly proliferating will have shorter intermitotic time
If a cancer has a very short intermitotic time, you are dealing
with a very aggressive cancer; the doubling time decreases

C. Contents of Cancerous Tissues
Actively proliferating cells (clonogenic stem cells)
Non-actively proliferating cells but maintaining clonogenic
capacity
o Proliferation may have been inhibited by lack of nutrients
or other homeostatic factors
Cells that have lost clonogenic capacity

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SURGERY 3.4
Clonogenic stem cells remain latent and thus are hard to treat
when given chemotherapy since they are not replicating.
Chemotherapy only works on rapidly dividing cells.
Tumor cells in the periphery where neovascularization is
present, are well oxygenated and rapidly dividing
o Rapid cell division promote detachment & entry to
lymphatics
Centrally located cells subject to decrease in PO2 retain
clonogenic activity and can metastasize




Figure 8.Contents of Cancerous Tissue
Clinical implication
The best area to biopsy is the periphery, not the center of the
tumor.
o The areas at the periphery are usually the areas most
oxygenated and where cells are rapidly dividing. The tissues at
the center usually becomes necrotic.
A tumor on diagnostic imaging that is hypervascular is
probably cancerous.
o Difficult to penetrate by cytotoxic agents
Why?
Tumor cells in the periphery where neovascularization is
present, are well-oxygenated and rapidly dividing.
o Rapid cell division promote detachment & entry to
lymphatics
Centrally-located cells subjected to decrease in PO2
retain clonogenic activity and can metastasize
C. Tumor growth
Expressed in terms of volume doubling time (DT)
Range: week to one year with median DT of 60 days
Table 1:
Breast 130 days
Lungs 160 days
Melanoma 140 days
Metastatic Melanoma 64 days
Situational example: If there is a suspicious lesion in the breast
that is not amenable to any kind of biopsy, then the best way
to see if there is an increase in size is to do a repeat
mammography 3-4 months after the initial testing. Knowledge
of the doubling time tells us when to do surveillance.

--------------------------------------------
FINALS Schedule
Pathology
Psychiatry
Mar 24, Mon
Mar 24, Mon
11am-1pm
3pm-5pm
Pediatrics
Parasitology
Mar 25, Tues
Mar 25,Tues
9am-11am
2pm-4pm
Surgery
Medicine
Mar 26, Wed
Mar 26, Wed
9am-12am
2pm-4pm
Pharmacology Mar 27, Thurs 1pm-3pm
Summative OSCE Mar 28, Fri 8am-5pm


D. Gompertzian Curve

Figure 9.Gompertzian Curve

Small tumor close to 100% of cells proliferating
As tumor enlarges, more cells drop out of proliferating cycle
due to the lack of nutritional supply
Decrease in growth rate with increasing size rather than a
linear/exponential growth
o Lack of nutrients/blood supply alter growth rate
o Large tumors may have many cells in G0 or G1
o Growth altered by immune system
1.0 cm tumor (clinically detectable) contains 10
9
cells that
are active
Clinical implication: The smaller the tumor, the better
response to treatment acting on rapidly dividing cells
(radio- or chemotherapy). Larger tumors are therefore
reduced in size via debulking procedures so that the
remaining cancer cells would be recruited into the cell
cycle.

E. Therapeutic Implications
RULE: Good response to cytotoxic tx (chemo/RT) of actively
proliferating cells
o Removal of primary tumor may increase growth rate in
metastatic foci thus vulnerable to cytotoxic therapy
o Cytoreductive (debulking) surgery reduces tumor bulk &
may increase growth rate to allow cytotoxic Tx to work
e.g. ovarian CA

F. Tumor Growth
FACTORS AFFECTING GROWTH RATE
1.Tumor aggressiveness (angiogenic factor, membrane
characteristics, enzymes, DNA factors)
2.Host defense mechanisms (host responses like T killer
cells, fibrosis, etc.)

Table 2:
Fast-growing Cancers Slow-growing Cancers
Short incubation (rapid doubling
time)
Long incubation period (long
doubling time)
Early recurrence is common Early recurrence is uncommon
Rare late recurrence Late recurrence is common
Only few people die after three
years post-resection
Most patients die after five
years or more

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SURGERY 3.4
G. Clinical Implication
Fast growing cancers (e.g Pancreatic AdenoCA, Gastric cancer,
Esophageal cancer)
o Intensive surveillance for 1
st
1 2 years
Slow growing cancers (e.g. Papillary Thyroid CA)
o Long period of surveillance necessary (>10 years)

Table 3: Clinical Implication of Cancers

II. CANCER METASTASIS
Tumor cells will detach, implant & grow (metastasis)
RULE: Carcinoma first metastasizes to the lymphatics
(lymphogenous) while sarcoma invades the bloodstream
(hematogenous)
o Generally, cancers metastasizes to the lymph nodes; they
can also spread hematogenously and transcoelomically.
o Once a sarcoma also spread through the lymph nodes, it
automatically considered Stage IV.
When lymphatic channel is entered, regional nodes filter it,
causing lymphadenopathy (nodal metastasis)
Organ selectivity: preference of cancer cells to implant in
specific organs (ex. mets to lung, liver, bone, ovary, brain and
peritoneal cavity)
Examples:
o Ovarian cancers dont usually go to the lymph node or to the
blood. They spread transcoelomically. Ovaries have thin
outer layer. When a tumor grows in it, it easily breaks the
outer layer and spill cancer cells into the abdominal cavity.
In the abdominal cavity, there is peritoneal fluid that
circulates around the peritoneum. This fluid carries the
cancer cells. When the cancer cell attaches to the surface of
the peritoneum, it grows there. This is called Peritoneal
Carcinomatosis
o Squamous Cell Carcinoma of the Skin doesnt usually
metastasize; they are more of local spread. This is also true
for Basal Cell Carcinoma of the Skin.
o Melanoma has high risk of metastasis to the lymph node, as
well as Breast Cancer.
o Abdominal CA metastasize via lymph nodes, blood, and
transcoelomic
o Head and Neck cancers metastasize via lymph nodes
A. Therapeutic Implications
RULE: Knowledge of stage, behavior, pattern of spread dictate
treatment
Example: Squamous Cell CA of the forehead. Treatment would
be local excision since it does not readily spread lymphatically
or hematogenously. However, for a 3 cm melanoma on the
forehead, the treatment would be excision of the primary
tumor and lymph node because melanoma metastasizes into
the lymph nodes.
Once the tumor invades the lymph nodes, there is always a
possibility that the tumor is already systemic. Thus, treatment
should also be given systemically (chemotherapy). Surgery
would not cure cancer cells in the blood.
Surgery is for LOCAL TREATMENT only.
Therapeutic Implications:
For carcinoma:
o examination of corresponding lymph node basins is a
must.
o Resection may involve not just primary tumor but also
nodal basins for regional control.
For sarcoma:
o Look for distant metatases even if LN are not involved.
Liver, lungs, bone, brain
o Resection of nodal basins usually unnecessary

Table 4. Early vs Late Metastasis
Early Metastasis Late Metastasis
1. Rarely curable when
reaches a certain size
2. Good correlation
between size and
survival
3. Potential for multi-site
involvement
4. Local recurrence does
not influence survival

5. Resection of metastatic
nodules no effect on
survival
1. Poor correlation of size
and survival
2. Correlated better with
depth of invasion

3. Few metastatic sites

4. Large tumors may still be
curable even with
extension
5. Success possible with
metastasectomy

Tumors w/ propensity for local invasion need wider resection
margins (e.g. BCC)
Locoregional treatment is indicated if:
o Dissemination likely in early stages (surgery +
chemotherapy)
o Local control doubtful (surgery + RT)
III. PREOPERATIVE PLANNING
The first thing you do when a patient who comes into the clinic
with a mass is to diagnose if it is a tumor or not. For example,
if you have a 5 cm mass on the breast, you do a biopsy. Once
you determine that it is cancer, the next thing to do is to know
the extent of the tumor.
Clinical Staging (TNM)
o PE, Imaging (CT, MRI, PET)
o In a PET scan, glucose is injected and cancer cells take up
the glucose. Large radioactive areas seen are usually
malignant type cancers. Non-malignant types dont
usually take up a lot of glucose.
Tissue diagnosis if possible and necessary
o Mandatory if patient presents with malignancy
Pre-operative Conference (with other specialists and the
patient and relatives)
o Planning multidisciplinary approach
o Explaining extent of surgery
o Explaining risks and outcome
Pre-operative preparation
o Medical risk evaluation
o Optimize patient condition
Pulmonary physiotherapy
Nutritional support
Bowel preparation
Antibiotic prophylaxis
o Timing of surgery (ex. Post RT)



Dissemination Occurs at
disease inception
Tumors with low
biologic potential
Lung cancer
Osteogenic sarcoma
Anaplastic thyroid CA
Ewing sarcoma
Esophageal CA
Basal cell CA
Desmoids/skin SCC
Chondroma
Well differentiated
thyroid carcinoma
Multimodal treatment Local Treatment

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SURGERY 3.4
IV. INTRAOPERATIVE CONDUCT OF OPERATION
1. Determine stage during surgery (curability and resectability)
A tumor can be resectable but can no longer be cured
For example, a tumor in the colon has undergone multiple
liver metastasis. The tumor in the colon can be resected but
the patient cannot be cured.
2. Histologic confirmation if necessary
3. En-bloc resection
Nodal dissection not picking
Avoid tumor spillage
4. Attain tumor free margins
If you leave behind a single cancer cell in the operating field,
there is always this possibility that the cancer cell will grow
and replicate and recur. That is why you must do a wide
excision, if possible.
Sarcoma: mandatory margins of resection is 5cm.
V. TYPES OF CANCER OPERATIONS
1. CURATIVE RESECTION (for Stages I, II, III)
o Resectable tumor & cure can be attained by surgery (e.g.
radical resection)
2. CYTOREDUCTIVE SURGERY
o Decrease tumor load prior to adjuvant therapy
o Indicated if other effective therapies are available to control
residual disease
o ex. Ovarian cancer - resection of bowel with infiltration to
prevent perforation during chemotherapy
3. DIAGNOSTIC SURGERY
o Biopsy to confirm diagnosis or histology of cancer

Figure 10 . Cytoreductive Surgery (Hyperthermic Intraperitoneal
Chemotherapy). An 82 year old Px with Ovarian Ca. All the tumors were
removed including the lining of the abdominal wall, the peritoneum. After the
procedure, chemotherapy was placed inside the abdomen. The patient
survived for another 2 years.

4. PALLIATIVE SURGERY
Unresectable tumor but longevity can be increased
Patient can be made comfortable
ex. Bypass & resection for obstruction

From Recording: * you perform surgical procedure to alleviate the
pressing problem of the px
*Ex. Px with colon cancer that has already metastasized to the lungs
and to the liver with only 4-6 months. The primary tumor is
obstructing her colon and so she couldnt eat. You have to perform
the procedure on this patient so she could eat. So what we do is we
remove the tumor or we do a diversion. We take out the colon
outside the abdomen and feces will come out that way. This is done
even if we know she will just live for 4-6 months.
* Px with tumor in the neck that has already metastasized to the
lungs and bones and has only 6 months to live. The tumor is pressing
on her neck so she couldnt breathe so you have to put in a tube or
remove the tumor.

5. PROPHYLACTIC SURGERY
Prevent future cancer from developing
Prophylactic mastectomy for high risk for breast CA
Total colectomy for multiple polyposis of colon

VI. POSTOP MANAGEMENT
Maintenance Of Records
o Accurate record keeping
o Indicate clinical/pathologic stage
o Document surgical and adjuvant therapy
Follow-Up And Rehabilitation
o Detect recurrences (Surveillance); Surveillance imaging
studies
For breast Ca px-chest xray, ultrasound every 6 months
for the next 2 years
For Colon CA Colonoscopy every 3 years; CT scan of
the abdomen every year for the next 5 years
o Monitor treatment outcome
VII. PRINCIPLES OF CHEMOTHERAPY
Goal:To kill cancer cells by interfering with its metabolic
pathway without serious damage to normal cells

A. Classification / Mechanism of Action
1. Alkylating Agents (i.e. Cyclophosphamide)
Binds to nucleic acids thereby altering the structure
Cell cycle nonspecific
Cross resistance with other alkylating agents
2. Antimetabolites (5-FU, Methotrexate)
Structural analogues of nucleic acid precursors results in
production of false intermediate metabolites
S phase specific agents
3. Antibiotics (ex. Adriamycin, Bleomycin)
Interferes with various points in sequence of DNA to RNA
to protein formation
Interferes with DNA replication or inhibition of RNA
synthesis
Cell cycle non-specific
4. Anti-Microtubular Agents
Plant origin
Causes disorganization of mitotic spindles
Produce mitotic arrest of the cell in metaphase
Cell cycle specific

4.1. Vinca alkaloids (ex. Vincristine, Vinblastine)
o inhibit assembly of microtubules
4.2. Taxanes (ex. Paclitaxel, docetaxel)
o inhibit microtubular disassembly
First Order Kinetic Phenomenon
o With the administration of a drug, a constant percentage
of cells is killed, not a constant number of cells
o First dose: A relatively constant proportion (not an
absolute number) of cells are killed
o Second dose will kill the same percentage of remaining
cells
o Subsequent doses will eliminate close to 100% of cells
o THERAPEUTIC IMPLICATION: CHEMOTHERAPY DRUGS ARE
USUALLY GIVEN IN SEVERAL CYCLES

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SURGERY 3.4
o Side Effects
- Vomiting
- Hair loss
- Depressed immunity

- Weakness/anorexia
- Anemia
- Organ specific (cardiac,
liver, kidney)

B. Therapeutic Implication
Intermittent Therapy (rationale)
o Allow recovery of immune system (2-3 weeks)
o Allows recovery of DNA damage in normal cells which is
faster than cancer cells
o Destruction of cancer cells by blocking DNA synthesis in
actively proliferating cancer cells
o Better effect than continous therapy
Combination of Drugs
o More effective tumor kill
o Less complications
o Provides maximum cell kill within the range of toxicity for
each that can be tolerated by the host
o Offers a broader range of coverage of resistant cell lines in
a heterogenous population
o Prevents or delays the emergence of drug resistance cell
lines.
o Drugs known to be active as single agents usually are
selected
o Drugs with different mechanisms of actions are combined
to allow for additive or synergestic effects. Drugs with
differing dose-limiting toxic effects are also combined to
allow for each drug to be given at therapeutic does. Same
goes with different patterns of resistance to avoid cross-
resistance.
o Combining cell-cylce specific and cell-cycle-nonspecific
agents are especially advantageous.
o Treatment-free interval between cycles is kept to the
shortest possible time that will allow for recovery of the
most sensitive normal tissue.
Sometimes chemotherapy is given prior to surgical procedure and
monitor the response. Thats the best way to see if there is any
response.

80% of the time, if you give chemo before surgery for breast CA,
then palpate it after some time, no tumor can be felt even with
imaging, even if you did biopsy of breast and have it examined under
the microscope, there are still some viable cancer cells, so you really
need to remove the breast, then therell be no more viable cancer
cells. That is complete pathological response
There is no difference in prognosis/survival if even if reduced to very
few cancer cells or 50% of total reduction after chemotherapy.

Complete pathological response will have a better chance of
survival compared to those who only have complete clincal
response
VIII. CANCER TREATMENT STRATEGIES
Neoadjuvant Therapy
o Down stage/shrink tumor and convert the procedure from
total removal of the organ to just removal of the tumor
itself
o Allow curative resection
o Test response to cytotoxic therapy
o Prior to surgery
Adjuvant Therapy
o Given in addition to primary treatment
o Eradicate microscopic CA cell not removed by primary
treatment
o Prevent distant mestastasis/local recurrence
o After surgery
Palliative chemotherapy (wont be on the exam)
o Incurable disease but death not imminent
o Can significantly prolong life and improve quality of life
o Patient must have good performance status
o Treatment is given out of guilt
o Patients usually just experience the drug side effects
Targeted Therapy
o Newest form of cytotoxic therapy
o Blocks the growth of cancer cells by interfering with
specific targeted molecules needed for carcinogenesis and
tumor growth
o Targets the processes (or marker) invovled in tumor
growth
o Rather than by simply interfering with rapidly dividing cells
(traditional chemotherapy)
o More effective, less harmful, more expensive than
chemotherapy
o Types of targeted therapy:
o Small molecules
- Gefitinib: targets EGF receptor tyrosine kinase, for lung
CA and some solid tumors
- Imatinib for CML, GIST
- Tamoxifen: targets estrogen receptors of breast
cancer. But not all breast tumors have estrogen
receptors, just only 70%
- Aromatase inhibitors: blocks formation of estrogen,
includes those estrogen from fat and adrenals
o Monoclonal Antibodies
- Trastuzumab: targets HER2/neu receptor of breast CA

IX. PRINCIPLES of RADIATION THERAPY
A. Radiation Therapy (RT)
A local (non-systemic) effect
Affects cells by interfering with reproduction and mitosis
Affects rapidly dividing cells
Aims to effect maximal damage to cancer cells but allows
recovery of normal cells
Just like surgery, only for local control of tumor
Uses ionizing radiation
Radiation deposition results in DNA damage manifested by
breaks in the strand in the sugar phosphate backbone of the
DNA
Manifests primarily by loss of cellular reproductive integrity.
Most cell types do not show signs of radiation damge until
they attempt to divide, so slowly proliferating tumors may
persist for months and appear viable. Some cell types undergo
apoptosis.

PRINCIPLES OF CHEMOTHERAPY
Response

1. Complete
2. Partial
3. None
4. Progression

Criterion

1. Complete disappearance
2. 50% reduction in T size
3. < 50% reduction in T size
4. > 50% increase in total
measurable disease
Criteria for objective response for
clnically measurable tumors

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SURGERY 3.4
B. Factors affecting Radiosensitivity
Oxygen Tension (work best in high oxygen tension)
o Necrotic tumors decrease O2 tension-resistant
o Anemic patients decrease O2 carrying hgb-resistant
o Work best if with high oxygen tension. Radiotherapy needs
higher oxygen cause it will cause overproduction of free
radicals which will cause damage to the DNA structure of
the cancer cell. Repair mechanisms of cancer cells
inhibited and thus death of cancer cell.
o Hypoxic cells are significantly less radiosensitive than
aerated cells because presence of oxygen is thought to
prolong the half life of free radicals
o Indirectly ionizing radiation is less efficacious in tumors
with areas of hypoxia. In contrast, radiation damage from
directly ionizing radiation is independent of cellular oxygen
levels.
o The extent of DNA damage from indirectly ionizing
radiation is dependent on the phase of cell cyle. The most
radiation sensitive phases are G2 and M.
Fractionation
o Redistribution
o Re-oxygenation
o work best in fractionation, little by little so that a small
amount of cancer cells die, and group will progress to
dividing stage, then give another dose of radiation. It gives
better results in survival and less recurrence and less
adverse effects

C. Curative Role of RT
SCC of the Head & Neck (Early)
Cervix CA
Lymphoma
1. PRE-OP RT (intact blood supply)
Reduction of tumor size (ex. Rectal cancer,
neoadjuvant radiotherapy)
Decreases recurrence
2. POST-OP RT
For bulky or aggressive tumors
Positive margins
Decreases recurrence
D. Combined Radiotherapy and Chemotherapy
Chemotherapy is prior to radiotherapy
Sensitize tumor cells to RT effects
For advanced head & neck and rectal cancer

E. Types of RT
1. External
X-ray
Gamma beam
Particle beam
Intensity Modulated Radiation Therapy (IMRT)
2. Interstitial radiation (brachytherapy)
Recurrences after external RT
Unresectable cancers
3. Intracavitary (Uterine Cervix Ca)
Insertion of radium packed tubes inside the cavity
4. Systemic RT
I131 Thyroid Ca
Phosphorus 32 bone metastasis


X. ON-GOING TRIALS IN CANCER THERAPY
Genetic & Molecular Medicine
Stem Cell Therapy
TYPES:
1. Remove normal cell then give high dose chemotherapy. When
the bodys system is down (supper suppressed bone marrow), the
stem cell it put back and reproduce normal cells.
2. Dendritic Cell Therapy. Get cancer cell and macrophage. Label
(tattoo) the macrophage that would detect the tumor cell (tumor
marker). Place the macrophage back to the system, that
macrophage would produce antibodies that hopefully would
recognize the cancer cells. Downside, not enough scientific
evidence that it works with solid tumors.
IMMUNOTHERAPY
1. Dendritic cell therapy
2. Nanotechnology in Medicine-we put a device inside
blood/system, give treatment and see if the treatment is
working. Nanoscale devices smaller than human cells (10,000 to
20,000 nanometers in diameter) and organelles and similar in
size to large biological macromolecules such as enzymes and
receptors ex: Hemoglobin is approximately 5 nm
in diameter, while the lipid bilayer surrounding cells is on the
order of 6 nm thick. Nanoscale devices smaller than 50
nanometers can easily enter most cells, while those smaller than
20 nanometers can transit out of blood vessels.


SURGICAL ONCOLOGY not all about techniques!
Understanding the behavior of cancer according to the
molecular biology, natural history and its response to
treatment applied under the concept of multidisciplinary
approach.



THE ONLY PREPARATION FOR TOMMORROW
IS THE RIGHT USE OF TODAY





So be strong and courageous! Do not
be afraid and do not panic before them.
For the LORD your God will personally
go ahead of you. He will neither fail nor
abandon you.- Deuteronomy 31:6