37. In what two phases of the course of AIDs is an infected person the most contagious?

Why?

Concentration or levels of AIDS is high in the blood or body fluids: Phase 1 and Phase 3, because those are the highest points of concentration of AIDS.

38. How do fusion inhibitors differ from reverse transcriptase inhibitors and anti proteases in terms “before/after” infection? What two surface proteins do fusion inhibitors attach to?

Fusion inhibitors work by preventing HIV from entering healthy CD4 cells (T cells) in the body, whereas the others are active against HIV after it has infected the CD4 cell.

1.      What mature blood cells do myeloid stem cells produce? Lymphoid stem cells?

Neutrophiles, eosinophils, basophils (mast cells), monocytes (Macrophages), platelets, erythrocytes,

-lymphocytes (CD4, CD8, NK, B cells)

2. No matter the type of leukemia, overcrowding of the bone marrow by malignant leukemia cells result in what three clinical manisfestations?

Anemia, Chronic Infection, bruising and bledding complications

3. Distinguish between acute and chronic leukemia in terms of age of onset, maturity of cells, and onset of treatment.

Acute: Rapid growth of immature blood cells (blast cells); Mostly in children, adolescaents and young adults; treatment must be immediate and strong.

Chronic: slow growth of more developed cells; mostly in adults >50 years of age; treatment depends on stage but usually is less aggressive.

4. How common is Acute lymphoblastic leukemia (ALL) in terms of pediatric cancers? In most cases, what is the pathophysiology of the transformed lymphoid cells? What environmental factors usually cause this transformation? What historical events clearly linked radiation exposure to leukemia?

95% is due to acute leukemia;

Translocation of a promoter gene

Genetics, radiation increases the risk (Japan churnobyle)

5. What are the signs and symptoms of ALL due to bone marrow overcrowding? Signs and symptoms of ALL due to metastasis outside of the bone marrow?

Fever and frequent infections sure to failure of bone marrow to produce WBC’s; fatigue,palenessand pallow due to anemia; petechiae under the skin due to low platelet count; easy bruising and bleeding due to low platelet count.

-Swollen or tender lymph nodes; hematomegally and splenomegaly; bone pain and joint pain caused by the spread of the keukemic “blast” cells to the surface of the bone or into the joint from the marrow cavity.

What three common tests are normally performed by a hematologist to determine not only if the child has leukemia but also the type of leukemia?

Bone marrow aspiration; CBC; Spinal tap lumbar puncture

*7. What two tests are commonly used to determine the type of ALL? Why is this important?

TerminalDeoxynucleotidyl Transferase (TdT) Assay, mAB “tags” intigen

8. When treating ALL chemotherapeutically, total treatment (i.e., all three phases) usually is given for what length of time?

2-3 years

Induction Chemo: 2-3 weeks

Consolidation Chemo: months

Maintenance Treatments

9. Induction phase treatment is to achieve remission—what five criteria determine that remission has been achieved?

No blast cells in the:

-Blood; CBC

-Bone marrow samples

-cerebral spinal fluid

-normal blood marrow begins to return

-Blood counts (Hct, WBC, Platelets) normalized

10. What are the two major routes that chemotherapeutic drugs are given during the induction phase of treatment?

Intravenously or intrathecally

11. What two methods are used for intravenous infusion?

Internal jugular venous cannulation; peripherally inserted central catheter.

12. What two methods are used for intrathecal infusion? To what cerebral anatomical location is the ommaya reservoir connected?

Ommaya Reservior and Spinal tap;

Catheter from reservoir to the lateral ventricle.

13. Chemotherapy is given in lower doses (i.e., less intense) to assist in prolonging a remission and drugs are usually given for brief periods every 4 to 8 weeks over a 2 - 3 year time period.

c. Maintenance

14. More than 95% of children with ALL enter remission after 1 month of treatment 

a. Induction 29

14.5. second phase of chemotherapy

15. Is also intense in terms of drug cycles and side effects and lasts about four to eight months

b. Consolidation

16. When considering hematopoietic stem cells transplantation (HSCT), what two sources are the stem cells derived from? Which one is used more and why?

Bone Marrow Transplant or peripheral blood (apheresis); apheresis: easier to get people to donate blood instead of bone marrow.

17. The traditional source of hematopoietic stem cells for use in autologous and allogeneic transplantations.

f. Bone marrow transplantation (BMT)

18. Refers to the use of hematopoietic stem cells collected from the umbilical cord and placenta.

d. Cord Blood Transplantation

19. The extraction of hematopoietic stem cells (HSC) from the patient and storage of the harvested cells in a freezer for reinfusion back into the patient at a later date.

b. Autologous HSCT

20. The incidence of patients experiencing rejection (graft-versus-host disease or GVHD) is very rare.

d. Cord Blood Transplantation

21. Refers to the use of stem cells from a human leukocyte antigen (HLA)–matched donor

c. Allogeneic HSCT

22. A process in which the blood of a donor or patient is passed through an apparatus that separates out one particular constituent of blood and returns the remainder to the circulation

e. Apheresis

23. With the availability of these factors, most hematopoietic stem cell transplantation procedures are now performed using stem cells collected from the peripheral blood via apheresis rather than from the bone marrow.

a. Granulocyte-macrophage colony-stimulating factor (GM-CSF) and Granulocyte colony-stimulating factor (G-CSF)

24. The use of this method of transplantation has rapidly increased because of several favorable factors, including ease of collection, expanded and prompt availability, a decreased risk of adverse effects (eg, GVHD, transmission of infections), and an increased tolerance to HLA-mismatch.

d. Cord Blood Transplantation

25. These factors are able to “move” hematopoietic stem cells from the bone marrow into the blood so that they can be collected via apheresis.

a. Granulocyte-macrophage colony-stimulating factor (GM-CSF) and Granulocyte colony-stimulating factor (G-CSF)

26. In Graft vs Host Disease (GVHD), what specific cells initiate the rejection process? What are the three target organs in GVHD?

Mature T helper cells

Liver, skin, GI tract

27. Disease of adults with most (>75%) people newly diagnosed with this leukemia are over the age of 50, and the majority are men

d. Chronic Lymphocytic Leukemia (CLL)

28. Because of its slow onset, early-stage of this leukemia is, in general, not treated since it is believed that early intervention does not improve survival time or quality of life.

d. Chronic Lymphocytic Leukemia (CLL)

29. Results from a reciprocal translocation between the long arms of chromosome 9 and chromosome 22, resulting in the formation of the bcr-able oncogene.

c. Chronic Myelocytic Leukemia (CML)

30. Accounts for 80% of acute leukemias in adults, 15 to 39 years of age

b. Acute Myelobastic Leukemia (AML)

31. The symptoms, diagnosis, and treatment of this type of leukemia are similar to ALL.

b. Acute Myelobastic Leukemia (AML)

32. This leukemia is grouped into several phases: chronic, accelerated, and blast crisis.

c. Chronic Myelocytic Leukemia (CML)

33. Malignant neoplasm of immature hematopoietic cells (e.g., blast cells) of the myeloid line.

b. Acute Myelobastic Leukemia (AML)

34. Accounts for 15% of all leukemias and occurs primarily in middle aged (40-60 yrs) adults

c. Chronic Myelocytic Leukemia (CML)

35. The most common leukemia diagnosed in children age 2-5 years.

a. Acute Lymphoblastic Leukemia (ALL)

36. The Philadelphia chromosome (Ph1) is the diagnostic marker of this leukemia.

c. Chronic Myelocytic Leukemia (CML)

37. The diagnosis of this leukemia is based on the demonstration of an abnormal population of B lymphocytes that display an unusual but characteristic pattern of molecules that includes the co-expression of cell surface marker clusters of CD5 and clusters of CD 23.

d. Chronic Lymphocytic Leukemia (CLL)

38. Criteria for diagnosing transition into this phase includes: 10–19% myeloblasts in the blood or bone marrow; >20% basophils in the blood or bone marrow; and new genetic abnormalities in addition to the Philadelphia chromosome

b. accelerated

39. Is the terminal phase

c. blast crisis

40. If started early in this phase, chemotherapeutic drugs have a good chance of stopping the progression

a. chronic

41. Approximately 85% of patients are in this phase at the time of diagnosis.

a. chronic

42. Clinically behaves like an acute leukemia. 31

c. blast crisis

43. During the chronic phase of CML, what is the cause of left side pain and abdominal fullness?

Splenal megaly

44. Multiple myeloma is a cancer of what cell line?

Plasma Cells

45. What are three specific symptoms of multiple myeloma not seen in leukemia?

Bone Lesion

Hypercalcemia

Kidney Complications

46. In multiple myeloma, myeloma cells produced incomplete or “pieces” of monoclonal immunoglobulins –what three terms are used to describe these products?

Paprproteins, M-proteins, AKA Bench Hones Proteins

47. What is the mnemonic is used help recall the common tetrad of multiple myeloma and what do each of the letters stand for?

CRAB: Calcium, Renal failure, Anemia, Bone Lesions

48. Adhesion of the multiple myeloma cell to the stromal cells in the bone stimulates production of two important growth factors—what are they and how do they contribute to the clinical manifestations of bone lesions and hypercalcemia?

Interleukin-6 and RANKL

49. What are the two processes in multiple myeloma that causes renal damage?

The accumulation of Bench Jones Proteins; and calcium that collect in the nephron of the kidney.

50. In multiple myeloma, what are the three possible reasons for anemia?

1. Bone Marrow replacement with myeloma cells

2. Defective production of Erythropoietin (Kidney damage)

3. Cumulative mone marrow suppression from chemotherapy.

51. Leukemia is considered to be a cancer of the bone marrow and multiple myeloma a cancer of the plasma cell line—of what are tissue are lymphomas a cancer ?

Lyphoid tissue

52. According the World Health Organization (WHO) classification system, into what three groups are lymphomas divided?

Bcell, T cell, NK, and Hodgkin’s lymphomas

53. What are the two common types of B cell lymphomas?

Follicular and Burkitts

54. Follicular lymphoma is described as an indolent cancer—what does that mean? What affect does indolence have when considering the stage that it is diagnosed? What factor increases risks?

Slow growing

      it already has spread to other tissues

      Age

55. What are two broad types of Burkitt’s lymphoma? Which one has a high incidence in equatorial Africa?

Endimic, (equatorial Africa), burkitts leukemia (sporadic);

- Endimic

56. What age group does endemic Burkitt’s lymphoma involve? To what are 95% of the cases related? What is the distinctive feature of endemic Burkitt’s lymphoma that is rare in sporadic Burkett’s lymphoma?

Children and adolescents.

Epstein bar

The jaw is involved

57. What age group does sporadic Burkitt’s lymphoma involve? Link between EBV? Extra lymphatic tissue notably affected?

same age growth as endemic: children and adolescants

Not as strong 20% as epstine cases

Extra lymphatic tissue is the abdomine and intestine

58. What is common to all types of cutaneous T cell lymphoma (CTCL) in terms of migration of the malignant T cells?

The skin

59. What is necessary for the diagnosis of Hodgkin lymphoma?

Reed-Sternberg cell

60. What is the term used to describe the spread of Hodgkin lymphoma and how does that differ from non-Hodgkin lymphoma?

 term: anatomically contiguous or adjacent lymph nodes, usually does not skip.  Does not spread ectranodally until stage 3 or 4

61. What is the typical presentation/symptoms of Hodgkin lymphoma?

Rubbery painless enlarged lymph nodes usually cervical

62. Describe the disease occurrence in terms of age of onset.

 one in adolescent and the other in elderly

63. Compare 5-year survival rate over the last 50 years of Hodgkin lymphoma to multiple myeloma, non-Hodgkin lymphoma and leukemia.

better success rate with the treatment of hodgkins lymph bc when compared, there is a higher and longest 5 year survival rate.

*23. How many genes control the beta chain protein production?

There’s two genes

24. What are the possible genotypes for beta-thalessemia minor? Which of these genetypes would produce the most RBCs?

Three alleles:

-B-N normal beta

-B-0+: can produce small amounts of beta chain.

-B-0: produces no beta chain

Beta thalasemia could be B-0+ or B-0

B-N/B-0+ would produce the most RBC’s

25. What are the similarities in clinical outcomes between beta-thalessemia minor and alpha-thalessemia minor?

Small red blood cells, mild anemia

26. Why is beta-thalessemia major called Cooley’s anemia? Why does the baby at birth with beta thalassemia major seem normal?

B/c he was the first one to identify it; fetal hemoglobin had alpha and gamma and didn’t need beta so theyre still rpducing fetal hemoglobin but then that gene turns off and the adult turns off but they have a defective beta.

27. For beta-thalessemia major, as well as sickle cell anemia and Hemehoglobin-H disease, what is the cause for skeletal abnormalities?

Erythroid hyperplasia= replacement of bone marrow fat with dark red hemopoietic tissue

28. For beta-thalessemia major, as well as sickle cell anemia and Hemehoglobin-H disease, what two conditions cause hemochromatosis? What are iron chelators and how do they affect hemochromatosis? 33

1. Excessive absorbtion of dietary iron

2. repeated blood transfusions required by the patients

Iron Chelators: they pull iron out of the blood

-They reduce the symptoms of hemochromotosis

29. What common metabolic role do vitamin B12 and folate play that is the cause of megaloblastic anemia? What effect does this have on cell division?

They are key co-enzymes in the metabolic pathway to make DNA.

-developing rbcs have difficulty undergoing cell division.

30. Why does a patient with megaloblastic anemia present with hyperbilirubinemia and anemia?

Bc these big ugly cells are going to be cleared by the spleen and liver prematurely and it will cause bilirubin build up and jaundice.

31. Why is there a need to continually include folate in your diet? What are the three main causes of folic acid deficiency?

-We don’t have large stores of folate

-Socioeconomic resources; history of bowel related symptoms; bowl surgery for weight loss, cancer medications

32. Explain how the body absorbs cobalamin and include the following in your explanation: intrinsic factor, R- binder protein, and transcobalamin II.

1. Cbl in food is released suring peptic digestion

2. nonspecific cbl-binding protein released in saliva

3. cbl binds to Rprot

4. IF secreted by parietal cell of stomach mucosa

5. IF:Cbl complex absorbed into mucosal cell of ileum (receptor mediated)

6. theres a plasma protein called transcobalamine 2 and it transmits cbl and it circulates throughout the body

7. distributes and gives Cbl into those cells in the body

(Cbl= Vitamin B12)

33. What plasma protein transports iron from the intestine to other tissues? What molecule “holds” iron in the cells of the liver and spleen?

-Tranferin

-Ferritin

34. What is the most frequent reason for iron deficiency anemia in infants, toddlers and teens especially those in households living at or below the poverty

Not getting enough food with Iron in it., poverty becoming a big problem bc of how expensive iron filled foods are.

37. In what two phases of the course of AIDs is an infected person the most contagious?

Why?

Concentration or levels of AIDS is high in the blood or body fluids: Phase 1 and Phase 3, because those are the highest points of concentration of AIDS.

38. How do fusion inhibitors differ from reverse transcriptase inhibitors and anti proteases in terms “before/after” infection? What two surface proteins do fusion inhibitors attach to?

Fusion inhibitors work by preventing HIV from entering healthy CD4 cells (T cells) in the body, whereas the others are active against HIV after it has infected the CD4 cell.

39. Why will the treatment of one RT inhibitor not continue to work over time?

Resistance builds after 6 months to a year and occurs more rapidly in patients that have been infected for a longer time.

(40.) Explain how protease inhibitors work. Integrase inhibitors. Which one of these is still in development?

Protease Inhibitors: They block the action of protease and prevent the “slicing and dicing” of long proteins into HIV functional proteins.

Integrase Inhibitors: The block the action of integrase and thus prevent the incorporation of the viral genome into the target cell genome

41. Explain HAART. During this therapy, what happens to the levels of HIV? Are these persons still infectious?

HAART: Combination of several (typically three or four, with a combination of 2-3 types of RTs and a protease) antiretroviral drugs is known as Highly Active Anti-Retroviral Therapy (HAART). The use of the HAART regimen of drugs can lead to undetectable levels of HIV in the bloodstream but there is still HIV in genital secretions. Thus these persons are still infective. Recently, patients have been appearing who have clearly been infected by a person who harbors

protease inhibitor-resistant virus. This means that patients on the HAART regimen are again having unprotected sex with their partners.

1. No matter the carcinogen, what area of the cell is altered that will trigger the changes necessary for cells to become cancerous?

The genes

2. What is lag time? Why does lag time suggest that cancer is a multi-step process involving a series of genetic mutations?

Lag time: the time between the initiation of the carcinogen and the appearance of the cancer.

B/c the more the person is being bombarded by carcinogens, the longer the lag time.

3. What are the five phases of the cell cycle and describe what occurs in each.

1. Mitosis: cell division

2. GO: Quiesence Ex: Producing memory T cell and B cell.

3. G1: cell growth, production of structural proteins and enzymes

4. S: DNA synthesis, chromosome replication (Double the DNA)

5. G2: Production of spindle apparatus (Meiotic spindle)

4. What is the purpose of “checkpoints” within the cell cycle?

To monitor and regulate the process of the cell cycle.

5. Why is the molecule p53 called “the guardian of the genome”? Include “checkpoints” in your answer.

“Guardian of the genome”: It is a tumor suppressor

It plays an important role in triggering the control mechanisms (Determine if the cell cycle can proceed) at both G1/S and G2/M checkpoints.

6. What two things can p53 do if there is DNA damage? Include “cell cycle arrest” in your answer. Why is p53 called a “tumor suppressor gene”?

1. Repair it and allow it to go on

2. If it can’t fix it, it will activate suicide genes.

7. What 4 types of proteins (specific names) are involved in the cell’s typical growth-control pathway?

1. Growth factors

2. Growth factor receptors

3. Signaling Enzymes: Kinases(RAS)

4. Transcription Factors: activate genes that promote growth proteins.

8. What are oncogenes in relationship to proto-oncogenes?

Oncogenes arise from the mutation of proto-oncogenes.  Comes from the alter versions of the growth control proteins.

9. Genetically, are oncogenes dominant or recessive over proto-oncogenes?

Dominant

10. Are tumor suppressor genes dominant or recessive?

Dominant: in order to lose suppressor activity, you hace to knock out both of the genes.

11. What two deadly characteristics do malignant cancers have that benign tumors do not?

They invade and they metastasize.

12. Give two examples (one of the female gender and one of the male gender) of how benign tumors (i.e., hyperplasia) can cause “complications” .

Female: fibroid tumors (Heavy menstrual bleeding)

Male: Hyperplasia: benign prostate hyperplasia: urination backup in the urethra.

13. Distinguish between hyperplasia and dysplasia in terms of cell division, structure, and arrangement. How is cervical dysplasia identified?

Hyperplasia: Excessive rate of cell division, they look like the cells they’re related to.

Dysplasia: Excessive cell proliferation characterized by the loss of normal tissue arrangements and cell structure.

Cervical dysplasia: can be identified with a pap smear and followed up with a colposcopy for further pathological examination.

14. Define angiogenesis and how does it allow cancer in situ to become invasive? What are four factors that could be released by cancer cells that would promote angiogenesis?

Angiogenesis: the growth of new blood vessels and is essential for a carcinoma in situ to grow. Result of the cancer producing angiogenic growth factors.

VEGF: Vacular endothelial growth factor

ANG: Angiopoietin

PDGF: Platelet derived growth factor

FGF: Fibroblast growth factor

15. What are matrix metalloproteinases and how do they allow tumor cells to invade?

-Epithelial tissue is surrounded by a basal lamina (boundary) and restricts cells to an area in the organ.  To escape that “Fence” the matrix metalloproteinases helps degrade the glue of the basal lamina to allow the tumor cells to invade.

16. What two factors reduce the chance of cancer cells, once entering the blood, to metastasized to other parts of the body?

Mecahnically destroyed from bouncing against cell walls; can be attacked by Cytotoxic CD8 cells or the natural killer cells.

17. How do cancer cells “select” the tissue to which it metastasizes? What site do metastatic prostate cancer commonly select?

They select tissues by very specific interations between molecules on the cancer cell surface and molecules on the surface of the endothelial cells that line the blood vessels in the new host tissue.

18. What is meant by a 5-year survival rate?

Refers to the percentage of patients who live at least five years after being diagnosed with cancer.

19. Survival rates for breast cancer, though improved, show a variation amongst the two classes. What are they and what is the main reason for this fact?

Money; its between those who can afford the checkups and exams and will catch it early on and those who can’t afford the preventative checkups and only come in when they notice syptoms.

20. Five year survival rate is 10%

e. Stage IV

21. Breast tumor measures 2-5 cm and cancer has spread to two or more axillary lymph nodes 50

22. Ductal-carcinoma in situ

23. The most advance form of breast cancer

24. Tumor is larger than 5 cm and has spread to axillary lymph nodes that are connected as well to surrounding breast tissue

25. Inflammatory breast cancer

26. Breast tumor is more than 5 cm, but the cancer has not spread to the axillary lymph nodes

27. Tumor is less than 2 cm in size, and has not spread to the lymph nodes nor outside the breast

28. Tumor is smaller than 5 cm but has spread not only to axillary lymph nodes but also lymph nodes above the collar bone

29. Five year survival rate is 86% to 91%

30. Known as locally or regionally advanced breast cancer

31. Cancer cells have spread to distance parts of the body (e.g., bones, lungs, liver).

32. The estimated five-year survival rate is 100%

33. Lobular-carcinoma in situ

34. What is Prostate-specific antigen (PSA)?

Cell produced by prostate

Why has PSA's effectiveness for early detection of prostate cancer been questioned?

Because it is false pos and false neg prone

35. What is the reference range for PSA?

36. Why is PSA considered false-positive prone? False-negative prone?

7/10 men will not have prostate cancer.

2.5/10 men with prostate cancer will have no elevations of PSA

Digital rectal exam

Irregular lumps, large , hard spots

40. Metastasis has not been assessed.

41. Tumor extends outside of the prostate, but has not spread to the seminal vesicles.

42. The cancer has not spread to the lymph nodes.

43. The cancer has spread to lymph nodes in the pelvis.

44. The cancer has spread to the bones and/or a distant part of the body.

45. Tumor involves both the left and right sides of the prostate. 

46. Tumor is confined to only the right or left side of the prostate.

47. Tumor is confined to the prostate and is not detectable by digital rectal exam (DRE) or ultrasound.

48. Tumor extends outside of the prostate, and has spread to the seminal vesicles.

49. The test to detect lymph nodes spread have not been assessed.

50. The cancer has not spread to other parts of the body.

51. What types of tumors can neither surgery or radiation therapy alone treat?

52. The extent or amount of breast tissue that is removed during breast surgery is dependent on what characteristic of the tumor?

Radical Mastectomy

D: Modified Radical Mastectomy

55. Shortens radiation treatment length following lumpectomy.

B: MammoSite 5-day targeted radiation therapy

A:Lumpectomy and quadrantectomy

C:Simple Mastectomy or Total Mastectomy

59. Involves removing the entire breast, the axillary lymph nodes, and the pectoralis major and minor muscles behind the breast.

E: Radical Mastectomy

61. Explain cancers in terms of radiosensitivity and radioresistant.

Radiosensitivity: if it’s highly sensitive then it’s Rapidly killed;

C. Brachytherapy

D. Radioisotope therapy (RIT)

A. Conventional external beam radiation therapy(2DXRT)

B. Stereotactic radiation therapy (SRT)

66. The optimal form of treatment for very small tumors in the brain or spine.

B. Stereotactic radiation therapy (SRT)

67. Consists of a single beam of radiation delivered to the patient from several directions: often front or back, and both sides.

A. Conventional external beam radiation therapy(2DXRT)

68. This therapy can be temporary (radioactive material placed near the tumor for a specific amount of time then removed) or permanent (radioactive source remains in place, but becomes inert as radioactive material decays).

C. Brachytherapy

69. Define the following chemotherapy strategies: remission, prolagation of life, and palliation.

Remission: the disappearance of all manifestations.

Prolongation of life: Living 10 years instead of 8

Palliation: Relieve symptoms with no curing effect.

69A. What are the four common side effects of chemotherapy?

Immunosuppression- due to decrease production white blood cells.

Anemia: due to decreased production of red blood cells

Mucositis- Inflammation of the lining of the digestive tract.

69B. Why is it important to determine the patient’s performance status before chemotherapeutic treatment?

Bc whether you use the Kamofsky scale or the Zubrod Scale, you are determining the individual and it checks the number of doses and intensity.

69C. Compare the sensitivity of chemotherapy on cancers with high growth fractions compared to cancers with a slow growth rate.

Cancers most susceptible to chemo have high growth rates; those with low growth rates are less susceptible to chemo treatment.

69D. What is the relationship between cancer resistance and ABC multidrug transporters?

When cancer becomes resistant to chemo, the problem becomes that specific drugs are transported out and also other types of drugs and can become resistant to other types of chemo.

A. Combined Modality Chemotherapy

71. This chemotherapy strategy is also known as postoperative treatment because it is used after surgery in which the surgeon believes all the observable cancerous tissue was removed, but is concerned with the risk of recurrence.

C. Adjuvant Chemotherapy

72. With this therapy, the drugs will differ in their mechanism and side effects, but this strategy carries with it the advantage of minimizing the chances of resistance developing to any one chemotherapeutic agent.

A. Combined Modality Chemotherapy

73. This strategy initially involves surgically removing or irradiate the tumors that are visible together with chemotherapy for those small tumors that are not visible or have metastasized

C. Adjuvant Chemotherapy

74. Commonly known as preoperative treatment because the patient is given chemotherapy before surgery or radiotherapy.

B. Neoadjuvant Chemotherapy

75. This strategy involves the combined use of chemotherapeutic drugs with other cancer treatments, such as radiation therapy or surgery.

A. Combined Modality Chemotherapy

76. This chemotherapy strategy is design to shrink the primary tumor, thereby rendering surgery or radiotherapy less destructive or more effective.

B. Neoadjuvant Chemotherapy

77. As a group, these chemotherapeutic drugs prevent the formation of DNA and RNA by blocking the formation of their building blocks, purines and pyrimidines.

b. Antimetabolites

78. A class of enzymes that alter the supercoiling of DNA, preventing the DNA helix from unwinding and thus blocking DNA transcription and replication  

d. Topoisomerase inhibitors

79. These chemotherapeutic drugs blocks the formation of microtubules from tubulin, thus preventing cells from forming the spindle fibers necessary for mitosis.

c. Plant alkaloids

80. Purine or pyrimidine analogues that prevent these bases from becoming incorporated into DNA during the S phase of the cell cycle, thus stopping normal division.

b. Antimetabolites

81 Attaches to the negatively charged sites on the DNA (oxygen, nitrogen, phosphorous and sulfur atoms). By binding to the DNA, steps (replication, transcription, and base pairing) leading to duplication of the cell's genetic material are significantly altered.

a. Alkylating agents

82. This chemotherapeutic bind and inhibit the enzyme dihydrofolate reductase (DHFR), and thus prevents the formation of an intermediate, tetrahydrofolate. Tetrahydofolate is essential for purine and pyrimidine synthesis and its deficiency can lead to inhibited production of DNA and RNA.

b. Antimetabolites

83. The effect of this drug is to inhibit the action of 5α-reductase

e. Anti-androgens

84. This treatment involves the removal of the testes to eliminate the source of testosterone.

85. This drug blocks the action of the estrogen in the breasts.

c. Selective estrogen receptor modulator (SERMs)

86. This drug prevents the pituitary from releasing a hormone that stimulates the testes to release testosterone.

b. Luteinizing hormone-releaing hormone-analogs

87. This drug will stimulate bone cells, reducing the risk of osteoporosis, yet may stimulate the endometrium of the uterus, increasing the risk for uterine cancer.

c. Selective estrogen receptor modulator (SERMs)

88. This drug is used by postmenopausal women against breast cancer

d. Aromatose inhibitors

89. The action of this drug can prevent the binding of dihydrotestosterone (DHT) to a DNA receptor which in turn would stimulate the growth of prostate cancer.

e. Anti-androgens

90. This drug is used against breast cancer and prevents androgens, released mostly from the adrenal gland, from being converted to estrogen. The latter takes place mostly in fat cells.\ 

d. Aromatose inhibitors

91. Composed of murine antigen sequence region fused onto human sequence regions resulting in mAb that are approximately 65% human, thus reducing the patient’s immune response against the mAb and increasing the serum half-life.

B. Chimeric mAb

92. Approximately 95% human origin and therefore with a longer half-life.

C. Humanized mAb

93. Produced by transferring human immunoglobulin genes into the murine genome, after which the transgenic mouse is vaccinated against a desired cancer antigen.

D. Human mAb

94. Historically, these were the initial therapeutic antibodies obtain from hybridoma technology but have been plagued with clinical failures because of a short half-lie in vivo due to type III hypersensitivity reaction (immune complex formation after repeated administration clears murine mAb before it can target cancer).

A. Murine mAb

95. Produce by grafting the murine antigen determinant region into the Fab portion human antibodies.

B. Chimeric mAb

96. Bind to the target cell (tumor) antigen, are trafficked into the cell where they are released and usually result in the activation of apoptosis

d. Antibody-Drug Conjugates (ADCs)

97. It recruits natural killer (NK) cells which, via the porferin/granzyme process, kills the B cells.

b. Antibody-Dependent Cell-Mediated Cytoxicity

98. Targeted α-particle, 213Bi, therapy offers the potential for higher biological effectiveness and more specific tumor cell kill with less damage to surrounding normal tissues compared with the more conventional high-dose external beam radiation.

c. Radioimmunotherapy

99. End result will be the formation of the membrance attack complex (MAC) that will cause lysis and death to the cell.

a. Complement Dependent Cytotoxicity