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Atienza, Austria, Balbin (09272265029), Bandoma, Bañez, 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. P53)

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.

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6th 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 – doesn’t 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 don’t 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 G0 phase – State of cells not in the active cell cycle but capable of entering G1 upon stimulation.

o Gap 1 phase (G1) – period from mitosis to start of DNA synthesis.

o DNA Synthesis (S) o Gap 2 phase (G2) – 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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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.

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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 109 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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G. Clinical Implication

Fast growing cancers (e.g Pancreatic AdenoCA, Gastric cancer, Esophageal cancer) o Intensive surveillance for 1st 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 don’t 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 doesn’t 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 don’t 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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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 couldn’t 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 couldn’t 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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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. That’s 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 there’ll 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 (won’t 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 body’s 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