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INT > INTRODUCTION TO CANCER THERAPY; TRADITIONAL APPROACHES > Flashcards

INTRODUCTION TO CANCER THERAPY; TRADITIONAL APPROACHES Flashcards

1
Q

TRADITIONAL CANCER TREATMENT

A
  • RADIATION
  • SURGERY
  • CHEMOTHERAPY (MAIN APPROACH)
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2
Q

PRECISION MEDICINE FOR CANCER TREATMENT, EXAMPLES

A
  • TARGETED THERAPY (TARGETS CANCER-SPECIFIC GENETIC CHANGES USED TO SLOW TUMOUR GROWTH AND/OR KILL CANCER CELLS)
  • IMMUNOTHERAPY (MEDICAL TREATMENT THAT HELPS PATIENT’S OWN IMMUNE SYSTEM TO FIGHT THE CANCER)
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3
Q

TIMELINE OF KEY TURNING POINTS IN THE TREATMENT OF CANCER

A

3000 B.C. - 1890; SURGICAL TRETAMENTS ONLY OPTION USED
EARLY 1890s; RADIOTHERAPY (MARIE AND PIERRE CURIE)
1940s; CHEMOTHERAPY (DEVELOPMENT OF ANTITUMOUR DRUGS FOR THE TRETAMENT OF HEAMTOLOGICAL AND SOLID TUMORS)
1980s; TARGETED THERAPY (TYROSINE KINASE INHIBITORS AND MONOCLONAL ANTIBODIES DIRECTED TO SPECIFIC TUMORS AND MOLECULAR ALTERATION)
2010; CHECKPOINT INHIBITORS (USE OF MONOCLONAL ANTIBODIES ABLE TO STIMULATE THE IMMUNE SYSTM AGAINST CANCER)

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4
Q

CANCER CHEMOTHERAPY?

A
  • A MODALITY OF CANCER THERAPY THAT INVOLVES ADMINISTRATION OF CHEMICAL AGENTS TO DESTROY CANCER CELLS (CYTOTOXIC)
  • THE AIM OF CANCER CHEMOTHERAPY IS TO CURE WHERE POSSIBLE AND PALLIATE WHERE CURE IS IMPOSSIBLE
  • THE EFFECTIVE USE OF CHEMOTHERAPY NEEDS AN UNDERSTANDING OF THE PRINCIPLES OF TUMOUR BIOLOGY, CELLULAR KINETICS, PHARMACOLOGY AND DRUG RESISTANCE
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5
Q

THE FIRST CHEMOTHERAPEUTIC DRUG

A
  • 2ND DECEMBER 1943, BOMBING OF SHIPS, ONE OF WHICH (NAMED SS JOHN HARVEY) WAS CARRYING A SECRET CARGO OF 100 TONS OF MUSTARD GAS (NITROGEN MUSTARD)
  • MANY SEAMEN ON SURROUNDING SHIPS WHO SURVIVED DEVELOPED BLISTERING OF EPITHELIAL SURFACES, REDUCED WHITE BLOOD CELLS (LEUKOPENIA) AND PROFOUND LYMPHOID AND MYELOID SUPPRESISON ON AUTOPSIES
  • USING THIS INFO, PHARMACOLOGISTS GOODMAN AND GILMAN REASONED THAT THIS AGENT COULD BE USED TO TREAT LYMPHOMA
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6
Q

IS COMBINATION OR SINGLE AGENT CHEMOTHERAPY USED MORE OFTEN?

A

COMBINATION, BECAUSE DRUG RESISTANCE DEVELOPS RAPIDLY WHEN SINGLE AGENT IS USED BECAUSE OF THE PLASTICITY OF CANCER CELLS

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7
Q

DIFFERENT WAYS OF USING CHEMOTHERAPY?

A

NEOADJUVANT (PREOPERATIVELY): ADMINISTERED PRIOR TO SURGERY TO FACILITATE RESECTION AND PREVENT METASTASIS
ADJUVANT (POSTOPERATIVELY): AFTER SURGICAL DEBULKING TO KILL MICROMETASTASES AND REDUCE RISK OF DISTANT RELAPSE; INCREASE DISEASE-FREE SURVIVAL
PALLIATIVE: IMPROVE THE QUALITY OF THE PATIENT’S LIFE BY CONTROLLING SYMPTOMS /PROLONG LIFE IN A PATIENT IN WHOM CURE IS UNLIKELY
SALVAGE: A POTENTIALLY CURATIVE, HIGH-DOSE REGIMEN GIVEN TO A PATIENT WHO HAS FAILED OR RECURRED FOLLOWING A PRIOR CURATIVE REGIMEN

(OVERALL CURE RATES LOW)

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8
Q

APART FROM AFFECTING CANCER CELLS, CHEMOTHERAPY AFFECTS:

A

OTHER, HEALTHY, FAST-GROWING!!! CELLS OF THE BODY (E.G. BONE MARROW, WHICH CRATES BLOOD AND IMMUNE CELLS, AS BLOOD IS NCREDIBLY FAST REPLENISHING, LEADING TO CANCER PATIENTS BECOMING IMMUNOSUPPRESED, HAIR FOLLICLES, MUCOSAL TISSUES INSIDE THE MOUTH ETC)

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9
Q

KEY MECHANISM OF CHEMOTHERAPY

A

INTERFERENCE WITH BIOLOGICAL PROCESSES NECESSARY FOR CELL DIVISION INCLUDING THE SYNTHESIS OF DNA AND RNA

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10
Q

ANTIMETABOLITES?

A
  • A GROUP OF CHEMOTHERAPY DRUGS
  • LIMIT THE SYNTHESIS OF NUCLEIC ACID PRECURSORS (LEADING TO CELL DEATH)
  • E.G. METHOTREXATE INHIBITS DIHYDROFOLATE REDUCTASE, REDUCING THE SYNTHESIS OF FOLATE WHICH IS NECESSARY FOR PURINE AND PYRIMIDINE PRODUCTION
  • OTHER EXAMPLES: 5-FLUOROURACIL, CYTARABINE
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11
Q

TOPOISOMERASE ENZYMES?

A
  • PARTICIPATE IN THE WINDING AND UNWIDING OF DNA AND ARE INHIBITED BY ANTHRACYCLINES, EPIPODOPHYLLOTOXINS AND CAMPTOTHECINS (DNA UNWIDING NEESSARY FOR REPLICATION, THIS STOPS THE CELLS FROM DIVIDING, A CHEMOTHERAPY APPROACH)
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12
Q

WHICH TYPE OF CHEMOTHERAPY DRUGS CAUSE STRUCTURAL DAMAGE TO MATURE DNA? EXAMPLE OF CANCER IN WHICH THEY ARE USED?

A
  • ALKYLATING AGENTS (CYCLOPHOSPHAMIDE, CHLOROAMBUCIL, PROCARBAZINE); A COMMON VARIETY OF THIS TYPE OF DRUG ARE PLATINUM DERIVATIVES (CISPLATIN, CARBOPLATIN) –> USED AGAINST E.G. OVARIAN CANCER
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13
Q

WHICH TYPES OF CHEMOTHERAPY DRUGS DISTURB THE FUNCTION OF MITOTIC SPINDLE?

A
  • VINCA ALKALOIDS (VINCRISTINE, VINBLASTINE)

- TAXANES (PACLITAXEL AND RELATED COMPOUNDS)

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14
Q

HORMONAL AGENTS IN CHEMOTHERAPY?

A
  • BLOCK PROLIFERATION OF HORMONE-RESPONSIVE CELLS (E.G. OVARIAN AND BREATS CANCER)
  • E.G. TAMOXIFEN, AROMATASE INHIBITORS
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15
Q

EXAMPLES OF MECHANISMS OF CHEMOTHERAPEUTIC DRUGS?

A
  • ANTIMETABOLITES (LIMIT NUCLEIC ACIDS PRECURSORS)
  • INHIBITING TOPOISOMERASE ENZYMES INVOLVED IN WINDING AND UNWINDING OF DNA
  • CAUSING STRUCTURAL DAMAGE TO DNA
  • DISURBING FUNCTION OF THE MITOTIC SPINDLE
  • HORMONAL AGENTS (BLOCK PROLIFERATION OF HORMONE RESPONSIVE CELLS)
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16
Q

MECHANISM OF ACTION OF CHEMOTHERAPEUITIC DRUGS; ALKYLATING AGENTS

A
  • TARGET DNA, PRODUCE ALKYLATION THROUGH FORMATION OF INTERMEDIATES
  • NOT CELL CYCLE PHASE SPECIFIC!!!
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17
Q

MECHANISM OF ACTION OF CHEMOTHERAPEUITIC DRUGS; ANTIMETABOLITES

A
  • INTERFERE WITH DNA SYNTHESIS
  • STRUCTURAL ANALOGUES OR INHIBIT SEVERAL ENZYMES
  • S PHASE SPECIFIC!!!!
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18
Q

MECHANISM OF ACTION OF CHEMOTHERAPEUITIC DRUGS; MITOTIC SPINDLE AGENTS?

A
  • BIND TO MICROTUBULAR PROTEINS INHIBITING MICROTUBULE ASSEMBLY THEREBY INTERRUPTING THE MITOIS PHASE OF CELL DIVISION
  • M PHASE SPECIFIC!!!
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19
Q

EXAMPLE OF DISCOVERY OF MITOTIC SPINDLE AGENT CHEMOTHERAPEUTIC DRUG, PACLITAXEL (TAXOL)

A
  • US PROGRAMME TO SCREEN PLANTS TO TRY AND FIND NEW ANTICANCER AGENTS
  • SAMPLE OF PACIFIC YEW TREE, IDENTIFIED CYTOTOXIC ACTIVITY IN A COMPOUND NAMED ‘TAXOL’
  • TAXOL FOUND TO INHIBIT THE DEPOLYMERISATION OF MICROTUBULE LEADING TO CELL ARREST AT MITOSIS AND SUBSEQUENT APOPTOSIS
  • LATER FOUND TO HAVE PARTIAL OR COMPLETE RESPONSE IN 30% OF PATIENTS WITH ADVANCED OVARIAN CANCER
  • 1992; FDA APPROVED FOR OVARIAN CANCER
  • 1994; FDA APPROVED FOR BREAST CANCER
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20
Q

MECHANISM OF ACTION OF CHEMOTHERAPEUITIC DRUGS; TOPOISOMERASE INHIBITORS?

A
  • DNA TOPOISOMERASES I AND II ARE ESSENTIAL ENZYMES FOR TRANSCRIPTION, REPLICATION AND MITOSIS (MODULATE THE STRUCTURE AND WINDING OF DNA)
  • INHIBITING THEM WILL LEAD TO CELL DEATH
  • DIFFERENT GROUPS OF DRUGS: TOPO I &TOPO II INHIBITORS
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21
Q

PRICIPLES OF COMBINATION CHEMOTHERAPY

A

COMBINATION CHEMOTHERAPY CAN OFTEN USE 3-4 DRUGS!!!!

  • USE DRUGS ACTIVE AS A SINGLE AGENT
  • USE DRUGS WITH DIFFERENT MECHANISMS OF ACTION
  • USE DRUGS WITH DIFFERENT MECHANISMS OF RESISTANCE
  • USE DRUGS WITH DIFFERENT SIDE EFFECTS
  • BE AWARE OF DRUG-DRUG INTERACTIONS
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22
Q

CATEGORISATION OF CANCER BY EFFECTIVENESS OF CHEMOTHERAPY

A

RESPONSIVENESS ( IN DECREASING ORDER OF EFFICACY):

CATEGORY 1 (TUMOURS WHICH CAN BE CURED BY MONO OR COMBINATION THERAPY, I.E. NORMAL LIFE SPAN AND PROLONGATION OF SURVIVAL IN MOST PATIENTS, E.G. GERM CELL, LEUKEMIAS, LYMPHOMAS, CHORICARCINOMA, TESTICULAR CANCER)

CATEGORY 2 (TUMOURS WHERE THE AVERAGE SURVIVAL IS PROLONGED WHEN CHEMOTHERAPY IS USE AS AN ADJUVANT TO LOCAL SURGERY OR RADIOTHERAPY IN THE ERLY STAGES OF DISEASE, E.G. BREAST, COLORECTAL, OVARIAN, OSTEOSARCOMA, EING’S SARCOMA, WILMS TUMOUR)

CATEGORY 3 (TUMOURS WHERE THERE IS EVIDENCE THAT A SINGLE DRUG OR A COMBINATION WILL PRODUCE CLINICALLY USEFUL RESPONSES IN MORE THAN 20% OF PATIENT. PROLONGATION OF SURVIVAL OCCURS IN MOST RESPONDING PATIENTS BUT MAY BE OF SHORT DURTAION, E.G. LUNG, BLADDER, PROSTATE, STOMACH, CERVICAL)

CATEGORY 4 (TUMOURS WHERE LOCAL CONTROL MAY BE IMPROVED BY USING CHEMOTHERAPY BEFORE, DURING OR AFTER SURGERY AND RADIOTHERAPY, E.G. HEAD AND NECK)

CATEGORY 5 (TUMOURS FOR WHICH THERE ARE CURRENTLY NO EFFECTIVE DRUGS. OBJECTIVE RESPONSES OCCUR IN LESS THAN 20% OF PATIENTS AND THERE IS NO EVIDENCE OF SURVIVAL BENEFIT IN RCTs WHEN COMPARED TO BEST SUPPORTIVE CARE, E.G. LIVER, MELANOMA, PANCREATIC, BRAIN, RENAL, THYROID)

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23
Q

PARMETERES TO BE EVALUATED IN SYSTEMIC CANCER TREATMENTS (WHOLE-BODY)

A

RESPONSE:

  • COMPLETE RESPONSE (CR); DISAPPEREANCE OF ALL TARGET LESIONS
  • PARTIAL RESPONSE (PR); AT LEAST A 30% DECREASE IN THE SUM OF THE LONGEST DIAMETER (LD0 OF TARGETED LESIONS
  • STABLE DISEASE (SD); NEITHER SUFFIECIENT SHRINCAKE TO QUALIFY FOR PR NOR SUFFICIENT INCREASE TO QUALIFY FOR PD
  • PROGRESSIVE DISEASE (PD); AT LEAST A 20% INCREASE IN THE SUM OF THE LD OF TARGETED LESIONS
  • DURATION OF RESPONSE OR TIME TO PROGRESSION (TTP): THE TIME FROM RESPONE TO PROGRESSION

SURVIVAL:

  • DISEASE FREE SURVIVAL (DFS); FROM THE TIME OF TREATMENT TO FIRST RECURRENCE
  • OVERALL SURVIVAL (OS); FROM THE TIME OF DIAGNOSIS TO DEATH
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24
Q

HOW CAN RESPONSE TO CANCER THERAPY BE CATEGORISED/EVALUATED?

A
  • COMPLETE RESPONSE (CR); DISAPPEREANCE OF ALL TARGET LESIONS
  • PARTIAL RESPONSE (PR); AT LEAST A 30% DECREASE IN THE SUM OF THE LONGEST DIAMETER (LD0 OF TARGETED LESIONS
  • STABLE DISEASE (SD); NEITHER SUFFIECIENT SHRINCAKE TO QUALIFY FOR PR NOR SUFFICIENT INCREASE TO QUALIFY FOR PD
  • PROGRESSIVE DISEASE (PD); AT LEAST A 20% INCREASE IN THE SUM OF THE LD OF TARGETED LESIONS
  • DURATION OF RESPONSE OR TIME TO PROGRESSION (TTP): THE TIME FROM RESPONE TO PROGRESSION
25
Q

CHEMOTHERAPY DELIVERY

A
  • INTRAVENOUS OR ORAL
  • LOCAL DRUG APPLICATION: (DECREASES OVERALL TOXICITY TO THE BODY)
  • – INTRA-ARTERIAL (I.E. HEPATIC INFUSION)
  • – INTRA-PERITONEAL (OVARIAN CANCER)
  • – INTRA-PLEURAL (PLEURAL METASTASIS)
  • DAY CARE OR OUTPATIENT SETING (REDUCED COSTS AND BETTER FOR PATIENTS AND FAMILIES)
  • NEED TO CONSIDER PROGNOSTIC FACTORS!!!: STAGE OF DISEASE, SITE OF METASTAIS, GENERAL MEDICAL CONDITION OF PATIENT, WILLINGNESS TO ACCEPT LIKELY TOXICITY…
  • RISK VS BENEFIT, MUST BE AN INFORMED DECISION
  • CONSIDERATIONS REGARDING DRUG COSTS
26
Q

POSSIBLE TOXICITIES OF ALKYLATING CHEMOTHERAPEUTIC AGENTS

A
  • GERM CELL DAMAGE (GONADAL DAMAGE; SPERM PRESERVATION SMETIMES RECOMMENDED)
  • PULMONARY TOXICITY (IF DETECTED EARLY CAN BE TREATED WITH CORTICOSTEROIDS)
  • SECOND MALIGNANCIES AS A RESULTS OF TREATMENT WITH ALKYLATINGS
27
Q

MUCOSITIS AND CANCER THERAPY?

A
  • ORAL MUCOSISTIS IS A COMMON COMPLICATION OF CANCER CHEMOTHERAPY
  • BEGINS 5-10 DAYS AFTER THE INITIATION OF CHEMOTHERAPY AND LASTS 7-14 DAYS
  • CAUSES THE LINING OF THE MOUTH TO ATROPHY AND BREAK DOWN, CAUSING ULCERS AND SORES

PATIENTS TYPICALLY EXPERIENCE THE FOLLOWING:

  • ORAL PAIN AND BURNING
  • ULCERATIONS
  • DIFFICULTY EATING, DRINKING AND SPEAKING
  • DIFFICULTY WITH MOUTH CARE REGIMENS
  • GRADES 0-4
28
Q

TREATMENT FOR MUCOSITIS INDUCED BY CYTOTOXIC CANCER THERAPY?

A
  • GOOD AND REGULAR ORAL HYGIENE
  • REGULAR MOUTHWASHES
  • PROTECT LIPS WITH MOUSTERISER
  • AVOIDING ACIDIC FOODS, ALCOHOL AND SPICY FOODS
  • ANALGESIA (E.G. PECFENT)
29
Q

DRUG RESISTANCE EVOKED BY CYTOTOXIC DRUGS

A
  • TUMOURS RELATIVE TO NORMAL TISSUE MAY BE INHERENTLY RESISTANT OR ACQUIRE RESISTANCE
  • MAINLY OCCURS FOR DRUGS OF SIMILAR STRUCTURE, BUT EXTENDS TO MULTIPLE CLASSES OF STRUCTURALLY UNRELATED AGENTS

4 MAIN MECHANISMS:

1) THE TRANSPORT OF A DRUG OUT OF THE CELL (PUMPING IT OUT)
2) THE METABOLISM AND THUS INTRACELLULAR CONCENTRATION OF THE DRUG
3) STRUCTURE OF THE TARGET PROTEIN TO WHICH DRUG BINDS TO CAUSE CYTOTOXICITY
4) PROTECTION FROM APOPOTOSIS

+ THE ISSUE OF CANCER STEM CELLS; QUIESCENT, INCREASED EXPRESSION OF ANTI-APOPTOTIC PROTEINS AND INCREASED ACTIVITY OF PRO SURVIVAL PATHWAYS

30
Q

A MAJOR TRANSPORT PROTEIN RESPONSIBLE FOR DRUG RESISTANCE IN RESPONSE TO CYTOTOXIC CHEMOTHERAPY:

A
  • P-GLYCOPROTEIN (PGP)
  • ENCODED BY THE MDR1 GENE
  • PUMPS OUT DRUGS
  • NORMAL PATHWAY IN HEALTHY CELLS, BUT CAN BECOME UPREGULATED IN SOME CANCERS
  • PGP OVEREXPRESSION THROUGH INCREASED EXPRESSION OF ITS mRNA (WITH OT WITHOUT MDR1 GENE AMPLIFICATION)
31
Q

EXAMPLES OF HOW DRUG RESISTANCE TO PLATINUM DRUGS IN CANCER CAN BE TACKLED?

A
  • INCREASING THE LEVELS OF PLATINUM REACHING TUMOURS IN A WAY THAT’S LESS TOXIC (E.G. LIPOSOMAL PLATINUM PRODUCTS)
  • COMBINING THE EXISTING PLATINUM DRUGS WITH MOLECULARY TARGETED DRUGS (E.G BEVACIZUMAB)
  • USING NOVEL PLATINUM DRUGS TARGETING RESISTANCE MECHANISMS (E.G. OXALIPLATIN) OR MODIFYING THE DRUG ITSELF TO BE LESS SUSCEPTIBLE TO RESISTANCE
32
Q

EXAMPLES OF HOW THE TUMOR MICROENVIRONMENT (TME) IS ASSOCIATED WITH DRUG RESISTANCE?

A
  • VASCULAR ABNORMALITY (AFFECTS DRUG DELIVERY, FLUID EXTRAVASATION)
  • HYPOXIA AND ACIDICITY (INDUCED ANGIOGENESIS, APLIFICATION OF GENE EXPRESION, INITIATION OF IMMUNOLOGICAL AND METABOLIC CHANGES OF TME
  • FIBROBLASTS (DRUG ENTRAPPING, CYTOKINES AND GF SECRETION)
  • IMMUNE CELLS (CYTOKINES AND CHEMOKINES SECRETION, SHAPING THE IMMUNOSUPPRESIVE TME)
  • ECM (BIOMOLECULES SECRETION, INDUCED PROGRAMMED CELL DEATH)
  • EXOSOMES (DELIVERY OF RESISTANT MOLECULES, DRUG EFFLUX AND METABOLISM ALTERATION, PROMOTE CELL SURVIVAL)
33
Q

SURGERY FOR CANCER IS ALSO KNOWN AS

A

SURGICAL ONCOLOGY

34
Q

DISOCVERIES THAT REVOLUTIONAISED SURGICAL ONCOLOGY

A
  • DISCOVERY OF ANASTHESIA
  • DISCOVERY OF ANTISEPTIC AGENTS
  • SUB SPECIALISTAIONS AND HYPERSPECIALISATIONS OF SURGEONS WHO CAN PERFORM MUCH MORE PRECISE SURGERIES (IN HISTORY; QUITE RADICAL APPROACHES USED, REMOVING WHOLE LARGE ORGANS)
  • MULTIDISCIPLINARY APPROACHES 9COMBINING SURGERY WITH RADIOTHERAPY, CHEMOTHERAPY ETC.)
  • INTRODUCTION OF PREVENTATIVE SURGERY (E.G. FOR BRAST CANCER)
  • SURGERY FOR PALLIATION (FOR DISABLING SYMPTOMS, E.G. IF A TUMOUR IS PRESING ON A CERTAI ORGAN)
35
Q

WHEN CAN SURGERY CURE CANCER PATIENTS?

A

WHEN THEY HAVE SOLID TUMOURS WHICH ARE CONFINED TO THE ANATOMIC SITE OF ORIGIN, ESP IF DETECTED EARLY

36
Q

TECHNOLOGICAL ADVANCES IN SURGICAL ONCOLOGY

A
  • DEVELOPMENT OF SURGICAL INSTRUMENTATION
    USE OF FINE NEEDLES AND FIBRE-OPTIC ENDOSCOPY (E.G. LAPAROSCOPY FOR THE DIAGNOSIS AND STAGING OF CANCER: OESOPHAGEAL, STOMACH, COLON, PANCREATIC)
    LIVER RESECTION FOR COLORECTAL LIVER METASTASIS
  • ROBOTIC SURGERY (OR ROBOT ASSISTED SURGERY) —> USUALLY ASSOCIATED WITH MINIMALLY INVASIVE SURGERY; PROCEDURES PERFORMED THROUGH TINY INCISIONS
37
Q

EXAMPLES OF WHERE SURGICAL ONCOLOGY CAN BE USED AS A MEANS OF CANCER PREVENTION

A
  • TESTICULAR CANCER (REMOVAL OF TESTICLES (ORCHIDOPEXY), E.G. IN CASE OF CRYPTORCHIDISM; WHEN ONE OR BOTH OF THE TESTICLES DO NOT DESCEND INTO THE SCROTUM WHILE THE FETUS IS DEVELOPING)
  • COLON CANCER (COLECTOMY IN CASES OF E.G. FAMILIAL COLON CNACER, FAP OR HNPCC, OR ILLNESSES LIKE ULCERATIVE COLITIS)
  • BREAST CANCER (MASTECTOMY, E.G. FAMILIAL BREATS CANCER, BRCA 1 OR 2 MUTATIONS)
  • OVARIAN CANCER (OOPHORECTOMY, FAMILIAL OVARIAN CANCER, BRCA 1)
  • MEDUALLARY CNACER OF THE THYROID (THYORIDECTOMY, FOR UNDERLYING CONDITIONS SUCH AS MULTIPLE ENDOCRINE NEOPLASIA, GENES MEN1 AND MEN2)
38
Q

TUMOUR MARGIN?

A

REMOVING A RIM OF NORMAL TISSUE SURROUNDING THE TUMOR WHEN PERFORMING ONCOLOGICAL SURGERY

  • THERE ISN’T A STANDARD DEFINITION OF HOW WIDE A ‘CLEAR MARGIN’ HAS TO BE
  • USUALLY 2MM OR MORE OF NORMAL TISSUE BETWEEN THE EDGE OF THE CANCER AND THE OUTER EDGE OF THE REMOVED TISUE
  • PARTICULARLY IMPORTANT IN BREATS CANCER!!!!! (LUMPECTOMY/PARTIAL MASTECTOMY)
39
Q

MODIFIED RADICAL MASECTOMY?

A
  • SURGICAL PROCEDURE PERFORMED WHEN BREATS CANCER HAS STARTED SPREADING
  • COMBINES A SIMPLE MASTECTOMY WITH REMOVAL OF THE LYMPH NODES UNDER THE ARM (AXILLARY LYMPH NODE DISSECTION)
40
Q

WHAT KIND OF SURGERY IS ROBOTIC SURGERY ASSOCIATED WITH?

A

MINIMALLY INVASIVE SURGERY, PERFORMED THROUGH TINY INCISIONS

41
Q

FUNDAMENTALS OF RADIATION THERAPY FOR CANCER

A
  • USE OF IONISING RADIATION TO TREAT CANCER; MODERN HIGH ENEGY X-RAY MAHCHINES CAN DELIVER TIGHT BEAMS TO WELL-DEFINED AREAS IN THE BODY (TARGET DEEP-SEATED TUMOURS WITH MINIMAL RADIATION TO SURROUNDING NORMAL TISSUE)
  • AIMS TO KILLS CELLS; DNA DAMAGE INDUCED BY IONIZING RADIATION!!!!
  • THE MAJOR TYPES OF DAMAGE INDUCED BY IR INCLUDE BASE AND SUGAR DAMAGE, SINGLE-STRAND BREAKS, DOUBLE-STRAND BREAKS AND COVALENT INTRASTRAND OR INTERSTRAND CROSSLINKING
42
Q

OVERVIEW OF DNA DAMAGE RESPONSE

A

3 STEP PROCESSES

1) DNA DAMAGE IS RECOGNIED BY DNA DAMAGE SENSOR PROTEINS
2) TRANSDUCER PROTEINS THEN SIGNAL TO EFFECTORS
3) THIS RESULTS IN EITHER CELL CYCLE ARREST, DNA REPAIR OR APOPTOSIS
(SENSORS —> TRANSDUCERS —> EFFECTORS)

(TUMOURS CAN DEVELOP THERAPY RESISTANCE BY ACTIVATING OR INHIBITING VARIOUS PROCESSES WITHIN THE DNA DAMAGE RESPONSE)

43
Q

FACTORS INFLUENCING TUMOUR RESPONSE TO RADIOTHERAPY

A

CELL INTRINSIC FACTORS:

  • CELL TYPE
  • PHASE OF THE CELL CYCLE
  • P53 AND ATM STATUS

MICROENVIRONMENT FACTORS:

  • OXYGEN TENSON
  • SERUM DEPRIVATION
  • pH

RADIATON FACTORS:

  • TOTAL DOSE
  • NUMBER OF FRACTIONS
  • RADIATION QUALITY
44
Q

DESCRIBE THE FORMS OF RADIOTHERAPY?

A

RADICAL RADIOTHERAPY:

  • INTENT TO CURE EITHER AS PRIMARY THERAPY (E.G. EARLY STAGE HODGKIN’S LYMPHOMA) OR AS AN ALTERNATIVE TO SURGERY
  • PRESERVES NORMAL ANATOMY, ACUTE MORBIDITY IS LESS SEVERE
  • FOR LOCALISED DISEASE
  • HIGH DOSE THERAPY DELIVERED IN DAILY FRACTIONS. TYPICALLY OVER UP TO 7 WEEKS TO REDUCE LATE ADVERSE EFFECTS
  • E.G. HEAD AND NECK CANCR (OFTEN COMBINED WITH CHEMO), LARYNGEAL CARCINOMA, LUNG CANCER FOR PATIENTS NOT FIT TO UNDERGO RADICAL SURGERY….

ADJUVANT RADIOTHERAY:

  • ADMINISTERED AS AN AJUNCT TO POTENTIALLY CURATIVE SURGERY
  • ERADICATE MICROSCOPIC RESIDUAL DISEASE WHICH REMAINS WITHIN THE TUMOUR BED, LYMPHATIC CHANNELS OR REGIONAL LYMPH NODES
  • BREAST CANCER IS MOST COMMONLY USED EXAMPLE ( USED TO REDUCE LOCAL RELAPSE RATES FOLLOWING PARTIAL MASTECTOMY

PALLIATIVE RADIOTHERAPY:

  • CONTROL OF DISTRESSING SYMPTOMS
  • NOT CURATIVE; IMPROVES THE QOL INSTED
  • RELIEVE PAIN DUE TO BONE METASTASES AND NERVE COMPRESSION
  • REDUCE HEMORRHAGE AND OBSTRUCTIONS
  • USED IN E.G. BRAIN METASTASES
45
Q

MOST COMMON EXAMPLE OF USE OF ADJUVANT RADIOTHERAPY?

A

BREAST CANCER (TO REDUCE LOCAL RELAPSE RATES FOLLOWING PARTIAL MASTECTOMY)

46
Q

EXTERNAL BEAM RADIOTHERAPY

A
  • X RAYS, GAMMA RAYS AND ELECTRON BEAMS FROM LINEAR ACCELERATORS
  • HIGH INTENSITY ELECTROM BEAM (4-20 MeV) HAS GREATER PEETRATION, LESS SCATTER, DELIVERS HIGH ENERGY TO DEEP-SEATED TUMOURS WHILE SPARING NORMAL TISSUES IN ITS PATHWAY
  • CONFORMAL AND INTENSITY-MODULATED RADIOTHERAPY SHAPE THE RADIATION BEAMS TO CLOSELY FIT THE TUMOR (PLANNED USING CT SCAN TO CREATE A 3D IMAGE OF TUMOUR LOCATION) —> COMPUTER PROGRAMME DESIGNS RADIATION BEAMS THAT FOLLOW THE SHAPE OF THE TUMOR
  • FRACTIACION DIVIDES DOSE OVER A TREATMENT COURSE LASTING MULTIPLE WEEKS (BALANCE BETWEEN TARGETING THE TUMOUR AND DAMAGING NORMAL TISSUE)
47
Q

NAME FOR INTERNAL RADIOTHERAPY?

A

BRACHYTHERAPY

48
Q

BRACHYTHERAPY?

A
  • USE OF RADIOACTIVE SOURCES IMPLANTED DIRECTLY INTO A TUMOUR OR BODY CAVITY TO DLIVER LOCALISED RADIOTHERAPY

E.G. RADIOACTIVE IRIDIUM-192 NEEDLES OR WIRES IMPLANTED INTO TUMOURS OF THE BREAST, TONGUE OR FLOOR OF THE MOUTH

  • MAJOR DISADVANTAGE IS RISK TO STAFF HANDLING RADIOACTIVE SOURCES
49
Q

RADIOISOTOPE THERAPY?

A
  • INTERNAL ISOTOPE TREATMENT GIVEN EITHER ORALLY OR SYSTEMATICALLY BY INJECTION
  • CAN ONLY BE USED WHERE A TUMOUR IS IN A TISUE THAT WILL PREFERENTIALLY ACCUMULATE A SPECIFIC ISOTOPE
  • E.G. RADIOIODINE (I-131) FOR THE TREATMENT OF THYROID CANCER
  • E.G. RADIOIMMUNOTHERAPY; RADIOLABELLED MONOCLONAL ANTIBODIES, E.G. AS TREATMENT FOR B CELL LYMPHOMA (BLOOD CANCERS)
  • E.G. TREATMENT FOR METASTATIC SOLID TUMORS; ANTIBODIES FOR BREAST CANCER (HER2), COLORECTAL CANCER (CEA), PROSTATE CANCER (PSMA ETC)
50
Q

PROTON THERAPY?

A
  • FORM OF RADIOTHERAPY THAT USES PROTONS INSTEAD OF X RAYS
  • HIGH ENERGY PROTON BEAMS TARGET TUMOURS MORE PRECISELY
  • GENERATED USING A SYNCHROTRON OR CYCLOTRON
  • LESS RADIATION DOSE OUTSIDE THE TUMOUR (LESS DAMAGE TO HEALTHY TISSUES) –> FEWER SHORT TERM AND LONG TERM SIDE EFFECTS
  • PROVEN TO BE EFFECTIVE IN ADULTS AND ESPECIALLY CHILDREN WITH BRAINCANCER
51
Q

HOW DOES RADIOTHERAPY INFLUENCE THE BODILY IMMUNE RESPONSE TO CANCER?

A

IT INCREASES IT (INDUCES RELEASE OF TUMOUR ANTIGENS WHICH ARE CAPTURD AND PROCESSED BY ANTIGEN-PRESENTING CELLS (APCs) TO ACTIVATE CYTOTOXIC T LYMPHOCYTES (CTL) WHICH WILL ATTACK THE PRIMARY TUMOUR OR METASTATIC TUMOUR CELLS)
(combining radiotherapy with immunotherapy?)

52
Q

ABSCOPAL EFFECT?

A

The abscopal effect occurs when radiation treatment—or another type of local therapy—not only shrinks the targeted tumor but also leads to the shrinkage of untreated tumors elsewhere in the body.

(RADIATION LEADS TO SHRINCAKE OF TARGETED TUMOUR BUT ALSO TO INCREASED IMMUNE RESPONSE TO CANCER WHICH ALSO AFFECTS THE UNTREATED CANCER CELLS WHICH WOULD HAVE BEEN HARD TO REAVCH)

53
Q

MOLECULAR MECHANISMS CONTRIBUTING TO A RADIORESISTANT PHENOTYPE IN CANCER?

A
  • EVASION OF APOPTOSIS
  • REPOPULATION BY CANCER STEM CELLS
  • HYPOXIA (OXYGEN NEEDED FOR CELLS TO BE SENSITIVE TO RADIATION)
  • EXPANDED TUMOUR SUBCLONES
  • IMMUNE EVASION
  • ALTERED CELL CYCLE
  • ENHANCED DNA DAMAGE RESPONSE
  • INFLAMMATION
  • ALTERED MITOCHONDRIAL AND ENERGY METABOLISM
54
Q

HOW MANY GROUPS OF SIDE EFFECTS OF RADIOTHERAPY ARE THERE?

A 
2:
EARLY EFFECTS (OCCUR DURING TREATMENT)
LATE EFFECTS (MOST SERIOUS, PROGRESIVE AND IRREVERSIBLE)
55
Q

DESCRIBE THE EARLY SIDE EFFECTS OF RADIOTHERAPY?

A
  • OCCUR DURING TREATMENT; USUALLY 2ND OR 3RD WEEK OF THE COURSE
  • SELF LIMITING
  • NON SPECIFIC EFFECTS (TIREDNES, LACK OF ENERGY, DEPRESION..)
  • SPECIFIC LOCAL EFFECTS RELATED TO AREA BEING TREATED (SKIN-ERYTHEMA, BOWEL-DIARRHOEA, BLADDER-FREQUENCY/DYSURIA, SCALP-HAIR LOSS, MOUTH/PHARYNX-MUCOSITIS)
56
Q

DESCRIBE THE LATE SIDE EFFECTS OF RADIOTHERAPY?

A
  • MOST SERIOUS, PROGRESSIVE AND IRREVERSIBLE
  • LOSS OF STEM CELL RECOVERY POTENTIAL, PROGRESSIVE DAMAGE TO SMALL BLOOD VESSELS RESULTING IN THEIR OCCLUSION
  • RARE, NOT USUALLY SEEN BEFORE 6 MONTHS
  • SPECIFIC LOCAL EFFECTS RELATED TO THE AREA BEING TREATED (SKIN-FIBROSIS, BOWEL-STRUCTURE, PERFORATION, FISTULAE, BLADDER-FIBROSIS/HAEMATURIA, CNS-MYELITIS CAUSING PARAPLEGIA, LUNG-FIBROSIS)
  • VERY RARE INDUCTION OF 2ND MALIGNANCY; LEUKEMIA/LYMPHOMA AROUND 3 YERS, SOLID TUMOURS AROUND 10-30 YEARS FTER EXPOSURE
57
Q

CYBERKNIFE?

A

3D IMAGE-GUIDED INTENSITY MODULATED RADIOTHERAPY

58
Q

RADIOSENTISIZERS?

A

Radiosensitizers are drugs or chemical compounds that enhance the lethal effects of radiation. Importantly, a good radiosensitizer must have a favorable therapeutic ratio. In other words, it must have a differential effect between tumors and normal tissues to be clinically useful.

INT (52 decks)

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