Principles of Surgical Oncology Tranx

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  • 8/6/2019 Principles of Surgical Oncology Tranx




    Cancer Statistics - according to theInternational Agency for Research onCancer, WHO (2008)

    Most Frequent Cancers in theworld:Female:

    Incidence Mortality

    1. Breast2. Colorectum3. Cervix Uteri4. Lung5. Stomach6. Corpus Uteri7. Liver8. Ovary9. Thyroid

    10. Others

    1. Breast2. Colorectum3. Cervix Uteri4. Lung5. Stomach6. Liver7. Ovary8. Corpus


    9. Thyroid10. Others

    Male:Incidence Mortality

    1. Lung2. Prostate3. Colorectum4. Stomach5. Liver6. Esophagus7. Bladder8. Non-Hodgkin

    Lymphoma9. Leukemia10. Others

    1. Lung2. Prostate3. Colorectum4. Stomach5. Liver6. Esophagus7. Leukemia8. Bladder9. Non-


    10. Others

    Both sexes:Incidence: Mortality

    1. Breast

    2. Prostate3. Lung4. Colorectum5. Cervix Uteri6. Stomach7. Liver8. Corpus Uteri9. Esophagus10. Ovary

    1. Lung

    2. Breast3. Stomach4. Liver5. Colorectum6. Cervix Uteri7. Prostate8. Esophagus9. Ovary10. Leuke


    Most Frequent Cancers in thePhilippines:Female:

    Incidence Mortality

    1. Breast2. Cervix Uteri3. Lung

    4. Colorectum5. Ovary6. Liver7. Corpus Uteri8. Thyroid9. Leukemia10. Stomach

    1. Breast2. Lung3. Cervix Uteri

    4. Liver5. Colorectum6. Ovary7. Leukemia8. Stomach9. Corpus Uteri10. Thyroid

    Male:Incidence Mortality

    1. Lung2. Liver3. Prostate4. Colorectum5. Stomach6. Leukemia7. Pharynx,

    Others8. Brain9. Non-Hodgkin


    10. Lip/Oral Cavity

    1. Lung2. Liver3. Colorectum4. Prostate5. Stomach6. Leukemia7. Brain8. Pharynx,

    Others9. Non-Hodgkin


    10. Lip/OralCavity

    Both sexes:Incidence: Mortality

    11. Breast12. Lung13. Cervix

    Uteri14. Liver15. Prosta

    te16. Colore

    ctum17. Ovary18. Stoma


    11. Lung12. Breast13. Liver

    14. CervixUteri

    15. Prostate

    16. Colorectum

    17. Stomach

    18. Leuke

    Subject: SurgeryTopic: Principles of Surgical OncologyLecturer: Dr. Malen M. GellidoDate of Lecture: 22 July 2011Transcriptionist: GluttonoidsPages: 13




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    19. Corpus Uteri

    20. Leukemia

    mia19. Ovary20. Brain

    Incidence Rate of NeoplasmsMalignant Neoplasms ranked

    number 3 in the over-all cause ofmorbidity in 2005

    -Causes of death in the Philippinesas of 2005 (DOH):

    1st and 2nd =Cardiovasculardisease 3rd = MalignantNeoplasms


    The Cell Cycle

    During the synthetic or Sphase, the cell generates a singlecopy of its genetic material,.

    Mitotic or M phase, the

    cellular components arepartitioned between two daughtercells.

    The G1 and G2 phasesrepresent gap phases duringwhich the cells preparethemselves for completion of theS and M phases, respectively.

    When cells ceaseproliferation, they exit the cellcycle and enter the quiescentstate referred to as G0.

    In human tumor cell-cycle

    regulators like INK4A, INK4B, andKIP1 are frequently mutated oraltered in expression.

    These alterationsunderscore the importance of

    cell-cycle regulation in theprevention of human cancers.

    Six Essential Alteration in CellPhysiology that Dictate MalignantGrowth

    1. Self- sufficiency in growth signals2. Insensetivity to antigrowth signals3. Tissue invasion and metastasis4. Limited replicative potential5. Sustained angiogenesis6. Evading apoptosis

    **RememberSALISE in patho.Self sufficiency in growth signalsAbility to invade and metastasizeLimitless replicative potentialInsensitivity to growth-inhibitorysignalsSustained angiogenesisEvasion of APOPTOSIS

    Angiogenesis is theestablishment of new bloodvessels from a pre-existingvascular bed which is essentialfor tumor growth and metastasis.

    Tumors develop an angiogenic

    phenotype as a result of accumulated genetic alterationsand in response to local selectionpressures such as hypoxia.

    Apoptosis is a geneticallyregulated program to dispose ofcells.

    o Cancer cells must avoidapoptosis if tumors are toarise.

    o The growth of a tumor

    mass is dependent not onlyon an increase inproliferation of tumor cellsbut also on a decrease intheir apoptotic rate.

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    Metastases arise from thespread of cancer cells from theprimary site and the formation ofnew tumors in distant sites.

    A feature of malignant cells istheir ability to invade thesurrounding normal tissue. Theability to invade involves

    o changes in adhesion,o initiation of motility, ando proteolysis of the

    extracellular matrix (ECM).

    Oncogenes counterpart: Proto-oncogenes

    they are originally proto-oncogenesthat become abnormal throughmutation, chromosomal transfer, oramplification

    These are:

    o PGFR (growth


    o HER 2 neu

    (growth factor receptor)

    o c-myc

    (nuclear transcription factor)

    o ras

    (intracellular signaltransduction molecules)

    Tumor supressor genes (mutationsin these genes leads to cancer):

    o RB1o p53o APCo BRCA 1 and 2-breast cancer genes


    A. Genetic Factors(See Last Page for table)

    General Features of HereditaryCancer Syndromes

    Same or linked forms of cancer intwo or more close relatives

    Earlier than usual cancer onset in

    one or more relatives

    Bilateral cancer in paired organs Multiple primary tumors in the

    same individual

    Specific constellation of tumorsare part of known cancersyndrome

    Evidence of autosomal dominant

    transmission of cancersusceptibility

    B. Chemical Factorso even chemotherapicagents can cause malignancies.

    o chemical carcinogensusually affect specific organs,targeting the epithelial cells (orother susceptible cells within anorgan) and causing geneticdamage (genotoxic)

    o the most commonlyassociated exposures that increasecancer risk are:


    diet, and

    reproductivefactors (e.g., sexual behaviorand hormones).

    o Chemically relatedDNA damage and consequentsomatic mutations relevant tohuman cancer can occur:

    Directy fromexogenous exposures

    Indirectly activation of endogenousmutagenic pathways (e.g.,nitric oxide and oxyradicals)

    Chemotherapeutic Agents

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    C. Viral Factors

    May cause or increase the risk ofmalignancy through:

    o direct transformation,

    expression of oncogenes thatinterfere with cell-cycle

    checkpoints or DNA repairo expression of cytokines or other growthfactorso alteration of theimmune system.

    Oncogenic viruses may beRNA or DNA types

    1. RNA Viruses

    Retroviruses that containreverse transcriptase.

    After infection, the single-stranded RNA viral genome istranscribed into a double-

    stranded DNA copy, which isthen integrated into thechromosomal DNA of the cell.

    Retroviral infection of thecell is permanent; thusintegrated DNA sequencesremain in the host chromosome

    2. DNA Viruses

    Unlike the oncogenes of the RNAviruses, those of the DNA tumorviruses are viral, not cellular, inorigin.

    These genes are required for viralreplication using the host cellmachinery.

    In permissive hosts, infection withan oncogenic DNA virus mayresult in a productive lyticinfection, which leads to celldeath and the release of newlyformed viruses.

    In nonpermissive cells, the viralDNA can be integrated into thecellular chromosomal DNA, andsome of the early viral genes canbe synthesized persistently,which leads to transformation ofcells to a neoplastic state.

    The binding of viral oncoproteinsto cellular tumor-suppressorproteins p53 and Rb isfundamental to thecarcinogenesis induced by mostDNA viruses, although sometarget different cellular proteins.

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    Biological Agents that CauseCarcinogenesis

    D. Physical Factors1. Radiation

    Damage nucleotides,cross linkage, DNA single anddouble stranded breaks,inactivates tumor suppressorgene, induces genomic instabilityin cells that persist at least 30generations

    Induces DNA lesions that

    damage nucleotide bases andcross-linking, and DNA single-and double-strand breaks(DSBs).

    Misrepaired DSBs are theprincipal lesions of importance inthe induction of chromosomalabnormalities and gene


    DSBs in irradiated cellsare repaired primarily by anonhomologous end-joiningprocess, which is error prone;thus DSBs facilitate theproduction of chromosomal

    rearrangements and other large-scale changes such aschromosomal deletions.

    It is thought that radiationmay initiate cancer byinactivating tumor-suppressorgenes.

    Radiation inducesgenomic instability in cells thatpersists for at least 30generations after irradiation.

    Therefore, even if cells donot acquire mutations at initialirradiation, they remain at riskfor developing new mutations forseveral generations.

    ** how radiation produce cancer allthe things are on the molecular level

    2. UV Rays

    UV light creates UV-specificdipyrimidine photoproducts in theDNA of the target cells.

    When these are not sufficientlyrepaired, errors in replication canresult in characteristic mutations

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    in critical genes.

    3. Asbestos

    Asbestos is a naturally occurringmineral silicone that results from

    fibrous crystallization

    Induce DNA damage, includingDSBs, mutations, andchromosomal damage.

    Asbestos fibers can impair mitosisand chromosomal segregation,which can result in aneuploidy.

    Due to formation of reactiveoxygen species

    Can cause Mesothelioma

    **In a cell cycle, there are a lot ofcheckpoints but if tumor suppressorgenes/oncogenes enter the cycle theywill bypass the checkpoints, causing alot of mutations and later on they willbecome cancer.

    (see last page for larger picture)




    An examination of tissue removedfrom a living body in order to

    determine the presence or extentof a disease.

    Origin 19th century French fromGreek bios (life) and opsis (sight)

    Types of BiopsyNeedle Biopsy

    - Fine Needle

    - Core NeedleOpen Surgical Biopsy

    - Incision Biopsy- Excision Biopsy


    1. Fine Needle Aspiration Biopsy

    A cytologic technique inwhich cells are aspirated from atumor using a needle and syringe

    with the application of negativepressure.

    Aspirated tissue consists ofdisaggregated cells rather thanintact tissues

    Other related terms:

    o Fine needle cytology

    o Fine needle biopsy

    o Needle aspiration biopsy


    Aspiration biopsyo Aspiration cytology

    o Needle biopsy

    Equipment needed:

    o 10 or 20ml syringe

    o Gauge 21- 27 needle

    o Glass slides

    o Local anesthetic

    Where is it done?o Office or clinic


    o Office procedure

    o Cheap

    o Fast

    o High sensitivity

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    o Needs experiencedcytopathologist

    o Low specificity

    o Can not distinguishinvasive from in-situmalignancies

    2. Core Needle Biopsy

    Performed with a large cuttingneedle, usually 14 gauge,deployed into the area of concernby a rapid-fire, spring-loaded,automated instrument.

    Retrieves a small piece of intacttumor tissue, which allows thepathologist to study theinvasive

    relationship between cancer cellsand the microenvironment.


    o Sampled material familiarto most pathologists

    o Insufficient samplinginfrequent (

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    o Needs heavy sedation,even general anesthesia

    o Done in the operating room

    Guiding Principles in BiopsyProcedures

    1. Needle tracks or scars should beplaced carefully so that they canbe conveniently removed as partof the subsequent definitivesurgical procedure.

    2. Care should be taken to avoidcontaminating new tissue planesduring the biopsy procedure.

    3. Adequate tissue samples must beobtained to meet the needs of thepathologist.

    4. When knowledge of theorientation of the biopsyspecimen is important forsubsequent treatment, thesurgeon should mark distinctiveareas of the tumor carefully tofacilitate subsequent orientationof the specimen by thepathologist.

    5. Placement of radiopaque clipsduring biopsy and staging

    procedures is sometimesimportant to delineate areas ofknown tumor and to guide thesubsequent delivery of radiationtherapy to these areas.

    Biopsy TechniquesFNA Core



    Yes Yes No

    Hemorrhage + ++ ++Widesampling

    + ++ +++

    Ease ofinterpretation

    + ++ +++

    Ability todetectinvasion

    No Yes Yes

    Cost + ++ +++Rapid


    +++ ++ +


    Pulmonary nodule

    Retroperitoneal mass

    Image-guided biopsy for non-palpable lesions of the breast

    Stereotactic guidance Ultrasound guidance Magnetic resonance imaging

    guidance Needle localization biopsy

    A. Stereotactic Guidance

    Uses the principle of parallax todetermine the lesion position in 3-D space

    Two angled xray views(stereotactic pair) acquired withthe beam 15 degrees on eitherside of the center are used tolocalize the mammographic lesion

    A computer algorithm /software isused to calculate the position of

    the lesion

    1. Automated core biopsyguns

    Multiple core biopsysamples are necessary toensure accurate sampling

    May need 5 -10 samplings

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    Require multiple needleinsertions

    2. Vacuum-assisted biopsydevice (Mammotome Stereotactic or ultrasoundguidance)

    Inserted once and rotated

    while in the breast to obtainsamples from different areas ofthe lesion.

    A vacuum is used to pulltissue into the sample notch

    and transported to thecollection chamber

    Using the vaccum-assistedbreast biopsy system, the probeis positioned at the lesion. Itvacuums, cuts, and removestissue samples, which arepassed through the probeshollow chamber into a collectiontray. This allows for multiplesamples to be collected wholeonly one incision into the breastis made.

    Mammographic Needle

    LocalizationCranio-caudal Magnification Microcalcifi-view view cationslocalized


    Mammographic Needle LocalizationBiopsy

    Specimen Mammography

    Excised breast tissue with needleintact is radiographed

    Mammographic abnormalitiesshould be included in thespecimen

    Not all tumors need to be biopsied

    prior to surgical removal Parotid neoplasms Tumors of the head of the

    pancreas or periampullary areacausing obstructive jaundice

    Liver tumors Retroperitoneal tumors

    **Biopsy may be omitted insituations whereby the histopathresult will not change thedecision to operate and surgically

    remove a tumor

    Biopsy is mandatory to establishthe presence of malignancy in

    Patients who have inoperabletumors and need to undergosystemic anti-cancer treatment(chemotherapy, targeted therapy,etc) or radiation therapy .


    Why is cancer staging needed?

    To be able to prognosticate

    To be able to choose theappropriate management

    Staging Systems

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    Which staging system to usedepends on the type ofmalignancy

    AJCC/UICC uses TNM and is themost commonly used for almostall solid tumors

    FIGO preferred by gynecologists

    Other systems for hematologicmalignancies

    Clinical Tumor Signaling

    TX: Primary tumor cannot beassessed

    T0: No evidence of primarytumor

    Tis: Carcinoma in situ

    Tis Ductal carcinoma in situ

    Tis Lobular carcinoma in situ

    Tis Pagets disease of the nipplewith no tumor.

    T1: Tumor < 2.0 cm or less

    T1mic: Microinvasion < 0.1 cm

    T1a: Tumor 0.1 cm 0.5 cm

    T1b: Tumor 0.5 cm 1.0 cm

    T1c: Tumor 1.0 cm 2.0 cm

    T2: Tumor 2.0 cm 5.0 cm

    T3: Tumor > 5.0 cm

    T4: Tumor of any size withdirect extension to chest wall orskin

    T4a: Extension to chest wall, notincluding pectoralis muscle

    T4b: Edema (including peaudorange) or ulceration of the skinof the breast or satellite skinnodules confined to the samebreast

    T4c: Both T4a and T4b

    T4d: Inflammatory carcinoma.

    Clinical Nodal Staging

    NX: Regional lymph nodescannot be assessed

    N0: No regional lymph nodemetastasis

    N1: Metastasis to movableipsilateral axillary lymph node(s)

    N2: Metastasis in ipsilateralaxillary lymph node(s) fixed ormatted, or in clinically apparentipsilateral internal mammarynodes in the absence of clinicallyevident axillary lymph nodemetastasis

    N3: Metastasis in ipsilateralinfraclavicular lymph node(s) withor without axillary lymph nodeinvolvement, or in clinicallyapparent iipsilateral internalmammary lymph node(s) and inthe presence of clinically evidentaxillary lymph node metastasis;

    or metastasis in ipsilateralsupraclavicular lymph node(s)with or without internal axillary ormammary lymph nodeinvolvement

    Pathologic Nodal Staging

    pNX: Regional lymph nodescannot be assessed

    pN0: No regional lymph nodemetastasis

    pN1: Metastasisin 1 to 3 axillarylymph nodes

    pN2: Metastasis in 4 to 9 axillarylymph nodes

    pN3: Metastasis in 10 or moreaxillary lymph node

    Distant metastasis

    MX: Presence of distantmetastasis cannot be assessed

    M0: No distant metastasis

    M1: Distant metastasis present

    Cancer Staging Metastatic work-ups, usually in

    the form of imaging studies, aredone to determine the presenceof distant spread.

    Distant spread is defined by thestaging system

    Usually refers to any area beyondthe regional lymph node groups

    AJCC Stage Groupings for BreastCancer





    0 Tis N0 M0

    I T1 N0 M0


    T0 N1 M0

    T1 N1 M0

    T2 N0 M0

    IIBT2 N1 M0

    T3 N0 M0

    IIIA T0 N2 M0

    T1 N2 M0

    T2 N2 M0

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    T3 N1 M0

    T3 N2 M0




    Any T N3 M0

    IV Any T AnyN M1

    Diagnostic Studies for Breast CancerPatients

    Cancer Stage0 I II II


    History & physical X X X X XCBC, platelets X X X XLiver functiontests

    X X X X

    Chest x-ray X X X XBilateralmammograms

    X X X X X


    X X X X


    X X X X

    Bone scan X X XAbdominal CTscan orultrasound orMRI

    X X

    Breast Cancer 5 Year SurvivalRates

    Stage I 94% Stage IIa 85% Stage IIb 70% Stage IIIa 52% Stage IIIb 48% Stage IV 18%


    1. Removal of primary tumorprovides local and regional controlof the malignant process.

    Local tumor itself withmargin of normal tissue

    Regional draining lymphnodes

    Questions before surgery Is there informed consent?

    Discuss risks and benefits Will the patient tolerate the

    procedure? Presence of co-morbid

    factors Nutritional status Performance status

    Curative or palliative?


    **The lymphatic drainage of lesions in variousanatomic locations throughout the colon.

    Tumor A in the cecum orascending colon.

    A -> A (left colon) local margin isfollowed on the surgical resectionto satisfy the regional control(lymph nodes) which are foundalong the vasculature (rightcolon)

    Remember:o carcinoma epithelial in

    origin metastasizes throughlymphatic system (lumphnodes).

    o Sarcoma - mesenchymal in

    origin metastized throughhematogenous route

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    Modified Radical Mastectomy vs.L umpectomy

    MRM = Lumpectomy with axillarydissection + radiation

    Radiation is needed tosterilize the breast tissue thatwas left behind after the surgery

    Lumpectomy for lessermagnitude

    Has a high chance ofrecurrence but with samerate of survival with TotalMastectomy.

    Breast is kept


    Used to determine the status ofaxillary lymph nodes withoutencountering the morbidities ofdoing full Axillary Lymph NodeDissection (ALND)

    usually performed before removalof the primary breast tumor

    ALND has complication like lymphedema (LE).

    To prevent LE, sentimental lymphnode is taken out.

    Nuclear Dye is used to localizedthe sentinel lymph node.

    Wide resection

    Local control is used by excising

    the tumor surrounding the normaltissue, regional control isdisregarded.

    Stage III Locally Advanced BreastCancer

    Preoperative Chemotherapy

    Mastectomy or Breast ConversationTherapy (BCT) if possible

    pre operative chemotherapy isgiven before the surgery to shrinkthe tumor.

    If chemotherapy is given beforethe surgery there will be lessrecurrence and improvedsurvival.

    But if chemotherapy is NOT givenbefore the surgery there is achance for an early recurrence.

    Neoadjuvant chemotherapy


    2. Cytoreductive Surgery

    MRM Lumpectomy

    Large incision ismade from axillaacross the breast

    Curvilinear orradial incisionconcentric to thenipple-areola

    complexBreast tissue isdissected frompectoralis muscle andremoved

    Carcinoma andsurrounding tissueis removedcompletely

    Large scar andabsent breast afteroperation

    Small scar afteroperation

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    In some instances, the extensivelocal spread of cancer precludesthe removal of all gross diseaseby surgery.

    The partial surgical resection ofbulk disease in the treatment ofselected cancers improves theability of other treatment

    modalities to control residualgross disease that has not beenresected.

    Burkitt's lymphoma and ovariancancer

    3.Metastatic disease

    Removal of tumors thathave spread to distant sites

    May lengthen a patientssurvival or even provide cure

    As a general principle,patients with a single site ofmetastatic disease that can beresected without major morbidityshould undergo resection of thatmetastatic cancer

    4. Oncologic Emergencies



    drainage of abscesses

    impending destruction ofvital organs



    Surgical resection often isrequired for the reliefof pain orfunctional abnormalities.

    The appropriate use ofsurgery in these settings canimprove the quality of life forcancer patients.

    Palliative surgery mayinclude procedures to relievemechanical problems, such as

    intestinal obstruction, or theremoval of masses that arecausing severe pain ordisfigurement

    6. Reconstruction andRehabilitation

    The ability to reconstructanatomic defects cansubstantially improve functionand cosmetic appearance

    Lost function (especially ofextremities) often can be restoredby surgical approaches.

    These includes lysis ofcontractures or muscletransposition to restore muscularfunction that has been damagedby previous surgery or radiationtherapy

    7. Therapies other thansurgical therapy (read the book toknow this nice to knows :p )

    Chemotherapy (Pharmao_0)

    Hormonal Therapy

    Targeted Therapy


    Gene Therapy

    Radiation Therapy(different lecture)




    Three Categories (not in the ppt butin the book)

    a. primary prevention

    i.e., prevention of initialcancers in healthy individuals

    b. secondary prevention

    i.e., prevention of cancer inindividuals with premalignantconditions

    c. tertiary prevention

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    i.e., prevention of secondprimary cancers in patientscured of their initial disease


    Metastases can sometimes arise several

    years after the treatment of primary


    o E.g breast cancer recurrences

    have been reported decades after

    the original tumor.

    Dormancy - cells remain viable in a

    quiescent state and then become

    reactivated by a physiologically

    perturbing evento Cells establish preangiogenic

    metastases in which they continue to

    proliferate but that proliferative rate

    is balanced by the apoptotic rate.


    Modern cancer therapy ismultidisciplinary, involving thecoordinated care of patients by:

    Surgical Oncologist

    Medical Oncologist

    Radiation Oncologist

    Primary Care Physician


    Gynecologic Oncologist

    Reconstructive surgeon

    Anesthesia/Pain Specialist

    Rehab Med Physician Radiologist

    Psycho Oncologist

    Palliative Care Specialist

    Nurse Oncologist

    Chaplain/ Pastoral CareStaff

    Hospice Care Staff

    Support Groups

    Family Members


    60 y/o male, presenting withmass on hisanterior neck

    DiagnosticProcedures and Treatment:

    History & PE = Clinicaldiagnosis Imaging studies( mammography +/- ultrasound if breast cancer) Biopsy Stage the disease Definitive treatment Additional treatment Surveillance


    I consider that our presentsufferings are not worth comparingwith the glory that will be revealedin us. Romans 8:18

    Conditions in Which ProphylacticSurgery Can Prevent Cancer





    Testicular Orchiopexy

    Polyposis coli Colon Colectomy

    Familial coloncancer

    Colon Colectomy


    Colon Colectomy

    Multipleendocrineneoplasia types2 and 3

    Medullarycancer of thethyroid


    Familial breastcancer

    Breast Mastectomy

    Familial ovariancancer

    Ovary Oophorectomy

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    RT @ medschooladvice: Memorize, take test,unload. Memorize, take test, unload. Medschool: the bulimia of learning.

    ~follow him on twitter :p


    ***This was not emphasized by Dr. Gellido but is included in his ppt.

    A genetic model for colorectal tumorigenesis.(**useful to know. The diagram part was not discussed extensively)

    Tumorigenesis proceeds through a series of genetic alterations involving oncogenes and tumor-suppressorgenes.

    In general, the three stages of adenomas represent tumors of increasing size, dysplasia, and villouscontent.

    Individuals with familial adenomatous polyposis (FAP) inherit a mutation on chromosome arm 5q.

    In tumors arising in individuals without polyposis, the same region may be lost or mutated at arelatively early stage of tumorigenesis.

    A ras gene mutation (usually K-ras) occurs in one cell of a pre-existing small adenoma which, throughclonal expansion, produces a larger and more dysplastic tumor.

    The chromosome arms most frequently deleted include 5q, 17p, and 18q. Allelic deletions of chromosome arms 17p and 18q usually occur at a later stage of tumorigenesis

    than do deletions of chromosome arm 5q or ras gene mutations.

    The order of these changes varies, however, and accumulation of these changes, rather than theirorder of appearance, seems most important.

    Easter Cooperative Oncology Group: Performance Scale and Corresponding Karnofsky Rating

    Grade Description Karnofscy Scale

    0 Fully active, able to carry on all predisease activitiease without restriction 100

    1 Restricted in physically strenuous activity, but ambulatory and able to carry 80 90

    out work of a light or sedentary nature (e.g., light houseworl/office work)

    2 Ambulatory and capable of all self-care but unable to carry out any work 60 70

    activities; up and about more than 50% of waking hours

    3 Capable of limited self-care, confined to bed or chair 50% or more of 40 50

    waking hours4 Completely disabled cannot carry on any self-care; totally confined to bed or chair 30 or less
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    **nasa libro itong table at nasa ppt din di doc...baka gusto nyong kabisaduhin.. Goodluck! :p

    o But the genes he emphasized were RB1, p53, APC, BRCA 1

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    and 2