ALU 201: Intermediate Medical Life Insurance Writing PDF

FOUR CANCERS Introduction appropriately assess that extra risk in the cases they do see. The best way to accomplish this is with the insurable range. Colon and rectal tumors have the third highest incidence and death rates ALU 201: Intermediate Medical Life Insurance Writing Page 60 Section A approp...

FOUR CANCERS Introduction appropriately assess that extra risk in the cases they do see. The best way to accomplish this is with the insurable range. Colon and rectal tumors have the third highest incidence and death rates ALU 201: Intermediate Medical Life Insurance Writing Page 60 Section A appropriately. pace at which the incidence rates have increased has diminished to some degree in the last 10 overall prognosis is quite good. Race and Gender Age Page 61 ALU 201: Intermediate Medical Life Insurance Writing survival, with a more aggressive disease that is more likely to be located on the head and neck. Sun Exposure intense, recreational exposure appears to impart a higher risk than the overall time spent in the sun. is 1.8 in blondes and 2.4 in those with red hair. protection. Organ Transplantation and Prior History of Cancer malignancies. Benign Nevi Atypical (Dysplastic) Nevi Page 62 melanoma within a dysplastic nevus is unusual and, thus, it is not necessary to remove all atypical marker 1. variable pigmentation 2. irregular outline 3. indistinct borders. existing skin lesion. 1. 2. 3. 4. 5. B = border irregularity C = color variation D = diameter greater than or equal to 6 mm E = evolving with changes over time (growth, color variation, itching, bleeding). Thus, the classic melanoma will be a large, pigmented lesion that has an asymmetrical shape, to diagnose. Page 63 ALU 201: Intermediate Medical Life Insurance Writing 1. 2. nodular melanoma 3. lentigo maligna 4. acral lentiginous melanoma. eventually enters a vertical phase in which spread is into the deeper dermal layers. As will be tumor increases. thin and tend to be indolent, or more slowly progressive, in character. They usually carry a better sole, or under the nail and are more common in individuals with black or dark complexions. They the other subtypes. the risk, and there is no critical level below which the risk is zero. It should be kept in mind that the Page 64 In this case, the measured depth on pathological examination can be less than the true prognostic depth. mean that the lesion has a classic ulcer crater. Instead, it means that pathologically (i.e., under the 1. lower expected death rate in younger individuals. 2. 3. to that seen with ulceration 4. a. Clark level I – epidermis only b. c. d. Clark level IV – reticular dermis e. account. Page 65 ALU 201: Intermediate Medical Life Insurance Writing 1. 2. and a greater response is associated with thinner tumors and a better outcome. 3. With increasing age, males 4. Tumor regression can, as previously noted, indicate that the tumor was at one time thicker 5. Elevated serum S-100 protein circulating melanoma cells. 6. Desmoplastic melanoma It is important to recognize that melanoma (and atypical nevus) pathology interpretation and dermatopathologist to always distinguish between an atypical nevus and an early melanoma, or to 1. 2. 3. th edition, with the current categories 1. 2. 3. 4. The reason these levels were chosen was primarily convenience, to allow clinicians and others Page 66 where ulceration is present. Thus, a melanoma that is less than 1.0 mm in depth that has ulceration is designated T1b and has the The 8th risk groupings that correlate reasonably well with survival outcomes (see below). The entire list 1. 2. 3. 4. 5. 6. Page 67 ALU 201: Intermediate Medical Life Insurance Writing Treatment chemotherapeutic trials. monoclonal antibodies, vaccines and other approaches that mobilize one’s individual immune is injected directly into the tumor, destroying malignant cells through a local immune response. Mortality clearly varies by stage, and it tracks well with the AJCC staging system (Figure 1). higher risk due to tumor ulceration, high mitotic rate, and scalp or neck location, those without Table 1 Figure 2). The risk rises rapidly as lesions get deeper. Because ulceration revises the stage to the next depth category, Page 68 lesions (Figure 3 melanoma in a given individual suggests either a genetic predisposition exists or that the individual Figure 4). Although not common, recurrences nodes, new liver or lung lesions) should not be ignored. Page 69 ALU 201: Intermediate Medical Life Insurance Writing Page 70 Melanoma Mortality By Stage SEER Data 600 500 400 Years 0-5 300 Years 5-10 200 100 0 IA IB IIA !!B IIC Stage Adapted from the Surveillance, Epidemiology, and End Results (SEER) Program Public-Use Data (1973-2008). National Cancer Institute, DCCPS, Surveillance Research Program. Cancer Statistics Branch. Released September 2011. Based on the November 2010 submission. Page 71 ALU 201: Intermediate Medical Life Insurance Writing Melanoma Mortality - Stages IA, IIA by Age and Location SEER Data 250 200 Years 0-5 150 Years 5-10 Years 10-15 100 Years 15-20 50 0 Extremity Extremity Axis Axis < 60 > 60 < 60 > 60 Adapted from the Surveillance, Epidemiology, and End Results (SEER) Program Public-Use Data (19732008). National Cancer Institute, DCCPS, Surveillance Research Program. Cancer Statistics Branch. Released September 2011. Based on the November 2010 submission. Melanoma Long-Term Mortality by Extent of Tumor SEER Data 600 500 400 Localized 300 Regional Distant 200 100 0 0-5 5-10 10-15 15-20 20-25 Years Adapted from the Surveillance, Epidemiology, and End Results (SEER) Program Public-Use Data (19732008). National Cancer Institute, DCCPS, Surveillance Research Program. Cancer Statistics Branch. Released September 2011. Based on the November 2010 submission. Page 72 Section B Prostate Cancer Epidemiology prostate cancer. Incidence rates increased dramatically in the early 1990s, peaking in 1992 at 237.4 cases per screening. The incidence rate has subsequently diminished and was 141.0 cases per 100,000 in cancer in the world (237.4 cases per 100,000 in the years 1975 to2012) and death rates that are Page 73 ALU 201: Intermediate Medical Life Insurance Writing prostate cancer. and exact mechanism by which this occurs is unclear. Etiology Screening and Diagnosis Digital Rectal Exam Page 74 that the negative predictive value is reasonably low. In addition, the positive predictive value even though the PSA level is in the normal range. In those situations, stability over time and the ruling out a malignancy. cancer. PSA is a serine protease glycoprotein that is produced almost exclusively by the epithelial distinguishes prostate cancer is that it produces more PSA per unit volume than does benign tissue. 1. 2. prostatitis 3. prostatic massage 4. surgery 5. ® ) and dutasteride (Avodart®), was established in an older population, and it has been recognized that levels vary with age. With Page 75 ALU 201: Intermediate Medical Life Insurance Writing 1. 2. 3. 4. PSA readings in the normal range, with a negative predictive value estimated to be around 85%. 4.0 ng/ml. PSA Velocity threshold in the 0.35 to 0.40 ng/ml per year range. For optimal accuracy, one should have at least three readings spaced out over at least 18 months when assessing PSA velocity. Controversy against recommendation has been controversial and continues to be debated in clinical circles. The advanced, incurable disease with early mortality, which makes it highly valuable in the insurance Page 76 Improving the performance of PSA Percentage Free PSA PSA Density The PSA density (PSAD) is another tool that has been employed, though also requires the PSA Isoforms Prostate Health Index Page 77 ALU 201: Intermediate Medical Life Insurance Writing Four Kallikrein Assays PCA3 The prostate cancer antigen 3 gene (PCA3) is highly overexpressed in almost all prostate cancer in independently predicting a positive biopsy, but as with the other predictive markers, it has not been shown to improve outcomes. Transrectal Ultrasound not Biopsy Page 78 Pathology 1. 2. 3. 1. 2. 3. 4. 5. Since the prostate cancer grade is so closely tied to prognosis, it is imperative to pay close Page 79 ALU 201: Intermediate Medical Life Insurance Writing Staging designate whether the categories were clinically or pathologically derived. using presently available treatments. 1. T1 lesions (T1a, T1b, or T1c) indicate clinical staging only when the cancer is not palpable (T1c). 2. 3. seminal vesicle invasion. 4. Tumors that are located in the apex or that invade the prostatic capsule without penetration through the capsule are considered T2, not T3 lesions. Page 80 Prognostic Factors 1. 2. 3. T stage cT1, cT2a, pT2 cT1, cTa, pT2 cT2b, cT2c T any Grade group 1 1 1 2 3 4 5 PSA >20 Any Any Stage Group I IIA IIA IIB IIC IIC IIIA IIIB IIIC Treatment Active Surveillance Most prostate cancers are now diagnosed while clinically localized. Taking into account the Page 81 ALU 201: Intermediate Medical Life Insurance Writing Surgery and Radiation progression during AS. Surprisingly, there are no good studies that directly compare the outcomes likely to be treated with radiation. The result is that the surgically treated group tends to be, in changed to such a large extent. This makes comparisons between surgery and radiation and among Page 82 closely. Though an increase in the PSA level is usually an indication that the tumor has recurred, and urinary incontinence. tumor while minimizing damage to the surrounding tissues. 1. 2. delivered to the tumor. Multiple studies show improved outcomes with the higher dosages. 3. Sometimes radiation can be combined with adjuvant hormonal therapy, which is given in improve response rates. implantation and generally take 18 months or longer to reach a nadir. In general, the complication divide. Since prostate tumor cells divide slowly, this delayed necrosis can take some time to to three years to reach its lowest level. The nadir, or lowest level reached, and the time it takes to Page 83 ALU 201: Intermediate Medical Life Insurance Writing External beam radiation therapy is occasionally used in individuals who have been treated with a radical prostatectomy but who then have a rising PSA level. In this case, the radiation is being one lasting at least several years, is an indication that the rising PSA was more likely due to local Hormone Therapy Prostate cancer is very sensitive to hormonal stimulation with androgens (i.e., testosterone and its the PSA to undetectable levels. Androgen removal can be accomplished surgically via castration or ® ® Cryotherapy cryosurgery can be used to destroy the prostatic tissue. The cooling process kills tumor cells directly, as well as via vascular damage. Cryotherapy has been used as primary treatment and Watchful Waiting requires therapy Mortality Prostate cancer is a slow growing tumor with a doubling time (i.e., the time required to double Page 84 disease, and survival curves are comparable to those seen with the general population. This is (Figure 1) Consequently, early mortality is not generally an issue with prostate cancer. Deaths within the ratios (data not shown here). As noted above, mortality peaks late and generally occurs at least 10 the prostate. For tumors extending outside the prostate, the surgical margins are important as well. This assessment is possible because surgical specimens provide the opportunity to determine the In contrast, those individuals treated with radiation are evaluated by clinical staging, which Individuals treated with radiation are thus divided into low risk, intermediate risk, and high risk groups using these clinical staging parameters. with active disease. This impacts outcomes seen with those Page 85 ALU 201: Intermediate Medical Life Insurance Writing treatment. This pattern is summarized in Figures 4 and 5. disease. For those at low risk, outcomes with AS appear to be excellent, but perhaps slightly less 13-15 years from PSA recurrence to mortality. This duration underscores the long clinical 1. 2. 3. See Figure 6. Page 86 Cumulative Survival Prostate CA Ages 40 up, Mod Diff Organ Confined, Surgery SEER Data 1.000 0.900 0.800 0.700 0.600 Observed Expected 0.500 0.400 0.300 0.200 0.100 0.000 1 3 5 7 9 11 13 15 17 19 21 Years Adapted from the Surveillance, Epidemiology, and End Results (SEER) Program Public-Use Data (1973-2006). National Cancer Institute, DCCPS, Surveillance Research Program. Cancer Statistics Branch. Released April 2008. Based on the November 2007 submission. Prostate Cancer Mortality - Surgical Therapy Localized - SEER Data 250 200 Years 0-5 150 Years 5-10 Years 10-15 100 Years 15-20 50 0 Well Mod Poor 50-59 Well Mod Poor 60-69 Well Mod Poor 70-79 Adapted from the Surveillance, Epidemiology, and End Results (SEER) Program Public-Use Data (1973-2006). National Cancer Institute, DCCPS, Surveillance Research Program. Cancer Statistics Branch. Released April 2008. Based on the November 2007 submission. Page 87 ALU 201: Intermediate Medical Life Insurance Writing Markov Model - Prostate Cancer - 15 Years Surgery v Radiation - All Groups 250 200 150 OC/Low EPE,M-/Intermed EPE,M+/High 100 50 0 Surg Rad 55 Surg Rad Surg 65 Rad 75 PSA Recurrence Free Survival T1, T2 Tumors Surgery (98% ) versus Radiation (94% ) 1 0.9 0.8 0.7 0.66 0.65 0.63 0.63 0.6 0.54 0.52 0.5 Radiation 0.4 0.3 0.2 0.1 0 5 10 Years Post Treatment Page 88 Surgery 15 Distant and PSA Recurrence Free Survival By Duration Post Surgery (45% T3 ) 1 0.9 0.8 0.7 0.6 Distant Free 0.5 PSA Free 0.4 0.3 0.2 0.1 0 5 10 15 20 25 Years. - Page 89 ALU 201: Intermediate Medical Life Insurance Writing - Page 90 Section C Breast Cancer Epidemiology it is the underwriting. 20% are called in situ lesions and have cells that show malignant changes but have not invaded replacement therapy. Age 8 (12.4%). Estrogen Exposure Page 91 ALU 201: Intermediate Medical Life Insurance Writing recent years. Family History the risk. Benign Breast Disease Environmental Factors 1. Page 92 2. lesion occurred at a young age. 3. 4. 5. 6. are at higher risk. Aromatase inhibitors (AIs) such as anastrozole and exemestane are also 7. Prior History of Breast Cancer Pathology In situ Carcinoma are considered to be DCIS. As with invasive breast cancer, the risk increases with age, and it is to consider is as lobular neoplasia, a designation that also includes atypical lobular hyperplasia Page 93 ALU 201: Intermediate Medical Life Insurance Writing Invasive Cancers Diagnosis Most breast cancers are asymptomatic at diagnosis. The disease is occasionally noted by the nipple discharge, or lymph node enlargement. Clinical breast examination by medical personnel also detects some tumors. also be used to direct needle biopsies or cyst drainage. Because ultrasound does not visualize Staging Page 94 adjuvant therapy (chemotherapy and/or radiation treatment based on the clinical stage and given subsequently determined. 1. Tis – carcinoma in situ 2. 3. 4. T3 – >5.0 cm 5. T4 – any size with extension to (a) the chest wall, (b) the skin, (c) both chest wall and skin, 1. 2. 3. 4. The M designation indicates whether distant metastasis is absent (M0) or present (M1). Page 95 ALU 201: Intermediate Medical Life Insurance Writing 1. 2. 3. 4. 5. 6. 7. 8. distant metastases. biomarkers. These biomarkers are the histologic grade, estrogen and progesterone receptor status, Though the anatomic staging noted above remains unchanged, it is to be used only in parts anatomic stage leads to much complexity (122 separate possibilities not including the recurrence score is less than 11, the case should be assigned pathological prognostic stage group IA, regardless Page 96 Prognostic Factors not control. tumor detected on microscopic examination or by specialized immunohistochemical testing carry cells. Tumor size is also critical in assessing risk, both in those with and those without nodal into the surrounding tissue (T4). The age of onset Lymphatic or vascular local and distant spread, particularly in higher grade tumors. While the estrogen and progesterone receptors early recurrence rates, while receptor positive individuals have higher later recurrence rates. In and long term outcomes. Page 97 ALU 201: Intermediate Medical Life Insurance Writing markers with more aggressive tumor behavior. oncogene is located on chromosome 17 and its overexpression is associated with increased tumor aggressiveness. Its overexpression also predicts an increased response to the humanized antibody ® ), a drug that can dramatically reduce recurrence rates in these tumors. poor prognosis. available. As previously noted, the recurrence score is already incorporated into the prognostic groups as that evidence becomes available. are important because they tend to be more aggressive with a poorer prognosis and are more likely limited treatment options, i.e., chemotherapy, as hormonal therapy and trastuzumab cannot be used. Treatment dissection (most DCIS tumors do not). Page 98 the usual approach is either prophylactic bilateral mastectomy, chemoprevention using hormonal (discussed below). Individuals with large tumors, an extensive intraductal component, or in whom a lumpectomy extensive intraductal component, radiation therapy may not be necessary. mammary or supraclavicular nodes may be involved at presentation, they rarely occur unless there hormonal therapy. Aromatase inhibitor drugs (Arimidex®, Femara®, Aromasin®) are now the androgens to estrogens in adipose tissue, the adrenal glands, and the breast tumors themselves do not 1. tumors. 2. positive individuals. Page 99 ALU 201: Intermediate Medical Life Insurance Writing 3. 4. not chemotherapy is used. 5. 6. 7. 8. third. 9. Extra mortality caused using adjuvant therapy is minimal. Mortality 1. lymph node status 2. tumor size 3. histologic grade. Figure 4) associated with older radiation techniques. With earlier diagnosis and more modern treatment Table 1 and Figure 5. Page 100 Figure 6). Individuals with metastatic Figure 7). over time, at approximately 0.3% per year in those not known to harbor a genetic predisposition. advanced by the time it is diagnosed. Page 101 ALU 201: Intermediate Medical Life Insurance Writing Survival By Node Status - Seer Data All Ages, All Sizes, All Grades 100.0% 90.0% 80.0% 70.0% Expected 60.0% 0-1 Nodes 50.0% 1-3 Nodes 40.0% 4+ Nodes 30.0% 20.0% 10.0% 0.0% 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 Years After Diagnosis Adapted from the Surveillance, Epidemiology, and End Results (SEER) Program Public-Use Data (1973-2006). National Cancer Institute, DCCPS, Surveillance Research Program. Cancer Statistics Branch. Released April 2008. Based on the November 2007 submission. Survival By Tumor Size - SEER Data All Ages, All Grades. All Nodes 100.0% 90.0% 80.0% 70.0% Expected 60.0% 0-1 cm 50.0% 1.1-2 cm 40.0% 2 cm up 30.0% 20.0% 10.0% 0.0% 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 Years After Diagnosis Adapted from the Surveillance, Epidemiology, and End Results (SEER) Program Public-Use Data (1973-2006). National Cancer Institute, DCCPS, Surveillance Research Program. Cancer Statistics Branch. Released April 2008. Based on the November 2007 submission. Page 102 Survival By Grade - Seer Data All Ages, All Sizes, All Nodes 100.0% 90.0% 80.0% 70.0% Expected 60.0% Well 50.0% Mod 40.0% Poor 30.0% 20.0% 10.0% 0.0% 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 Years After Diagnosis Adapted from the Surveillance, Epidemiology, and End Results (SEER) Program Public-Use Data (1973-2006). National Cancer Institute, DCCPS, Surveillance Research Program. Cancer Statistics Branch. Released April 2008. Based on the November 2007 submission. Breast Cancer Mortality By Size, Grade and Node Status 700 600 500 0-1 cm 400 1.1-2.0 cm 300 2.1 cm up 200 100 0 0 Nodes 1-3 Nodes 4+ Nodes Adapted from the Surveillance, Epidemiology, and End Results (SEER) Program Public-Use Data (1973-2006). National Cancer Institute, DCCPS, Surveillance Research Program. Cancer Statistics Branch. Released April 2008. Based on the November 2007 submission. Page 103 ALU 201: Intermediate Medical Life Insurance Writing Annual T1a, T1b T1c T2 T2 I II III (Moderate) nodes) Distant nodes) nodes) 2.0cm) 3.0cm) 5.0cm) 1.0% 1.9% 3.9% 0.5% 0.8% 1.5% 1.7% 0.4% 0.7% 0.9% 1.1% 1.7% 2.8% 0.8% 1.1% 1.4% 1.4% 0.8% 1.0% 1.5% yrs Percentage of Patients Recurring Per Year J Clin Oncol, 14:2738-46 15 10 Yearly Recurrence Rate 5 0 1 3 5 7 9 Yearly Inte rvals Page 104 11 Breast Cancer Mortality By Size, Grade and Duration No Nodes 300 250 200 0-1 cm 150 1.1-2.0 cm 2.1 cm up 100 50 0 Year 0-5 Year 5-10 Year 10-15 Adapted from the Surveillance, Epidemiology, and End Results (SEER) Program Public-Use Data (1973-2006). National Cancer Institute, DCCPS, Surveillance Research Program. Cancer Statistics Branch. Released April 2008. Based on the November 2007 submission. Breast Cancer- Metastatic Disease - All Grades Long-Term Mortality 1400 1200 1000 800 All Mets 600 400 200 0 0-5 5-10 10-15 15-20 20-25 Years Adapted from the Surveillance, Epidemiology, and End Results (SEER) Program Public-Use Data (1973-2006). National Cancer Institute, DCCPS, Surveillance Research Program. Cancer Statistics Branch. Released April 2008. Based on the November 2007 submission. Page 105 ALU 201: Intermediate Medical Life Insurance Writing Section D Colon Cancer Epidemiology to 14.7 per 100,000 in 2012. Increased screening, lower smoking rates, and improvements in diet more aggressive disease while those who are older at diagnosis tend to present at earlier stages. Weight gain is also thought to play a part in increasing risk. Individuals who are physically active have a lower risk. Page 106 surveillance is recommended in these diseases. colorectal cancer. recurrent and advanced adenomas. Etiology other genes permit the tumor to metastasize. 1. 2. tumor development than do tubular adenomas. 3. generally more rapid in proximal lesions. In addition, polyp development, and consequently cancer a common phenomenon. Page 107 ALU 201: Intermediate Medical Life Insurance Writing Inherited Colon Cancer Syndromes malignancies as well, especially endometrial and ovarian cancer (39% and 9% risk by age 70, respectively). Screening and Diagnosis Page 108 mortality, but has limited sensitivity due to its ability to visualize only the distal colon. It is generally used in conjunction with FIT. is considered preventive. CT colonography is nearly as sensitive as colonoscopy, and though it requires a similar bowel exposure, the inability to biopsy or remove polyps or other suspicious lesions, and that incidental capsule containing a tiny wireless video device that views the colon during the device’s transit. The procedure requires no sedation and does require a bowel preparation preceding the capsule’s Clinical Presentation Colon cancer can present as exophytic (growth extending into the lumen) or polypoid lesions, 1. 2. bowel. 3. gross blood in the stool or symptoms related to obstruction, such as a change in bowel habits. In general, tumors that present with symptoms are more likely to be advanced and carry a screening programs. Page 109 ALU 201: Intermediate Medical Life Insurance Writing Pathology 1. 2. 3. Staging 1. muscularis mucosae adjacent organs or structures). 2. subserosa, mesentery, or nonperitonealized pericolic tissues indicates 7 or more nodes) In assessing nodal metastases, it is important to note that nodal micrometastases isolated tumor cells are not counted. 3. M1b, and M1c.13 Page 110 1. 2. 3. 4. 5. 6. 7. 8. Prognostic Factors 1. 2. 3. 4. 5. lymphovascular and perineural invasion 6. high preoperative carcinoembryonic antigen (CEA) level (discussed below) 7. 8. 9. Page 111 ALU 201: Intermediate Medical Life Insurance Writing approved. Treatment low rectal cancers. Chemotherapy and radiation treatment, used as adjuvant therapy, can eradicate micrometastasis and increase cure rates in individuals who have been treated primarily with surgery. In individuals with metastatic disease, chemotherapy alone is not curative but may be able surgical removal can be necessary. 1. 2. 3. been shown to yield a roughly 30% reduction in recurrence and mortality rates, 4. with monoclonal antibodies have been used with some improved response. Surgery can be employed with palliative or symptomatic, but only rarely curative, intent (e.g., bowel in up to 20%. Page 112 additional three years. Colonoscopy is generally done at one year postoperatively and then every worse. Page 113 ALU 201: Intermediate Medical Life Insurance Writing colon cancer and its precursor lesion, the colonic polyp. years (and, thus, probable cure) may approach 20%. Stage At diagnosis I 94% 96% 98% IIA 85% 90% 96% IIB 71% 80% 92% IIIA 83% 89% 95% IIIB 64% 74% 89% IIIC 42% 57% 80% IV 5% 15% 48% Page 114 Colon Cancer Mortality by Node Status SEER Data 700 600 500 Years 0-5 400 Years 5-10 Years 10-15 300 Years 15-20 200 100 0 0 1-3 4 up Positive Nodes Adapted from the Surveillance, Epidemiology, and End Results (SEER) Program Public-Use Data (1973-2008). National Cancer Institute, DCCPS, Surveillance Research Program. Cancer Statistics Branch. Released September 2011. Based on the November 2010 submission. Colon Cancer Mortality by Grade SEER Data 600 500 400 Years 0-5 Years 5-10 300 Years 10-15 Years 15-20 200 100 0 Well Moderate Poor Grade Adapted from the Surveillance, Epidemiology, and End Results (SEER) Program Public-Use Data (1973-2008). National Cancer Institute, DCCPS, Surveillance Research Program. Cancer Statistics Branch. Released September 2011. Based on the November 2010 submission. Page 115 ALU 201: Intermediate Medical Life Insurance Writing Colon Cancer Mortality by Local Extent (T Stage) No Nodes - SEER Data 350 300 250 Years 0-5 200 Years 5-10 Years 10-15 150 Years 15-20 100 50 0 T1 T2 T3 T4 Extent - T Stage Adapted from the Surveillance, Epidemiology, and End Results (SEER) Program Public-Use Data (1973-2008). National Cancer Institute, DCCPS, Surveillance Research Program. Cancer Statistics Branch. Released September 2011. Based on the November 2010 submission. Colon Cancer Mortality by Local Extent (T Stage) 1-3 Nodes - SEER Data 600 500 400 Years 0-5 Years 5-10 300 Years 10-15 Years 15-20 200 100 0 T1 T2 T3 T4 Extent - T Stage Adapted from the Surveillance, Epidemiology, and End Results (SEER) Program Public-Use Data (1973-2008). National Cancer Institute, DCCPS, Surveillance Research Program. Cancer Statistics Branch. Released September 2011. Based on the November 2010 submission. Page 116 Colon Cancer Mortality by Stage and Grade Stages I and II - SEER Data 250 200 Years 0-5 150 Years 5-10 Years 10-15 100 Years 15-20 50 0 Well Moderate Poor Well Stage I Moderate Poor Stage II Adapted from the Surveillance, Epidemiology, and End Results (SEER) Program Public-Use Data (1973-2008). National Cancer Institute, DCCPS, Surveillance Research Program. Cancer Statistics Branch. Released September 2011. Based on the November 2010 submission. Colon Cancer Mortality by Stage and Grade Stages III and IV - SEER Data 2000 1800 1600 1400 Years 0-5 1200 Years 5-10 1000 Years 10-15 800 Years 15-20 600 400 200 0 Well Moderate Stage III Poor Well Moderate Poor Stage IV Adapted from the Surveillance, Epidemiology, and End Results (SEER) Program Public-Use Data (1973-2008). National Cancer Institute, DCCPS, Surveillance Research Program. Cancer Statistics Branch. Released September 2011. Based on the November 2010 submission. Page 117