Patho Chapters 9/10/11 – Flashcards
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Benign tumors
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Benign tumors are larger than normal tissue growths that still show resemblance to normal tissue, have continuing cellular differentiation, a low mitotic index, and have a well-defined stroma or capsule. One of the key defining characteristics is that benign tumors do no grow outside of their capsule.
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Malignant Tumors
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Malignant tumors on the other hand, have an accelerated rate of growth, a thick irregular stroma, anaplasia, pleomorphism, and an absence of normal tissue organization. The key defining characteristic of malignant tumors is that they infiltrate tissues beyond their capsule (metastasis).
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Carcinoma
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a cancer arising from the epithelium
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Adenocarcinoma
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A cancer that arises from or forms ductal or glandular structures.
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Lymphoma
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A cancer originating from lymphatic tissue.
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Sarcoma
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Cancer arising from mesenchymal tissue (including connective tissue, muscle, and bone).
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Leukemia
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Cancer of blood forming cells.
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How can tumor markers be used?
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1) To screen and identify individuals at high risk for cancer. 2) To help diagnose the specific type of tumor in individuals with clinical manifestations relating to their tumor. 3) To follow the clinical course of the tumor.
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Why are tumor markers important?
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Identification of tumor markers that are present in elevated levels in the early courses of common tumors, is an essential part of early diagnosis, and improves the treatment outcome.
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Identify the two mutational routes resulting in uncontrolled cellular proliferation.
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1) Small DNA changes/Point Mutations. (most common) 2) Large DNA changes/ Chromosome Translocations
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Point Mutation
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Alteration of one or few nucleotide base pairs.
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Chromosome translocation
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Part of a chromosome is transferred to another part of another chromosome.
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How do translocations activate oncogenes?
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1) Causing excess and inappropriate production of a proliferation factor. 2) Causing the production of a nouveau protein with growth-promoting properties.
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Autonomy
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Cancer cells dependence from normal cellular controls.
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Anaplasia
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Loss of differentiation. Marked increase in molecular size, with evidence of ongoing proliferation such as mitotic figures.
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Proto-oncogenes
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the normal non-mutated form of an oncogene. These genes promote proliferation, but are regulated heavily.
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Cellular Oncogenes
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mutated oncogenes that show high expression and low regulation, leading to over-promotion of proliferation.
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Tumor Suppressor Genes
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or anti-oncogenes, act as the brakes for cellular proliferation.
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The function of stem cells in cancer
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In the cancer stem cell model, there is a rare cancerous stem-cell that is able to produce non-stem cell offspring that divide a limited number of times. Although drugs may kill the majority of the cancer cells, if the cancerous stem cell is not killed, the recurrence of a complex tumor is possible.
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The role of chronic inflammation in the development of cancer cells.
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Chronic inflammation is associated with the release of cytokines, growth, and survival factors by immune cells. These factors in non-cancerous chronic inflammation are probably used to sustain endothelial cells, and help with remodeling and healing. This chronic inflammation is caused by infection. However, with cancer, the factors also support the growth and proliferation of the tumor. Furthermore, ROS are released in the inflammation process, leading to further genetic lesions in the tumor cells.
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What causes Liver cancer?
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Hepatitis B and C viruses are associated with 80% of liver cancer cases worldwide.
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What causes cervical cancer?
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Human papilloma virus (HPV). (HPV only causes cancer when the viral DNA is integrated into the host's cells, and directs the production of viral oncogenes)
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Epstein-Barr Virus (EBV) In individuals with AIDS or those taking immunosuppressive drugs
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can cause B-Cell Lymphomas. B-Cell Lymphomas after organ transplants are termed: post-transplant lymphoproliferative disorder (PTLD).
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Kaposi sarcoma herpesvirus
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causes Karposi sarcoma and several rare lymphomas.
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Human T-Cell leukemia-lymphoma (HTLV)
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adult T-cell leukemia and lymphoma (ATLL)
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Helicobacter pylori
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gastric carcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphomas.
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What factors are indicative of the metastasis of tumors in cancer (e.g. rate of growth)?
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Local spread, Stimulation of neoangiogenesis and lymphangiogenesis by VEGF (so maybe elevated VEGF levels), Inflammation (which recruits immune cells)
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Mechanisms hat favor metastasis of cancer
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Recruitment of macrophages and other cell types to the primary tumor; Stimulation of neoangiogenesis and lymphoangiogenesis; Survival in circulation; Inheritable changes that provide increased heterogeneity (versatility), which give certain cells in the cancer mass new abilities to facilitate metastasis.
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What are the clinical manifestations of cancer that lead to diagnosis?
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Paraneoplastic symptoms like endocrinopathies, nerve & muscle syndromes, dermatologic disorders, osseous, articular, and soft tissue changes, vascular & hematologic changes and nephrotic syndrome. Pain, fatigue, cachexia, Anemia, Leukopenia & thrombocytopenia, infection
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What are the treatment strategies for cancer?
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Chemotherapy, radiation therapy, and surgery,
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What is the mechanism of action of common chemotherapeutic agents?
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All chemotherapeutic agents take advantage of specific vulnerabilities in target cancer cells.
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What side effects are associated with cancer treatment?
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Vomiting and alopecia.
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Why is smoking a major risk factor for cancer?
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Smoking is the most important cause of cancer. It is a major risk factor because it produces chemicals that are carcinogenic.
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Why is radiation exposure a major risk factor for cancer?
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Radiation affects many cellular processes, including gene expression, mitochondrial function, nucleotide base damage and single and double strand DNA breaks. These changes can lead to carcinogenesis.
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How does smoking alter cellular structure and function?
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Smoke contains several carcinogenic pyrolytic products that bind to DNA and cause many genetic mutations. There are more than 45 known or suspected chemical carcinogens in cigarette smoke.[9] Tobacco also contains nicotine, which is a highly addictivepsychoactive drug. When tobacco is smoked, nicotine causes physical and psychological dependency. Tobacco use is a significant factor in miscarriages among pregnant smokers, and it contributes to a number of other threats to the health of the fetus such as premature births and low birth weight and increases by 1.4 to 3 times the chance for Sudden Infant Death Syndrome (SIDS).
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How does radiation exposure alter cellular structure and function?
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Radiation is a mutagen and a carcinogen that can penetrate cells and tissues and deposit energy in tissues at random in the form of ionizations.
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What effects does UV radiation have on the skin?
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Skin exposure to UVR produces ROS in large quantities that can overwhelm tissue antioxidants and other oxygen-degrading pathways. Imbalances in ROS can lead to oxidative stress, tissue injury and direct DNA damage. UVR can activate transcription factor NF-Kb and other free radicals important in regulating genes that induce inflammation. Inflammation is a critical component of tumor progression. UVR (sunlight) causes basal cell carcinoma and squamous cell carcinoma. UV radiations is known to cause specific gene mutations; for example, squamous cell carcinoma involves mutation of the TP53 gene, basal cell carcinoma in the patched gene, and melanoma of the p16 gene. In addition, UV light induces the release of TNF-alpha in the epidermis, which may reduce immune surveillance against skin cancer.
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What are the components of a cancer prevention diet?
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Increase: Fruits and veggies, Fiber, Foods containing vitamins A,C,D, and E; mineral selenium (not to exceed 200 mcg/day).Vitamin B6, Foods containing folate, Epigallocatechin gallate (found in green tea), Spices, Whole grains instead of refined grains, Lycopene, Legumes, Nuts. DECREASE: Fat (especially large amounts of omega-6 fatty acids), High-glycemic-index carbohydrates, sugar, Foods with high amounts of preservatives, Alcohol, Grilled, blackened food, Fried foods, High levels of calcium (≥ 2000 mg), Refined grain products.
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Identify the three areas of epigenetics
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-Methylation - the addition of a methyl group [ch3] to the cytosine ring of DNA; aberrant methylation can lead to silencing of tumor-suppressor genes. -Histone modifications (e.g. histone acetylation, alterations in chromatin) can result in gene silencing. -Micro-ribonucleic acids (miRNAs) are small RNA molecules that can target gene expression post-transcriptionally. They act like volume control lever to modulate the production of defined proteins in cells.The expression of miRNAs has been linked to carcinogenesis because they act as either oncogenes or tumor suppressor genes.
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What genetic mechanisms promote carcinogenic action in individuals that consume both alcohol and smoke cigarettes?
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Alcohol interacts with smoking, increasing the risk of malignant tumors, possibly by acting as a solvent for the carcinogenic chemicals in smoke products. Inherited factors also put some individuals at increased risk in DNA repair ability, carcinogen metabolism, and cell cycle control. Individuals having the genes encoding 32-ADH or the dominant negative allele for ALDH2 are at reduced risk for alcoholism, despite being at much higher risks for oropharyngeal cancer. Mechanisms involved in alcohol-related carcinogenesis: -Effect of acetylaldehyde , the first metabolite of ethanol oxidation -Induction of CYP-450 2E1 (genetic variant of CYP2E1), leading to the generation of reactive oxygen species (ROS) -Increased pro-carcinogen activation (e.g. nitrosamines) and modulation of cellular generation (cell cycle) -Nutritional deficiencies (retinol, retinyl, esters, folic acid, other vitamins)
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What is the bystander effect?
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The directly irradiated cells also can lead to genetic effects in so-called bystander cells or innocent cells even though they themselves received no radiation exposure. This is known as the bystander effect.
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Risk factor for HPV and Cervical Cancer
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HPV-16 in most developing countries, followed by HPV-18, 31, and 45. long-term use of oral contraceptives and smoking. Newer risk factors include drug addiction and reproduction factors (i.e. age at menarche and menopause), number of sexual partners, and can be transmitted through sexual contact.
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risk factors of endometrial cancer.
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Primary risk factor is unopposed estrogen exposure w/ resultant hyperplasia. Others include post-menopausal women and higher in white vs. black women (mortality rate in blacks is nearly twice as high). -Tamoxifen -Early Menarche -Late menopause -Anovulatory cycles (PCOS, perimenopause) -Nulliparity -Obesity -Diabetes -Gallbladder Disease -Physical Inactivity -High-fat, low-fiver diet -Hypertension -Family history
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clinical manifestations of endometrial cancer
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Abnormal vaginal bleeding
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risk factors for ovarian cancer
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-Family history of ovarian, breast, uterine, pancreatic, or colon cancer. -Personal history of breast and colorectal cancer -Obesity -Age: postmenopausal -Infertility or prolonged use of fertility drugs w/o achieving pregnancy. -Early menarche, late menopause, or no children, or first child after age 30. -Genetic predisposition, esp BRCA1, BRCA2, HNPCC, ARID1A.
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clinical manifestations of ovarian cancer
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Silent disease meaning that by the time the individual experiences symptoms and seeks treatment, the disease has spread beyond the primary site. -Pelvic pain and abdominal swelling (ascites). GI symptoms are anorexia, early satiety, upset stomach, and constipation. Fatigue. Urinary urgency or frequency, back pain, dyspareunia, and pelvic pressure. Abnormal vaginal bleeding may occur.
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risk factor for breast cancer
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Black women under the age of 45-50yrs old experience a higher incidence of early-onset breast cancer and higher breast cancer mortality. Early menarche 55 Never breast fed children High alcohol consumption Smoking Recent oral contraceptive use Current or recent use of combined hormone replacement therapy Physical inactivity Obesity or adult weight gain (postmenopausal) Family history of breast cancer Personal history of breast cancer High dose radiation to chest/breast Inherited genetic mutations BRCA1/2 High breast density Atypical Hyperplasia Prior benign breast disease No full term pregnancies Late age at first full-term pregnancy
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clinical manifestations for breast cancer
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a painless lump in the breast, palpable nodes in the axilla, retraction of tissue (dimpling), or bone pain caused by metastasis to the vertebrae
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diagnostic testing for breast cancer
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clinical breast exam, mammography, ultrasound, thermography, MRI, percutaneous needle aspiration, biopsy or minimally invasive biopsy, hormone receptor assays, and gene expression profiling.
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What is the most prevalent type of childhood cancer?
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leukemia
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What are the some of the characteristic differences between cancer in children and cancer in adults?
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Although research suggests there are environmental factors associated with childhood cancers, there are very few of these factors as compared to adulthood cancers.
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What are the risk factors for development of secondary malignancies in survivors of childhood cancer?
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The risk factors associated with secondary malignancies include a variety of factors such as previous chemotherapy or radiotherapy, genetic factors, and type of primary cancer.
