Chapter 7: Neoplasia Flashcards
Benign Tumor Histology
Typical of tissue of origin and few mitoses
Benign Tumor Growth Rate
Slow
Benign Tumor Localization
Strictly local, often encapsulated/ no metasis
Benign Tumor Necrosis
Rare
Benign Tumor Recurrence after treatment
Rare
Benign Tumor Prognosis
Good, unless in critical area
Malignant Tumor Histology
Anaplastic, with abnormal cell size and shape mitoses, many mitoses
Malignant Tumor Growth Rate
Rapid
Malignant Tumor Localization/Metasis
Infiltrative/ frequent metases
Malignant Tumor Necrosis
Common
Malignant Tumor Reccurence after treatment
common
Malignant Tumor Prognosis
Poor if untreated
What is the purpose of grading and staging Tumors?
To predict clinical behavior of malignant tumor and guide therapeutic management
Grading (histological evaluation)
Anaplasia - lack of the degree of cell differentiation
Grade: 0-4
What is the grade of a benign tumor?
Grade 1-2
What is the grade for malignant tumors?
Grade 3-4
Staging (Clinical evaluation)
T (tumor size): 0-5
N (lymph node): 0-2
M (Metasis): 0-2
Examples of tumors that use different staging systems
Leukemia and Kidney tumor
Degree of Anaplasia
Greater degree of anaplasia, greater degree of grade, low degree of differentiation, and greater degree of aggressive malignancy = greater degree of malignant potential
What terminology indicates malignant tumors?
-carcinoma, and -sarcoma
Carcinoma
epithelial origin (adenocarcinoma)
Sarcoma
Mesenchymal (nerve, bone, muscle) origin
Leukemia
White blood cells
Carcinogen (external factors)
Potential cancer-causing agent
Oncogene (internal factors)
Proto-oncogene which enhances growth-producing pathways
Tumor Suppressor Gene (Internal Factors)
Inhibits Cell Proliferation. Cancers may arise when tumor suppressor gene function is lost or abnormally inhibited
Proto-Oncogenes
Normal Cellular genes that can be transformed into oncogenes by activating (gain of function) mutations
- Overactivation
- Overpdocution
Gain of function mutations code for
Growth factors, receptors, cytoplasmic signaling molecules, and nuclear transcription factors
When do proto-oncogenes become activated oncogenes?
When mutations alter their activity so that proliferation-promoting signals are generated inappropriately
Retrovirus
One of the mechanisms to turn proto-oncogene to oncogene with overactivity
Examples of retroviruses
HIV (Kaposi’s sarcoma)
Epstein-Barr Virus (Burkitt Lymphoma)
Human T-lymphocyte virus type 1 (Adult T-cell leukemia/lymphoma)
Hepatitis B (DNA virus, but not retrovirus)
Hepatitis C
Tumor-Suppressor Genes
Contribute to cancer only when not present (Loss of functions). It also stops cell cycle for reparment.
Autosomal Recessive
Both copies of tumor suppressor genes are inactivated when cancer develops
What happens where there is a defective copy of tumor suppressor gene?
There’s a much higher risk for cancer development
Rb Gene
“Master Brake” for the cell cycle. It blocks/stops cell division. It binds to transcription factors to inhibit cell entering cell cycle. Inhibits these factors from transcribing genes that initiate cell cycle (before entering cell cycle).
p53 Gene
Most common tumor-suppressor gene defect identified in cancer cells. More than 1/2 of all types of human tumors lack functional p53. Normally, inhibits cell cycling and accumulates only after cellular damage, binds to damaged DNA and stalls division to allow DNA to repair itself. May direct cell to initiate apoptosis.
BRCA1 and BRCA2 Genes
Associated with breast cancer
Tumor Metastasis
Process by which cancer cells escape their tissue of origin and initiate new colonies of cancer in distant sites. Cancer cells generally spread via circulatory or lymphatic systems.
Effects of Cancer on the Body
Pain, Cachexia, Immune System Deficits, and other effects
Cachexia
Overall weight loss and generalized weakness due to the fact that rapidly growing cancer cells demand o2 and nutrients, loss of appetite, increased metabolic rate, and nausea
Immune system Deficits
Suppressed by cancer cell secretions, cancers can also elude detection, and bone marrow suppression
Bone Marrow Suppression
Contributes to anemia, leukopenia, and thombocytopenia. Due to invasion and destruction of bone marrow cells, poor nutrition, and chemotherapy. Can all be managed by blood replacement theraphy.
Anemia
Deficiency in circulating red blood cells( Male: HGB<13 mg/dl; female: <12 mg/dl)
What are the clinical manifestations of Anemia?
Pallor, fatigue, malaise, shortness of breath, and decreased activity tolerance
Leukopenia
Deficiency in circulating white blood cells due to malignant invasion of bone marrow, malnutrition, and chemotherapy
Clinical Manifestations of Leukopenia
Lymphadenopathy, joint swelling and pain, weight loss, anorexia, hepatomegaly, splenomegaly
Neutropenia
Definitive diagnosis is made after bone marrow aspiration or lymph node biopsy. Absolute neutrophil count <500 cells/microL(normal range is 1,500-8,000).
Thrombocytopenia
Deficiency in circulating platelets. Predispose to life-threatening hemorrhage if count is below 200,000.
Clinical Manifestations of Thrombocytopenia
Petechiae, easy bruising, bleeding gums, occult hematuria, and retinal hemorrhages
Hair Loss and Sloughing of mucosal membranes
Complications of chemotherapy and radiation therapy
Paraneoplastic Syndromes
Tumor production of hormones or cytokines
Examples of Paraneoplastic Syndromes
Hypercalcemia, Cushing syndrome secondary to ACTH secretion, Hyponatremia and water overload secondary to excess ADH secretion
Types of Cancer Therapy
Surgical procedure, radiation therapy, drug therapy/chemotherapy, immunotherapy, targeted molecular therapy, stem cell transplantation and bone marrow transplantation
Radiation Therapy
Kills tumor cells by damaging nuclear DNA(radiolysis). Initiates Apoptosis for the cells. Side effects are bone necrosis and bone marrow suppression.
Drug Therapy/Chemotherapy
Systemic administration of anticancer chemicals to treat cancers known or suspected to be disseminated in the body. Most drugs are cytotoxic. Most effective on rapidly dividing cells. A side effect is bone marrow suppression.
What are used in Immunotherapy?
Interferons, interleukins, and monoclonal antibodies
Interferons
Glycoproteins produced by immune cells in response to viral infection
Interleukins
Peptides produced and secreted by white blood cells. Also called lymphokines and cyotkines.
Monoclonal Antibodies
Antibodies with identical structure that bind with specific target antigens
Stem Cell Transplantation
Provides a method to restore bone marrow function after high-dose irradiation or chemotherapy. Used in malignant and nonmalignant disorders. Used to manage life-threatening disorders in which patient’s bone marrow cannot manufacture WBC, RBC, or platelets.
