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Pathophys. - Mod. 2
Neoplasia
| Question | Answer |
|---|---|
| (define) oma | - suffix - tumor |
| adenoma | benign tumor of glandular epithelial tissues |
| osteoma | a benign tumor of bone tissue |
| papilloma | a benign ginger-like projection that grows on any surface |
| carcinoma | a malignant tumor of epithelial tissue orgin |
| adenocarcinoma | a malignant tumor of glandular epithelial tissues |
| sarcoma | a malignant tumor of mesenchymal (multipotent) origin |
| carcinoma in situ | localized pre-invasive lesion - typically can be removed surgically - (i.e. breast ductal carcinoma in situ) |
| (name benign/malignant tumors) epithelial: surface | benign: papilloma malignant: squamous cell carcinoma |
| (name benign/malignant tumors) epithelial: glandular | benign: adenoma malignant: adenocarcinoma |
| (name benign/malignant tumors) connective: fibrous | benign: fibroma malignant: fibrosarcoma |
| (name benign/malignant tumors) connective: adipose | benign: lipoma malignant: liposarcoma |
| (name benign/malignant tumors) muscle: smooth | benign: leiomyoma malignant: leiosarcoma |
| (name benign/malignant tumors) neural: nerve cell | benign: neuroma malignant: neuroblastoma |
| (name benign/malignant tumors) neural: glial cell | benign: glioma malignant: glioblastoma/astrocytoma |
| (name benign/malignant tumors) hematologic: granulocytic | benign: (none) malignant: myelocytic leukemia |
| (name benign/malignant tumors) hematologic: lymphocytic | benign: (none) malignant: lymphocytic leukemia/lymphoma |
| (name benign/malignant tumors) endothelial: blood vessels | benign: hemangioma malignant: hemangiosarcoma |
| (this characteristic in normal/cancer cells) growth | Normal: regulated Cancer: unregulated |
| (this characteristic in normal/cancer cells) differentiation | Normal: high Cancer: low |
| (this characteristic in normal/cancer cells) Genetic Stability | Normal: stable Cancer: unstable |
| (this characteristic in normal/cancer cells) Growth Factor Dependence | Normal: dependent Cancer: independent |
| (this characteristic in normal/cancer cells) Density-dependent | Normal: high Cancer: low inhibition |
| (this characteristic in normal/cancer cells) Cell-to-cell adhesion | Normal: high Cancer: low |
| (this characteristic in normal/cancer cells) anchorage dependence | Normal: high Cancer: low |
| (this characteristic in normal/cancer cells) Cell-to-cell communication | Normal: high Cancer: low |
| (this characteristic in normal/cancer cells) Cell life span | Normal: limited Cancer: unlimited |
| (this characteristic in normal/cancer cells) antigen expression | Normal: absent Cancer: may be present |
| (this characteristic in normal/cancer cells) substance production (proteases, hormones) | Normal: normal Cancer: abnormal |
| (this characteristic in normal/cancer cells) cytoskeletal composition and arrangement | Normal: normal Cancer: abnormal |
| At the tissue level, what is one of the first signs of cancer? Why? | bleeding, (or a growth/sore that does not heal) ulceration, and/or necrosis....the blood vessels become eroded |
| In regards to bodily fluid, how does cancer present itself | unusual accumulation of fluid in various cavities: - lung/breast/lymphomas have PE's (CP/SOB/cough) - Ovarian - fluid accumulation in peritoneal cavity (abdominal discomfort and swelling) |
| what is wasting | - weight loss - wasting of body fat and muscle tissue - can cause weakness, anorexia, anemia |
| define cancer anorexia-cachexia syndrome | the wasting of body fat and muscle tissue due to cancer - causes weakness, anorexia, anemia |
| explain the correlation of cancer and wasting | - lack of appetite is common, but extent of weight loss is more than what can be caused by lack of appetite. - can be a significant cause of morbidity and mortality (especially with those who have advanced cancers) |
| in regards to fatigue what are two common side effects to cancer | - fatigue (some form of tiredness, weakness, lack of energy) - sleep disturbance (this can be a result of the disease itself or the cancer treatment) |
| in cancer, what can cause anemia | - can be an effect of the treatment - blood loss - hemolysis - impaired RBC production - insufficient level of healthy blood cells |
| cancer- related anemia can also cause | - less effective treatments -increased mortality - increased blood transfusions - decreased performance and quality of life |
| how can cancer- related anemia be treated | recombinant human erythropoietin |
| what are paraneoplastic syndromes | symptoms in sites that are not directly affected by the disease ---- sometimes the first clue that a person has cancer |
| what are some possible causes of paraneoplastic syndromes | - hormones secreted by the tumor - hematopoietic, neurologic, dermatologic syndroms |
| name three common endocrine syndromes seen with cancer | - inappropriate ADH secretion - Cushing syndrome (d/t ectopic ACTH production) - hypercalcemia |
| an important secondary prevention strategy for early cancer detection | screening |
| three ways cancer screening is done | - observation - palpation - lab tests and procedure |
| when screening for cancer: what is observed for possible changes | - skin - mouth - external genitalia |
| when screening for cancer: what ways do we palpate the body for changes | - breast - thyroid - rectum/anus - prostate - lymph nodes |
| what kind of lab tests can be performed for cancer screening | - pap smear - colonoscopy - mammography |
| two ways tumor markers present | 1) antigens expressed on surface of tumor cells 2) substances released from normal cells in response to presence of a tumor |
| what are tumor markers used for | - establishing a prognosis - monitoring treatment - detecting recurrent disease |
| describe the Prostate Specific Antigen (PSA) | - most well-known tumor marker - elevated in cancer situations - screened via blood test |
| histologic and cytologic studies are used to examine what | -structural, compositional, and functional characteristics of tissues and cells |
| name a few methods histologic and cytologic studies are performed | - cytologic smears -tissue biopsies - needle aspiration |
| how does a papaniculaou (PAP) test detect cancer | - pathologist examines a prepared slide (smear) for abnormal cells |
| what is the most common use for pap smear | cervical cancer detection/cancer |
| other than a cervical cancer, what else does a pap smear test for | - other bodily secretions - pleural fluid - peritoneal fluid - nipple drainage - gastric washings - anal washings |
| what is a tissue biopsy | - removal of a tissue specimen for microscopic study. - essential procedure in diagnosing the correct cancer and histology |
| what is excisional biopsy | the removal of part or all of the tumor through a surgical excision |
| what is fin-needle aspiration | the drawing up (removal) of cells and fluid with a small-bore needle and syringe/vaccum |
| fine-needle aspiration is commonly used for which organs | thyroid, breast, lymph nodes |
| how does immunohistochemistry help diagnose cancer | uses antibodies that bind to specific cell products/surface markers to correctly identify the desired antigen(s) ---- helps to correctly identify the type of cancer that the clinician is dealing with |
| this diagnostic cancer test uses "gene chips" to help diagnose cancer | Microarray Technology |
| how does microarray technology work | uses "gene chips" that can simultaneously perform hundreds or even thousands of miniature assays to detect and quantify the expression levels of a large number of genes |
| what is the benefit of using the microarray technology | - analyzes the large number of molecular changes present in cancer cells ----helps to determin the overall patterns of behavior |
| how are microarray's used in cancer treatment | - guide clinical decisions ---- determining best course for treatment |
| name the two main strategies for classifying cancers | 1) grading 2) staging |
| what is cancer grading based on | - cellular characteristics of the cells in the tumor and the degree of abnormalities present |
| name all the grade clacifications | I, II, III, IV ---- each grade has a specific set of associated characteristics |
| what is are the stages of cancer | - the spread of the disease ---- classifications are: I, II,III, IV ---- Stage IV is most widespread (often to different parts of the body) |
| what is the TNM System | - a more sophisticated/detailed staging system of the American Join Committee on Cancer (AJCC) - classifies disease into stages using the following components ---- Tumor ---- Nodes ---- Metastasis |
| in the TNM Classification System - "T" means | Tumor - the size and local spread of the primary tumor |
| in the TNM Classification System - "N" means | Nodes - the involvement of the regional lymph nodes |
| in the TNM Classification System - "M" means | Metastasis - the extent of the metastatic involvement |
| cancer treatment categories | 1) curative 2) control 3) palliative |
| most common forms of cancer treatment | 1) surgery 2) radiation therapy 3) chemotherapy 4) hormonal therapy 5) biotherapy |
| describe the use of surgery in cancer treatment | - multifactorial -------- cancer/tumor removal -------- helps with diagnosis -------- helps with staging -------- helps with palliation (relief of symptoms when cure is not possible) |
| for solid tumors, or if the tumor is small with well0defined margins __________________ is often the first treatment | surgery |
| describe the use of radiation therapy for cancer | - primary method of treatment for many - can be used in adjunct with surgery/chemo/or both - can be used palliatively to reduce pain - helps treat emergencies |
| how does radiation therapy work | uses high-energy particles/waves to destroy cancer cells - can interrupt the cell cycle process - injures ALL proliferating cells in the radiation field |
| what are common side effects from radiation treatment | - skin irritation - suppressed bone marrow function -------- decreased leukocyte/platelet/RBC |
| describe the use of chemotherapy for cancer treatment | - can be used alone of in combination with radiation/surgery - uses drugs to reach the tumor site - main treatment for hematologic and some colid tumors - can be used as a palliative option |
| how does chemotherapy work | - prevents cell growth and replication by halting protein/DNA/DNA synthesis - inhibits cell mitosis - especially effective at treating tumors that contain rapidly dividing cells ------ can also kill normal tissue |
| what are the two major categories of chemotherapy drugs | -direct DNA-interacting - indirect DNA-interacting |
| why can many chemo drugs lead to neutropenia (risk for infections), anemia (causing fatigue), and thrombocytopenia (risk for bleeding) | chemo drugs cause a reduction in all three blood cell types (RBC, WBC, and platelets) |
| what types of cancer drugs cause alopecia (hair loss) | chemo- from impaired proliferation in the hair follicles during treatment (usually temporary and will grow back once treatment ends) |
| what is the purpose of hormonal therapy in cancer treatment | - disrupt the hormonal environment of cancer cells ------- helps deprive the cancer cells of hormonal signals ------- examples: breast, prostate, and endometrium |
| describe hormones therapy and surgery combined to treat cancer | - surgery first, removes organ responsible for producing the hormones responsible -- then drugs are used to suppress the circulating hormone levels |
| what is biotherapy | immunotherapy and biologic response modifiers to change the person's immune response to cancer. Includes: ---- monoclonal antibodies ---- cytokines ---- adjuvants |
| what are monoclonal antibodies (mAbs) | - highly specific antibodies made from cloned cells - IgG most commonly used |
| define neoplasia | a disorder of altered cell differentiation and growth |
| define neoplasm | the "new growth" |
| define proliferation | a process of cell division, an adaptive process for cell growth to replace old cells of when additional cells are needed |
| define differentiation | the process in which cells become more specialized with each mitotic division |
| name the four phases of cell division | - G1 (Gap 1) - S phase - G2 (gap 2) - M phase (Mitotic phase) |
| what is occurring in the G1 phase | - DNA synthesis stops - the Cell enlarges - RNA synthesis occurs - protein synthesis occurs |
| what is occurring in the S phase | - DNA synthesis - 2 sets of chromosomes by the end ----- 1 set for daughter cell |
| what is occurring in the G2 phase | - dna synthesis stops - RNA and protein synthesis starts again |
| what are checkpoints during the cell cycle | - type of surveillance ----- ensures that the cell is ready for the next phase |
| what happens if the cell fails the checkpoint of the cycle | - DNA is allowed to replicate/repair |
| name the four phases of the mitotic phase | - prophase - metaphase - anaphase - telophase |
| cytokinesis occurs during what phases of mitosis | anaphase and telophase |
| what is G0 | the resting state of a cell ------highly specialized cells may stay in G0 phase (nerve and muscle cells) |
| why would a cell be in resting state | - decreased nutrients - decreased growth - decreased stimuli |
| what are the 3 main groups of cells that proliferate | 1 - well-differentiated cells that rarely divide and reproduce 2 - Progenitor/parent cells - continue to divide and reproduce, like blood, skin, liver 3 - undifferentiated stem cells producing lots of progenerator cells |
| what are progenitor cells | cells that are not fully differentiated and are capable of dividing into well differentiated cells (example: basal layer of the epidermis) |
| what are the benefits of the stem cell | - dormant until needed - (when needed) ------- can divide ------- produce other stem cells ------- carryout other functions |
| two important properties that stem cells poses | - self-renewal - potency |
| what is stem cell self-renewal | stem cells can undergo numerous mitotic divisions while maintaining an undifferentiated state |
| what is stem cell potency | describes the differentiation potential of stem cells |
| describe a benign neoplasm | - well-differentiated - resemble tissue of origin - slow to progress - remains localized (incapable of metastasizing) - contains a fibrous capsule ------ rim of connective tissue ------ aids in surgical removal - generally non-life threatening |
| describe a malignant tumor | - invades + destroys tissue - rapid growth - spreads to other part of the body - not well-defined margins ---- can cause ischemia/tiss. injury ---- out grows blood vessels - some can ---- secrete hormones ---- liberate toxins |
| what is a polyp | a growth that projects from the mucosal surface (i.e. intestines). - can be benign or malignant |
| the process of metastasis | - cancer breaks loose from primary tumor - invades surrounding extracellular matrix - gains access to blood vessel - survives passage in blood stream - emerges at favorable location - invades surrounding tissue. - begins to grow - esta. blood flow |
| what are two broad categories of malignant neoplasms | - solid tumors - hematologic cancer |
| what is a carcinoma in situ | a localized preinvasive lesion - can be surgically removed/treated - less likely to recur |
| what is seeding | - tumor cells are shed into other body cavities - (most often seen with ovarian cancer) occurs into the peritoneal cavity |
| what is important about the sentinel node | - the lymph node that drains the tumor area ----- it maybe the first evidence of disease ----- it may be examined for the presence of cancer cells |
| what is angiogenesis | - the development of new blood vessels within the tumor ------ usually occurs after the tumor reaches a distant site and establishes a new tumor |
| two broad etiologic causes of cancer | 1) genetic/molecular 2) external factors (age, hereditary, environmental) |
| what are the two cancer associated genes | - proto-oncogenes - tumor suppressor genes |
| what are three genetic events that lead to oncogene formation and activation | - point mutation - chromosomal translocation - gene amplification |
| what are 6 molecular and cellular mechanisms that are known to faciitate the development of cancer | - defects in DNA repair genes - defects in growth factor signalling pathways - evasion of apoptosis - avoidance of cellular senescence - development of sustained angiogenesis - metastasis + invasion |
| what are 7 risk factors that can lead to the development of cancer | - heredity -hormonal factors - obesity - immunological mechanisms - environmental agents (chemicals, radiation, cancer-causing viruses) |
| give an example of a hereditary cancer | - BRCA 1, 2 causes breast and ovarian cancer, retinoblastoma, - familial adenomatous, polyposis causes colon cancer |
| what organs do hormones and the development of cancer target | - breast - ovary - endometrium - prostate |
| list some lifestyle factors that contribute to the development of cancer | - smoking - alcohol use - chewing tobacco use - high/low fiber diet - high intake smoked meats - sun exposure - obesity |
| what are the 4 oncogenic viruses that can induce cancer | - Human Papillomavirus (HPV) - Epstein-Barr Virus (EBV) - Hepatitis B Virus (HBV) - Human Herpesvirus - 8 (HHV-8) ------ causes Kaposi sarcoma in people with AIDS |
| list some common symptoms people with cancer have: | - bleeding - pleural/peritoneal fluid - anorexia - weight loss - wasting of body fat and muscle - weakness - fatigue - sleep disterbances - anemia |
| why is anemia common in people with cancer | it could be because of blood loss, hemolysis, impaired red blood cell production, treatment effects |
| what are paraneoplastic syndromes? | cancer can also produce symptoms in sites not directly affected by the disease. These manifestations are termed paraneoplastic syndromes |
| give an example of paraneoplastic syndromes | - in appropriate ADH secretion - Cushing's syndrome dur to ectopic ACTH production - hypercalcemia |
| what body parts do we screen through observation | - skin - mouth - external genitalia |
| what body parts do we screen though palpitation | - breast - thyroid - rectum/anus -prostate -lymph nodes |
| how do we screen for lab tests and procedures | - pap smear - colonoscopy - mammography |
| what are tumor markers helpful for | - establishing prognosis - monitoring treatment - detecting recurrent disease |
| what is the most important procedure in diagnosing the correct cancer and histology | tissue biopsy |
| define the grading | the histologic/cellular characteristics of the tumor |
| define staging | the clinical spread of the disease |
| what is the purpose of grading and staging | both methods are used to determine the course of the disease in selecting an appropriate treatment or management plan |
| what are three possible goals of cancer treatment | - curative - control - palliative |
| when is surgery appropriate in the treatment of cancer | - tumor is small with well-defined margins - to treat oncologic emergencies - prophylactically |
| how does radiation kill cancer cells | - uses high-energy particles or waves to destroy/damage cancer cells -leads to the creation of free radicals, which damagee cell structures. - radiation interrupts the cell cycle process, kills cells, or damages DNA in the cells |
| list some side effects of chemo therapy | - neutropenia (risk of infections) - anemia (causing fatigue) - thrombocytopenia (bleeding) - anorexia - nausea - vomiting - alopecia - hair loss |
| list 5 possible treatments for cancer | - surgery - radiation - chemotherapy - hormone therapy - biotherapy |
| what is anaplasia | the loss of cell differentiation (the cells begin to resemble embryonic cells) |
| what happens to chromatin with anaplasia | chromatin becomes COARSE and CLUMPED |
| what happens to the nuclei of cells under going anaplasia | nuclei become larger than normal and contain an abnormal amount of chromosomes |
| on the differential grading system, the lower the grade = | the more differentiated the cells are |
| describe a grade I cell | well-differentiated neoplasm |
| describe a grade IV cell | poorly differentiated/anaplastic cell |
| the hallmark of cancer is | genetic instablitiy |
| how does genetic instability contribute to cancer | cancer cells have: - high frequency of genetic errors - aneuploidy (a lost or gained a chromosome) - intrachromasomal instability - microsatellite instability - point mutations |
| what is intrachromosomal instability | - insertions - deletions - amplification |
| what is microsatellite instability | short/repetitive sequences of DNA |
| what are point mutations | - specific - single nucleotide affected |
| what is the relationship between cancer proliferation and growth factor | cancer are able to grow in the absence of growth factor |
| describe how cancer is able to grow without growth factors present | - growth factor is not needed - some cancers produce their own growth factor - some have abnormal receptors (the pathway is inappropriately signalled) |
| what is cell density dependence | the cessation for growth after cells reach a certain density |
| in cancer, what happens to cell density dependence | cell density dependence is lost in cancer cells |
| what are contact inhibitors | tell the cell to stop growing once contact is made |
| in cancer, how are cell cohesiveness and adhesion | cell adhesiveness and adhesion are lost and cells do not stick together ------ this allows the outer limit of the tumor to shed into the surrounding fluid/tissues |
| what is anoikis | apoptosis when a cell is detached from it's basement membrane |
| describe the hormone production done by cancer cells | this is only done in cancer, they secrete hormones/enzymes that promote metastasis |
| give examples of fluid accumulation (locations) after seeding occurs | - ascites - pleural effusion |
| tissue growth rate is dependent on: | 1) number of cells actively dividing or moving through cell cycle 2) duration of cell cycle 3) number of cells being lost relative to new cells being produced |
| what is the growth fraction | number of dividing cells/number of resting cells |
| what is doubling time | the time it takes for total mass of cells in tumor to double |
| what is the relationship between growth fraction and doubling time | there is a direct relationship between growth factor and doubling time. (if one goes up, so will the other and vice versa) |
| what is a point mutation | - a change in a ***single*** nucleotide ----- insertion ----- deletion ----- substitution |
| what is the ras gene | one of the genes that regulates cell growth and death |
| a point mutation of the ras gene can give rise to | the ras oncogene (which is seen in many cancers) |
| what is chromosomal translocation | rearrangement of a segment of chromosomal DNA ----- Burkitt Lymphoma ----- Chronic Myelogenous Leukemia (CML) --myc protooncogene is translocated from chromosome 8 to chromosome 14 |
| what are the purpose of tumor suppressor genes | - slows down cell division - repairs DNA mistakes - tells cells when to die - inhibits proliferation |
| what is gene amplification | - unusual increase in number of copies of a certain gene - leads to over expression of a gene ------ increase in unwanted proteins |
| example of an over expressed gene that can cause cancer | - human Epidermal Factor Receptor - 2 gene ----- breast cancers ----- associated with aggressive tumors that have a poor prognosis |
| what is the growth factor pathway (any one of these steps can become bypassed during cancer) | - growth factor binds to receptor - the inner surface receptor activates - 2nd messenger enters the nucleus - DNA transcription is initiated - enter into the cell cycle |
| importance of apoptosis failure | enables DNA damaged cells to survive |
| which organelle helps to regulate apoptosis | the mitochondria(l) (membrane) |
| what is cellular senescence | - cells stop dividing in response to DNA damage (in cancer this is bypassed) |
| how does an increase in telomerase affect cell growth and senescence | - cell growth = promoted - senescence = prevented |
| a type of chemo therapy that prevents angiogenesis | anti-angiogenesis therapy |
| how do external carcinogenic agents work | - initiation - promotion - progression |
| initiation of an external carcinogenic agent | - exposure to carcinogen ---- physical ---- chemical ---- biological ---- any thing that causes irreversible damage to the genome |
| during the initiation phase of exposure to an external carcinogen, which cells are most suseptable | the ones that are *actively* synthesizing DNA |
| promotion of an external carcinogen | - reversible if promotor substance is removed - cancer may occur long after exposure (have long latency period) |
| what is the final step needed for an exposure to an external carcinogen to turn into cancer | progression |
| what happens during the progression phase of the external carcinogen exposure | - hightened level of evasiveness - ability to spread - grow unregulated - genomic alterations |
| the link between hormones and cancer is unclear. however it is strongly suggested by research. why might there be a link? | - hormones play a role in cell/proliferation (think of a uterine cycle) - there is a concern with clinical administration of hormones for clinical purposes |
| what is the purpose of immunotherapy in cancer treatement | it works on the theory that there is a link between one who is immunocompromised and cancer rates; --- increased immune response can lead to an increase in tumor destruction |
| what are tumor antigens | - receptors/identification molecules on tumor cells that help the immune system identify and destroy tumors |
| list the types of immune cells that help with attacking tumor cells. which ones have antibodies | - T lymphocytes (produces antibodies) - B lymphocytes (produces antibodies) - macrophages - natural killer cells |
| of all the immune cells that help with attacking tumor cells. which are most important in growth the antigenic tumor cells | t lymphocytes |
| what is the function of CD4+? what type of immune cell produces this | Helps identify cancer (produced by helper T cell) |
| what is the function of CD8+? what type of immune cell produces this | signals the presence of and elimination of tumor cells (cytotoxic T cells) |
| what is a carcinogen | - anything that causes cancer |
| the ways that chemical can cause cancer | - direct-reacting agents (active once contact is made) - indirect-reacting agents (procarcinogens/initiators-metabolize 1st ) |
| __________________ may enhance carcinogenicity of some chemicals | promoters |
| polycyclic-aromatic carbons can cause cancer. where can they be found | - fried foods (animal fat, smoked meat, smoked fish) - can be found in common place |
| nitrosamines can cause cancer. where can they be found | - foods that have been prepped/baked/preserved by using nitrites or nitrates - may reduce vitamin c (which is an antioxidant) |
| name the ways lifestyle habits can play a role in the development of colon cancer | - high fat/red meat diet - low fiber diet - low physical activity - obesity |
| in regards to ionizing radiation the type of cancer one gets after exposure is dependent on.... | - dose of radiation - gender - age during exposure |
| how is age related to the development of cancer after being exposed to ionizing radiation | - the younger a person was exposed. the sooner the cancer begins to develop |
| describe the TNM system | - American Joint Committee on Cancer (AJCC) - more sophisticated and detailed staging system - uses three major components (Tumor, Nodes, Metastasis |
| T (Tumor) Tx T0 Tis T1-4 | T0 - No evidence of primary tumor Tis - Carcinoma in situ T1-4 - Progressive increase in tumor size or involvement |
| N (Node) Nx N0 N1-3 | Nx - Regional lymph nodes cannot be assessed N0 - no evidence of regional node metastasis N1-3 - increasing involvement of regional lymphnodes |
| M (metastasis) Mx M0 M1 | Mx - Not assessed M0 - no distant metastasis M1 - distant metastasis present, specify sites |
| TNM system: what is "T" looking at specifically | The sized and local spread of the primary tumor |
| TNM system: what is "N" looking at specifically | the involvement of the regional lymph nodes |
| TNM system: what is "M" looking at specifically | the extent of the metastatic involvement |
Created by:
kandriot
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