Biology of Cancer and Tumor Spread – Flashcards
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What does benign mean?
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not cancer
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What does malignant mean?
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cancer
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What is a tumor?
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(AKA neoplasm)-new growth
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What are the characteristics of a benign tumor?
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grow slowly (could be years), well-defined capsule, not invasive, well differentiated (looks like cells of that location), low mitotic index, do not metastasize
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What are the characteristics of a malignant tumor?
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glow rapidly, not encapsulated, invasive, poor differentiated (cant tell what type of cell it is), high mitotic index, cell metastasize
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How are benign tumors named?
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according to the tissues from which they arise, and include the suffix "oma"
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Examples of benign tumors
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lipoma, glioma, leiomyoma, chondroma
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lipoma
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fat
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glioma
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neural; connective tissues, not the neuron itself
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leiomyoma
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smooth muscle
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chondroma
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cartilage
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malignant epithelial tumors are referred to as?
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carcinomas
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adendocarcinoma
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ducts, glands (the actual duct); bile duct, fallopian tubes; not glandular cells; adrenal gland or thyroid gland
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malignant connective tissue tumors are referred to as?
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sarcomas
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Rhabdomyosarcoma
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skeletal muscle
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cancers of the lymphatics are called?
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lymphomas
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cancers of the blood are called?
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leukemias
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Carcinoma in situ (CIS)
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preinvasive epithelial malignant tumors of glandular or squamous cell origin (stationary RIGHT NOW)
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Where is CIS often found?
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cervix, skin, GI, bronchi
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autonomy
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cancer cell's independence from normal cellular control; not playing by the rules, push even harder, grow bigger
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anaplasia
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loss of differentiation; cells don't even look like each other
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pleomorphic
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various shapes/sizes; disorganized, increased division; big nuclei, cells in division
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Tumor markers
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produced by cancer cells that are found on plasma cell membranes, in the blood, CSF, or urine
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Examples of tumor markers
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hormones (catecholamines, ACTH), enzymes (tyrosine kinase in CML), genes (philadelphia chromosome), antigens (prostate-specific antigen [PSA]), antibodies (Bence-Jones protein)
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Tumor markers are a way to diagnosis what?
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cancer!
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What is required before cancer can develop?
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multiple mutations (increase as we age)
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Knudson's 2-Hit Hypothesis
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Has to happen in both alleles
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Tumor-suppressor genes
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encode proteins that, in their normal state, negatively regulate proliferation; "anti-oncogenes"; turned off in cancer
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Oncogenes
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mutated genes that, in their non-mutant state, direct protein synthesis and cellular growth; turned on in cancer (aka proto-oncogenes)-> when functioning regularly, causes growth to occur when growth is needed
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Caretaker genes
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encode for proteins that are involved in repairing damaged DNA; "loss of function" of caretaker genes-> increases mutation rates; can lose whole arms (p or q) and translocation can occur
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telomeres
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protective caps on each chromosome; held in place by telomerase; become smaller with each cell division (each time it divides, one/two caps fall off); in cancer, caps don't fall off; cancer cells activate telomerase, allowing it to divide indefinitely
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What happens if mutation occurs in the somatic cells?
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it is not passed to progeny
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What happens if mutation occurs in germline cells?
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it can be passed on to future generations
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Oncogenic viruses: Hep B and C
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liver cancer; causes cancer b/c constant inflammation (releases ROS)
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Oncogenic viruses: EBV
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Post Transplant Lymphoproliferative Disorder (PTLD): mono like symptoms, along with lymphoid tumors, reactivation of EBV
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Oncogenic viruses: Kaposi's sarcoma herpesvirus (KSHV)
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AIDS; people who are immunosuppressed; HIV patients ten to get; connective tissue coming to skin (considered metastasis)
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Oncogenic viruses: HPV
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cervical, anal, oral, and penile cancer
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Oncogenic viruses: HTLV
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Human T cell leukemia-lymphoma virus; virus among IVDA that may take years to develop; T cell immune deficiency
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IVDA
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IV Drug abusers
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Helicobacter Pylori
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free radicals; invades GI tract; CHRONIC infections associated with: peptic ulcer disease, stomach carcinoma, mucosa-associated lymphoid tissue lymphomas (MALT-Tomas)
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What is an important factor in the development in cancer?
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chronic inflammation; cytokine release from inflammatory cells; free radicals -> mutation promotion; decreased response to DNA damage by caretaker genes
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Angiogenesis
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growth of new vessels; advanced cancers can secrete angiogenic factors (cytokines);
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VEGF
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vascular endothelial GF; normal in healthy tissue repair; but cancer cells can figure out how to do it, too
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Hallmarks of cancer: Self-suffiency
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autonomy, autocrine, RAs, increase receptors
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Hallmarks of cancer: Insensitivity
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loss of tumor suppressors (Rb, BRCA)
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Hallmarks of cancer: Apoptosis
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p53 mutations
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Hallmarks of cancer: Limitless replication
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activated telomerase
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Hallmarks of cancer: Angiogenesis
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secrete GFs
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Mutation in the p53 gene
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resists apoptosis; tumor suppressor gene; doesn't normally resist, helps apoptosis to occur
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Inactivation of the Rb tumor suppressor
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tumor suppressor gene; involved in a lot of cancers; retinoblastoma, lung, breast, bone
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3 steps in tumor spread
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1. direct invasion of contiguous organs, known as local spread 2. metastasis to distant organs, lymphatics and blood (good news for diagnosis) 3. metastasis by way of implantation (can occur with transplant); sometimes someone has so much cancer, just close them back up--by trying to remove, it could seed it somewhere else
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Paraneoplastic Syndrome
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NOT PART OF CANCER; may be the first sign that cancer exists; caused by secretion of multiple factors or body's response. ex. weight loss, acanthosis nigricans
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acanthosis nigricans
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gastric, lung, uterine Ca (looks dirty, wont wash off; picture on back of neck)
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Acute
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abrupt, undifferentiated (blast) cells, immature and ineffective (poor prognosis)
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Chronic
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insidious (subtle), more differentiation, decreased mortality (body actually adapts)
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Myelocytic
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(myeloid, myelogenous, myeloblastic, myelomonocytic)- granulocytes and monocytes; also includes RBC
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Lymphocytic
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T and B lymphocytes
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Causes of leukemia
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radiation/chemo, viruses (HTCL/lymphotrophic virus), chromosomal defects, environmental carcinogens
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What is the leading cancer in children?
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leukemia
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Acute Lymphocytic Leukemia (ALL)
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immature lymphocytes; 80-85% from B cell line; children and young adults; good prognosis with treatments we have today
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Acute Myelocytic Leukemia (AML)
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affects mostly adults; toxins and genetic diseases; only 20% survival rate; also affects RBCs and platelets; people treated for other cancers might develop this type
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Chronic Lymphocytic Leukemia (CLL)
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increase incidence in older adults; incompetent B lymphocytes (can be T); 2-10+ year survival (even without treatment)
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Chronic Myelocytic Leukemia (CML)
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30-50 y.o.; philadelphia chromosome; long term remission OR cure; 1st chromosome change associated with disease
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Multiple Myelomia
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Older adults; malignancy of plasma (B cells) in bone marrow; tumor masses throughout the bone marrow; causes unknown..virus?; unique proteins; NOT CURABLE!; people get FRACTURES
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M-Protein
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Malignant plasma cells-> heavy defective antibody; hyperviscosity- thicker blood; normal antibodies are suppressed
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Bence-Jones Protein
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The light chain of the antibody (Ig) may damage renal tubules while being excreted; found in urine; nothing else cause this besides multiple myeloma
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Bone destruction through cytokines in multiple myeloma
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B cells secrete cytokines: increase bone resorption (bone to blood)-> bone breakdown and increase Ca+ in blood (peroneoplastic syndrome)
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Manifestations of multiple myeloma
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fractures, hypercalcemia, bone pain, renal failure
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Diagnosis for multiple myeloma
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electrophoresis, bence-jones in urine, bone x-rays
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electrophoresis
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determines heavy and light chains (heavy M)
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Manifestations of leukemias
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weight loss, hepatomegaly, splenomegaly, lymph node enlargement (result from infiltration)
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Manifestations of acute leukemias
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fatigue and pallor (anemia), infection and fever (neutropenia), bruising and bleeding (thrombocytopenia), leukemic infiltration (leukemic cells enter brain, CSF, etc)
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Diagnosis of leukemias
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bone marrow aspirate and or biopsy; look at cells and maybe tissues; blood work (increase WBC, decrease RBC and platelets); lumbar puncture (LP)- looking for infiltrates
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Leukemia
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malignancy of hematopoietic stem cells (occurs in bone marrow); [in stem cells that have nucleus that create other RBCs; once divide and mature-> never divide again]; accumulation-leukocytosis; clonal disorder
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clonal disorder
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replacement with immature blasts (abnormal/cancerous) BLASTS are never normal/never going to grow up
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Leukocytosis
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increase leukocytes (WBC)
