INTRODUCTION TO CANCER CANCER refers to malignant NEOPLASMS (group of disorders where cells grow & multiply uncontrollably) TUMORS

RS Changes in normal body functions (due to pressure of cancer cells) Family of complex diseases Vary on the affected system of the body BIG C Group of distinct diseases with different causes, manifestation, tx & dx number of abnormal cells that arises from normal cells CAUSES: Exposure to carcinogen; Problem within the body itself Proliferation & overgrowth NEOPLASM NEW GROWTH BENIGN/MALIGNANT

ONCOLOGY science that deals with physical, chemical & biological properties and features of neoplasm (ONCOLOGIST) MALIGNANT NEOPLASM tumor capacity to invade the surrounded tissue 1. PRIMARY one area is surrounded 2. SECONDARY distant site is invaded (METASTASIS) TYPES OF CANCER 1. SOLID 2. HEMATOLOGIC * 12 MAJOR & 50 MINOR TYPES OF CANCER * 75% OF CANCER can be prevented by PRIMARY PREVENTION (SCREENING TEST) MOST COMMON: Breast Cancer BREAST SELF-EXAMINATION Prostatic Cancer PROSTATIC SERUM ANTIGEN * 5 YEARS of survival from cancer (free from manifestations) INCIDENCE AND MORTALITY Most common in people >60-65 years old immune system MEN > WOMEN Industrialized sectors & nation Second-hand smoking ovarian & uterus cancer 2nd leading cause of death (1st CVD) Leading cause of death in America FEMALE: Lungs, Breast, Colorectal MALE: Lungs, Prostate, Colorectal ETIOLOGY: Unknown FACTORS: Exposure to carcinogens, Economic factors, Education, Access to health care 1

NORMAL CELLS VERSUS CANCER CELLS NORMAL CELLS I. PARTS OF THE NORMAL CELL - NUCLEI PROTOPLASM (CYTOPLASM + NUCLEUS) NUCLEUS CHROMOSOMES DNA - DNA giant molecule that is important for MITOSIS controls activity of cytoplasm carry genetic information - GENES subunit of chromosomes contain portion of DNA specify the production of a set of protein FUNCTION: Order the production of enzyme Instruct cells to produce specific chemicals Instruct cells to develop specific structures Determine individual trait and characteristics Control other DNA to switch on and use some portion of genetic info stored in it - REPRODUCTION begins in the NUCLEUS Duplication of the 23 pairs of chromosomes Mitosis of the 2 sets into 2 separate nuclei Splitting of the cell into 2 daughter cells CHARACTERISTICS OF NORMAL CELL 1. Uniform in size and shape 2. Limited cell division (MITOSIS) - DEVELOP normal tissue REPLACE damaged/loss tissue 3. Undergo APOPTOSIS (cell self-destruction/death/suicide) - necrotic, O2, inadequate nutrient 4. SMALL NUCLEAR-CYTOPLASMIC RATIO small nucleus & wide cytoplasm 5. Perform specific DIFFERENTIATED FUNCTIONS (specific task to perform) to maintain homeostasis 6. When adverse condition occurs PROTECTIVE ADAPTATION ALTERATION in some cells some are helpful & other cases beyond usefulness UNPRODUCTIVE CELLULAR DESTRUCTION DURING CELL DIFFERENTIATION a. HYPERPLASIA - number & density of normal cells Under normal DNA control IN RESPONSE TO: stress, metabolic demand, hormonal level EXAMPLE: HYPERPLASTIC ENDOMETRIUM(normal, if asymptomatic; shrink on menopause) b. METAPLASIA change in the normal pattern of differentiation Normal for its particular type; not in normal function Under normal DNA control IN RESPONSE TO: adverse reaction (good sign) EXAMPLE: CHRONIC IRRITATION OF CERVIX WITH HPV INFECTION c. DYSPLASIA - LOSS OF DNA CONTROL over differentiation Abnormal degree of variation in size, shape & appearance 2

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7. 8. 9. 10. 11. 12. III.

Disturbance in the visual arrangement of the cell IN RESPONSE TO: adverse condition EXAMPLE: CONTINUED IRRITATION OF THE CERVIX (tissue changes in the cervix) PRE-CANCEROUS STATE! d. ANAPLASIA - regression of cell to an IMMATURE/UNDIFFERENTIATED CELL TYPE Characteristic of malignant cell/malignant transformation NOT UNDER DNA CONTROL IN RESPONSE TO: overwhelming destructive condition inside cell & surrounding tissue EXAMPLE: T-CELL LEUKEMIA * HYPERPLASIA & METAPLASIA reversible when irritant is removed; normal protective mechanism DYSPLASIA & ANAPLASIA irreversible ADHERE tightly together NON-MIGRATORY Grow in an ORDERLY & WELL-REGULATED manner do not divide unless time for cell division CONTACT INHIBITED divide only when not in direct contact with another cell surface Presence of GAP JUNCTION allow movement of molecules and ions to come into this gap EUPLOID balanced set of chromosomes

CELL CYCLE interval from mitosis of cell to mitosis of 2 daughter cells 2 DISTINCT ACTIVITY PERIOD A. INTERPHASE period of cellular growth between divisions - The cell grows - Carry out metabolic activities - Replicate cell DNA in preparation for cell division - RESTING PHASE - SUBPHASES: 1. G1 PHASE GROWTH 1/GAP 1 PHASE - Initial cellular growth to cell division - Rapid growth & metabolic activity (RNA & PROTEIN) - Getting ready for division extra nutrients, more energy, extra membrane, cytoplasm - LONGEST PHASE of all cell cycle 2. SYNTHESIS - Begins with DNA replication - Cells continue to grow - Synthesis of DNA 3. G2 PHASE GROWTH 2/GAP 2 - Starts upon completion of DNA replication - Cells continue to grow - Prepare for cell division 4. G0 PHASE ACTUAL RESTING PHASE - Carry out its function but does not divide B. PERIOD OF MITOSIS (MULTIPLICATION/DIVISION PHASE) - The process of normal cell multiplication takes place in response to a need and then stop - NO EXTRA CELLS ARE REPRODUCED 3

SUBPHASES: 1. PROPHASE shortening/condensing of chromosomes into well-defined thread a. PROMETAPHASE nuclear membrane disappears; chromosomes attached to microtubules 2. METAPHASE chromosomes lives up at the centrioles; pushed apart by the spindle 3. ANAPHASE each pair of chromosomes break apart into 2 daughter cells 4. TELOPHASE chromosomes become completely separated into 2 daughter cells CANCER CELLS

NEOPLASM (NEW GROWTH) characterized by uncontrolled cellular growth that fails to conform to normal pattern of grown of particular time. TUMOR GROWTH when lost cells have been replaced normal cells stop multiplying cancer cells keep on growing & multiply TUMOR I. TYPES OF CANCER CELLS 1. BENIGN - Expands but does not invade - Local and cohesive (CONTACT INHIBITED) - Well-defined boarders - Grows slowly - Frequently encapsulated - Cause pressure on vital structures - Easy to recover - Does not recur - GROWTH IN THE BRAIN 2. MALIGNANT - Abnormal cells/non cohesive - Grows aggressively; spreads (invasive)/metastasize - Destroys surrounding tissue - Does not respond to the bodys homeostatic control - Not easy to remove - Can recur

II. CANCER DEVELOPMENT (BASIC CONCEPTS) - Neoplastic cells originate from normal cells - Transformation of normal cells involves MUTATION - OVEREXPRESSION develop into a tumor - ONE CELL to undergo malignant transformation to cancer to begin III. CHARACTERISTICS OF CANCER CELLS - Rapid and continuous cell division (NO G0/RESTING PHASE) - Do not respond to signals for apoptosis (UNLIMITED LIFESPAN) - Show ANAPLASTIC MORPHOLOGY loose specific appearance of parent cell 4

- LARGE NUCLEAR CYTOPLASMIC RATIO - Loss some/all of differentiated function (UNDIFFERENTIATED) no useful purpose - ADHERE LOOSELY no connection with each other - NOT CONTACT INHIBITED continue to divide even when touched - ANEUPLOID - >23/<23 pairs of chromosomes MIGRATE & INVASION DEFINING CHARACTERISTIC!

THEORY OF CARCINOGENESIS CARCINOGENESIS/ONCOGENESIS development of cancer ONCOGENIC ACTIVATION main mechanism of carcinogen, regardless of specific cause I. ONCOGENIC THEORY - Genes that directed early embryonic development days after conception - Genes capable of triggering characteristics - TURNED ON when cells need to divide for normal growth replacement of dead or damaged cells under controlled conditions - TURNED OFF suppressed by SUPPRESSOR GENE (to prevent overreaction) - If it continues to activate cellular mutation damaged cells of the body - ONCOGENES due to exposure to carcinogen in the environment Turning on/off cannot be controlled - ACTIVATION MUTATION & Damage - SUPPRESSOR GENES OVEREXPRESSION of oncogenes UPSET THE BALANCE between the cell growth limitation CANCER CELLS - Cancer arise from normal cells abnormal cells - EXTERNAL FACTORS Activation Cancer 1. ENVIRONMENTAL CHEMICAL (alcohol, tobacco) - Mild carcinogenic substances - Act as co-carcinogen - LONG-TERM EXPOSURE: Damage & development of cancer cells - TOBACCO single-most important source of preventable carcinogen PHYSICAL - RADIATION IONIZING (from rocks & soil) Uranium, Radon, Radium ULTRAVIOLET RAYS - Exposure to sunlight SKIN CANCER - X-ray - Cosmic radiation (Protons & Atomic nuclei) - CHRONIC IRRITATION Scar r/t burn SKIN CANCER Chronic cell irritated tissue Free cell division DNA mutation

VIRAL - Break the DNA strands Virus inserts it own genetic material into Human DNA Damage to normal cells Mutation of the cells Damage to the suppressor gene Development of cancer - COMMON VIRUSES THAT CAUSE CANCER: HEPATITIS B & C LIVER (PRIMARY) HUMAN PAPILLOMA VIRUS (HPV) CERVIX, OVARY & UTERUS HUMAN LYMPHOTROPHIC VIRUS 1 ADULT T-CELL LYMPHOMA HUMAN LYMPHOTROPHIC VIRUS 2 HAIRY CELL LEUKEMIA EPSTEIN BARR VIRUS BURKITTS LYMPHOMA; B-CELL LYMPHOMA GULLAIN-BARRE SYNDROME BACTERIA - H.PYLORI the only bacteria that can cause cancer CHRONIC GASTRITIS (TYPE 2) gastric changes ATROPHY & METAPLASTIC changes GASTRIC CARCINOMA DIETARY - FIBER COLON CANCER - RED MEAT - ANIMAL FAT - METHOD OF PREPARATION - PRESERVATIVES: SODIUM NITRATE/NITRITE (contains NITROSAMINES) - FROM: bacon, hotdog, corned beef, ham, luncheon meat, etc. SODIUM BENZOATE (BENZOIC ACID) + VITAMIN C = BENZENE - SOURCE OF SODIUM BENZOATE: caffeinated beverages, pickles - SOURCE OF BENZENE: o TOBACCO - 32 cigarette/day = 1.8 mg of Benzene/day Secondhand smokers have 10x risk o PETROLEUM, CRUDE OIL, GASOLINE o EXHAUST o INDUSTRIAL EMISSION o GAS EMISSION (volcano & forest fire) - ACUTE MYELOID LEUKEMIA long-term exposure to Benzene - ADDITIVES: MONOSODIUM GLUTAMATE flavoring ASPARTAME sweeteners Food coloring - ANTIOXIDANTS: GREEN/YELLOW LEAFY VEGETABLES & FRUITS - Banana, Pineapple, Babana, Strawberry, Grapes - Black/Green tea, Wine, Fresh orange juice - PINEAPPLE JUICE (lipid) taken before breakfast with meals 6

2. PERSONAL FACTORS IMMUNE FUNCTION - when immunocompromised AGE >60 years old GENETIC RISK first degree relatives - Abnormal oncogenes passed from generation to generation - PATTERNS FOR GENETIC RISK: Inherited predisposition for SPECIFIC cancer - BREAST, PROSTATE, COLORECTAL CANCER Inherited condition ASSOCIATED with cancer GASTRIC CANCER FAMILIAL clustering CHROMOSOMAL alteration 3. OTHER POSSIBLE RISK FACTORS POVERTY inadequate access to health care (PREVENTIVE SCREENING & COUNSELING) STRESS Continuous unmanaged stress Stress hormones (EPINEPHRINE & CORTISONE) SYSTEMATIC FATIGUE & IMPAIRED IMMUNOLOGIC SURVEILLANCE GENERAL WEAR & TEAR/DEPRESSION OF THE IMMUNE SYSTEM TYPE C PERSONALITY people with unhealthy coping behavior to life stressor - Lead to physical & emotional isolation - CHRONIC DEPRESSSION & HOPELESSNESS ENERGIZING CHEMICALS (EPINEPHRINE, DOPAMINE, SEROTONIN) Repressed immune system OCCUPATION farmer, construction worker, x-ray personnel USE OF RECREATIONAL DRUGS - DIFFERENT EFFECTS: Unhealthy lifestyle Inadequate nutrition Suppressive effect on the immune system MARIJUANA DNA DAMAGE & GENETIC MUTATION OBESITY - Cancer cells (BREAST, COLON, ENDOMETRIUM, OVARY, PROSTATE) feed on SEX HORMONES (being synthesized from fat) HORMONAL AGENTS (ORAL CONTRACEPTIVES & ESTROGEN THERAPY) - DIETHYL STILBESTROL (DES) synthetic estrogen USED BEFORE: to prevent abortion & premature labor risk of OVARIAN CANCER CAN CAUSE: HEPATOCELLULAR, ENDOMETRIAL, BREAST CANCER VAGINAL CARCINOMA HORMONAL CHANGES - Early menarche (<12 years old) - Late menopause (>55 years old) - Delayed childbirth (>35 years old) - Nulliparity 7

FREE RADICAL molecule from the body which accumulates CANCER DEVIATION 7 DANGER SIGNS OF CANCER: Change in bowel habit and bladder habit A sore that doesnt heal Unusual bleeding/discharges (LATE MENOPAUSE) Thickening/Lump anywhere in the body Indigestion (Difficulty of swallowing) Obvious change in a ward or mole Nagging cough/Hoarseness in the voice II. CELLULAR TRANSFORMATION/DERANGEMENT THEORY - overexpression of oncogene A. STAGES OF CARCINOGENESIS/MALIGNANT TRANSFORMATION: (normal abnormal cells) 1. INITIATION - Brief, irreversible interaction - Between CARCINOGEN and PREDISPOSED CELL (normal nuclei is altered) - Body is initially exposed to carcinogen (IRREVERSIBLE) 2. PROMOTION - Normal cells has been initiatedi - Becomes a tumor if growth is enhanced (ANAPLASIA) - PROMOTER substances that enhance tumor after coming in contact with carcinogen - Promote growth of predisposed cell (full-blown) - LATENCY PERIOD 10-20 years of exposure to different carcinogen 3. PROGRESSION - Stage wherein the cancer cells have grown - 1 TUMOR = 1 BILLION CANCER CELLS - DETECTABLE TUMOR SIZE MALFUNCTION of the body HEALTH PROBLEMS 4. METASTASIS - Capacity of cancer cells to from SATELLITE TUMOR - Move from PRIMARY POSITION (by breaking off from original growth) - Established REMOTE COLONIES (SECONDARY) - STEPS: EXTENSION INTO SURROUNDING TISSUE - Secretion of ENZYMES that opens up surrounding areas - PRESSURE on the area BLOOD VESSEL PENETRATION - Form an EMBOLI - Tumor moves into CIRCULATION - Invades LYMPHATIC CELLS RELEASE OF TUMOR CELLS - Loosely held/loose connection with each other - Able to migrate to other sites

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INVASION - BLOOD CIRCULATION, LYMPH, SURROUNDING TISSUES - MOST THREATENING characteristic of malignant cells - REGIONAL/DISTANT sites - QUALITIES: Ability to cause PRESSURE ATROPHY Ability to DISRUPT THE BASEMENT MEMBRANE of normal cells MOTILITY RESPONSE TO CHEMICAL SIGNALS from adjacent tissues CHEMOTAXIS movement of cells in response to chemical signals Secretion of ENZYMES IMPAIRED BONE MARROW IMMUNE RESPONSE FAILURE IMMUNE SYSTEM - protects against invaders & non-self cells Immune surveillance (CELL-MEDIATED IMMUNITY T cells & B cells) Competent immune response ensures that cancer cell destruction exceeds proliferation NON-SELF CELL (INVADER) cancer cell HUMAN LEUKOCYTE ANTIGEN (HLA) normally found on the surface of a tumor

AUTOCRINE MOTILITY FACTOR protein that calls other malignant cells to move to distant side. ROUTES OF SPREAD 1. LOCAL SEEDING shedding of cancer cells into local area of primary tumor (REGIONAL) 2. BLOOD BORNE released into the blood - MOST COMMON CAUSE OF DISTANT SPREADING - Disrupt the bone marrow of blood vessel - INTRAVASATION ENTRY of cancer cells to blood vessels SYSTEMIC CIRCULATION 3. LYMPHATIC SPREAD replacement of normal node into cancerous node - EXTRAVASATION - MOVE OUT from blood vessels invade area where it came out (SECONDARY) IATROGENIC inability to seed out during surgery (DIAGNOSTIC/REMOVAL OF TUMOR) COMMON SITES: LIVER, LUNGS, BONE MARROW, BRAIN

FACTORS THAT ENABLE CANCER CELLS TO ESCAPE IMMUNE SURVEILLANCE: Aggressive cancer may compile into a LARGE MASS (>1 CM) SO RAPIDLY NO HLA (TUMOR-ASSOCIATED ANTIGEN) at the surface IMMUNE RESPONSE accumulated stress, depression, age, chronic disease, pregnancy, chemotherapy for primary cancer

* Metastasis may regress/disappear without apparent cause; may be dormant for many years; may resume growth later

CLASSIFICATION/NAMING I. ACCORDING TO CELL TYPE ORIGIN (HISTOLOGIC ORIGIN) A. CARCINOMA epithelial tissue - ADENOCARCINOMA glandular malignancy from epithelial tissue B. SARCOMA supportive tissue - FIBROSARCOMA fibrous connective tissue - LEIYOMYOSARCOMA smooth muscle layer C. SEMINOMA seminal/germ layer II. ACCORDING TO CELLULAR MATURITY/DEGREE OF DIFFERENTIATION A. BENIGN well-diffentiated B. MALIGNANT undifferentiated/immature III. ACCORDING TO SCIENTIST A. HODGKINS Thomas Hodgkin B. WILMS Max Wilm IV. ACCORDING TO ORGAN FROM WHICH THEY ARISE A. HEPATOMA liver B. OSTEOMA bone GRADING One of the first step in confirming cancer Estimate the rate of growth based on mitotic rate Measures amount of differentiation Vary in aggressiveness/sensitivity to treatment Determines prognosis & appropriate therapy Determine favorable outcome (EVALUATION) GRADE 1 most differentiated; least malignant GRADE 4 most malignant; least differentiated

PLOIDY Number of chromosome & appearance PHILADELPHIA CHROMOSOME (+) for CHRONIC MYELOGENOUS LEUKEMIA EUPLOIDY equal set of chromosomes ANEUPLOIDY - >23 OR <23 set of chromosomes degree of aneuploidy = degree of malignancy

STAGING Determine the exact location & degree of metastasis Early diagnosis = good prognosis Influence selection of therapy TYPES: o CLINICAL assess the manifestation & signs and symptoms o SURGICAL SURGICAL BIOPSY; size, number, site & spread by inspection at surgery o PATHOLOGIC size, number, site & spread by pathologic examination during surgery 10

STAGE 0 TUMOR IN SITU (TIS) pre-cancerous tumor at original site; starts as a growth STAGE 4 widespread malignancy

TNM SYSTEM Method now used to stage tumor To guide doctors during therapy Provides an accurate tumor description that is adjustable as the cancer progresses TUMOR anatomic extent of primary tumor NODES (REGIONAL LYMPH NODES) size, motility/mobility, & firmness, capsular invasion, depth of invasion, number of nodes, ipsilateral/contralateral/bilateral, distant node involvement METASTASIS (DISTANT METASTASIS) presence/absence of metastasis STAGE 1 T1 N0 M0 2 T2 N0 M0 3 T3 N0 M0 T1 N1 M0 | T2 N1 M0 | T3 N1 M0 4 A T4A N0 M0 | T4A N0 M1 T1 N2 M0 | T2 N2 M0 | T3 N2 M0 | T4 N2 M0 | B any T N3 M0 | T4B any N M0 C any M1 lesion LEGEND: T0 No evidence of primary tumor TIS tumor in situ T1-T4 ascending degree of tumor (size/involvement) N0 no abnormal regional lymph nodes M0 no mets N1A N2A regional nodes without mets N1B, N2B, N3B regional nodes with mets suspected NX regional nodes cannot be assessed clinically M1, M2, M3 ascending degree of mets involvement of the hosts; involving distant nodes PSYCHOPATHOLOGIC EFFECTS I. DISRUPTION OF FUNCTION - Destroys normal tissue - function - Death (by metastasis to vital organs) - Disrupt physiologic process - IF LEFT UNTREATED: *IMPAIRED IMMUNOLOGIC FUNCTION - infection *IMPAIRED HEMATOPOEITIC FUNCTION - platelet (thrombocytopenia bleeding tendencies) RBC (anemia) * LEUKEMIA/LYMPHOMA/ANY TYPES OF CA THAT METASTASIZED TO BONE MARROW 11

ALTERED GI STRUCTURE/FUNCTION ANOREXIA-CACHEXIA SYNDROME o IMPAIRED NUTRITION impaired ability to do task o METABOLIC RATE need for nutrient o LIVER FUNCTION metabolism of nutrient MOTOR & SENSORY DEFICITS BONE/SPINAL NERVE/CORD/BRAIN o BONE SITES MOST OFTEN AFFECTED: Vertebra, Ribs, Pelvis, Femur o COMMON SITES: Humerus, Scapula, Sternum, Skull, Clavicle o Possible motor changes (BONE) & sensory changes (BRAIN & SPINAL CORD) o NOT ALL CANCER CAN CAUSE PAIN (LUNG CANCER pain only if with mets) RESPIRATORY FUNCTION o DISRUPT GAS EXCHANGE DEATH (NASOPHARYNGEAL CANCER) o LUNG CAPACITY when lung tissue is involved (LUNG CANCER) o PULMONARY EDEMA & DYSPNEA pressure on blood & lymph vessels @ chest that would block the flow of blood through the lungs o GAS EXCHANGE thickened alveolar membrane; damaged pulmonary vessels

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HEMATOLOGIC ALTERATION Impair the normal function of blood cells Invades the bone marrow RBC & platelet proliferation of immature WBC (LEUKEMIA) Suppression of WBC IMMUNOSUPPRESSION RBC ANEMIA PLATELET BLEEDING TENDENCY Cancer cells with eroded blood vessels & tissues (BREAST, CERVICAL, GASTRIC) SEVERE BLEEDING GI TUMOR disrupt the absorption of VITAMIN B AND IRON GROWING TUMOR can deprive BONE MARROW of PURINE & FOLATE (ERYTHROPOEISIS) RENAL CELL CARCINOMA - large RBC at circulation viscosity of blood Impaired circulation Formation of THROMBUS INFECTION Impaired function of WBC LEUKOPENIA - WBC GRANULOCYTOPENIA - NEUTROPHILS It is important to determine ability of the body to fight infection risk of infection if immunosuppressed SIGNS OF INFECTION: o SEPSIS NOT ALL CLIENTS HAVE FEVER o SWELLING, REDNESS, DRAINAGE, PAIN *FEVER may not occur if immunosuppressed; but at times, it could be the only manifestation of patient HEMORRHAGE THROMBOCYTOPENIA (Bone marrow depression [may not be due to mets], chemotherapy, radiation, tumor infiltration of the bone marrow, enlargement of spleen, abnormal antibody function) 12

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>20-50 million/mm - risk for bleeding >20 million/mm - risk for SPONTANEOUS bleeding (needs PLATELET TRANSFUSION) ANOREXIA-CACHEXIA SYNDROME ALTERED TASTE o Mineral deficiencies o circulating amino acids o cellular metabolites o Administration of chemotherapeutic agents SENSE OF FULLNESS (EARLY SATIETY) o digestive enzymes o Abnormal metabolism of glucose & triglycerides o Prolonged stimulation of gastric volume receptors NAUSEA AND VOMITING o Chemotherapy CANCER CACHEXIA Feature of cancer Loss of body weight, adipose tissue, visceral protein & skeletal muscle NITROGEN IMBALANCE - nitrogen OUTPUT; nitrogen INPUT COMPLAINS OF: loss of appetite, early satiety, fatigue RELATED TO: inadequate nutrient intake, metabolism demand, energy expenditure DUE TO: o Anaerobic metabolism of tumor o Neoplastic cell inhibit food intake & divert nutrition for own use o Altered glucose & lipid metabolism o Suppressed appetite o Production of CYTOKINNINS (TUMOR NECROSIS FACTOR/CACHECTINS) Enhance or metabolic consumption of nutrients Robbing the body of nutrients (EARLY SATIETY & CACHEXIA)

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