This document summarizes evidence that early cancer detection through screening and diagnostic imaging can lead to overdiagnosis. The key points are:
1) There exists a reservoir of subclinical cancers that can be detected early, before they cause symptoms, based on autopsy studies finding cancers in prostate, thyroid, and breast tissues.
2) Screening programs and increased diagnostic imaging tap into this reservoir by detecting cancers earlier. Randomized trials provide the strongest evidence, showing an excess of cancers detected by screening that does not disappear over time.
3) Estimates from randomized trials suggest around 25% of mammographically detected breast cancers, 50% of chest x-ray and sputum-detected lung cancers, and 60%
A 49-year-old asymptomatic man presents for a vasectomy
evaluation. His past medical history is noncontributory, and his
family history is remarkable for prostate cancer in his father. On
genitourinary examination, his left testicle is notably larger than
his right testicle, with concern for a firm, nontender upper pole
mass palpated on the left side.
Association between ABO Blood Group and Various Types of Cancer: A Case–Contr...asclepiuspdfs
Introduction: The association between ABO blood group and cancer has been identified in many epidemiological researches. The aim of the current research was to investigate the association between ABO blood group and the risk of several types of cancer in a Greek adult population. Materials and Methods: A total of 459 individuals who suffered from various types of cancer and 918 non-cancer individuals were enrolled. Blood group data obtained from registration on identity patient’s card. The associations between ABO blood group and cancer estimated using a multivariate logistic regression analysis model, whereas a multinomial model was carried out to estimate adjusted odds ratios for each type of cancer separately. Results: The risk of overall cancer in blood groups A and B individuals was significantly higher than that in O and AB groups, (P = 0.001, OR = 1.96, 95%CI = 1.33–2.87, and P ≤ 0.0001, OR = 2.04 95% CI=1.43–2.90, respectively). Compared to blood type O, blood type A was significantly associated with an increased risk of gastric (P = 0.002, OR = 2.55, 95% CI = 0.55–4.30), colorectal (P = 0.046, OR = 2.06, 95%CI = 0.82–2.58), pancreatic (P = 0.034, OR = 2.23, 95% CI = 1.02–2.83), and lung cancer (LC) (P = 0.022, OR = 2.78, 95% CI = 1.63–5.49), whereas blood type B was significantly associated with an increased risk of esophagus cancer (P = 0.051, OR = 1.26, 95% CI = 0.83–1.50), after adjusting for age, gender, educational and socio-economic status, smoking, and family history of cancer. Conclusion: The overall cancer risk in blood groups A and B individuals was significantly higher compared to blood type O and AB, whereas blood type A was significantly associated with an increased risk of gastric, colorectal, pancreatic, and LC.
A 49-year-old asymptomatic man presents for a vasectomy
evaluation. His past medical history is noncontributory, and his
family history is remarkable for prostate cancer in his father. On
genitourinary examination, his left testicle is notably larger than
his right testicle, with concern for a firm, nontender upper pole
mass palpated on the left side.
Association between ABO Blood Group and Various Types of Cancer: A Case–Contr...asclepiuspdfs
Introduction: The association between ABO blood group and cancer has been identified in many epidemiological researches. The aim of the current research was to investigate the association between ABO blood group and the risk of several types of cancer in a Greek adult population. Materials and Methods: A total of 459 individuals who suffered from various types of cancer and 918 non-cancer individuals were enrolled. Blood group data obtained from registration on identity patient’s card. The associations between ABO blood group and cancer estimated using a multivariate logistic regression analysis model, whereas a multinomial model was carried out to estimate adjusted odds ratios for each type of cancer separately. Results: The risk of overall cancer in blood groups A and B individuals was significantly higher than that in O and AB groups, (P = 0.001, OR = 1.96, 95%CI = 1.33–2.87, and P ≤ 0.0001, OR = 2.04 95% CI=1.43–2.90, respectively). Compared to blood type O, blood type A was significantly associated with an increased risk of gastric (P = 0.002, OR = 2.55, 95% CI = 0.55–4.30), colorectal (P = 0.046, OR = 2.06, 95%CI = 0.82–2.58), pancreatic (P = 0.034, OR = 2.23, 95% CI = 1.02–2.83), and lung cancer (LC) (P = 0.022, OR = 2.78, 95% CI = 1.63–5.49), whereas blood type B was significantly associated with an increased risk of esophagus cancer (P = 0.051, OR = 1.26, 95% CI = 0.83–1.50), after adjusting for age, gender, educational and socio-economic status, smoking, and family history of cancer. Conclusion: The overall cancer risk in blood groups A and B individuals was significantly higher compared to blood type O and AB, whereas blood type A was significantly associated with an increased risk of gastric, colorectal, pancreatic, and LC.
Сулаєва О.М. - Молекулярна діагностика в менеджменті пацієнтів з рмзAlinaPokhilko
Навчальний курс: «Молекулярна онкологія, патологія та генетика»
Медична лабораторія CSD спільно з Center for research and education of translational biology and medicine (www.tbm.center ) пропонує безкоштовний курс навчальних лекцій для усіх бажаючих.
Thyroid Papillary Carcinoma and Noninvasive Follicular Thyroid Neoplasm with ...CrimsonPublishersGJEM
Papillary thyroid carcinomas (PTC) are well differentiated malignante pithelial tumors with characteristic nuclear features and they originate from epithelial cells of thyroid follicle. Papillary thyroid carcinoma is the most common type of thyroid cancers, which composes 85-90% of all thyroid carcinomas. Number of patients diagnosed with thyroid cancer has significantly increased during the last two decades due to increased awareness of nodular thyroid diseases, developments in diagnostic methods, wide applicability of thyroid fine needle aspiration, new descriptions of histopathology criteria and increased radiation exposure. It is more common in males than females with some ethnic variations. Although it is very rare during early childhood, it is the most common thyroid cancer of this age group. The mean age is 46 years at the time of diagnosis. Tumor has some histologic variants, the most common ones are being classical and follicular variants
https://crimsonpublishers.com/gjem/fulltext/GJEM.000505.php
For more open access journals in Crimson Publishers
Please click on link: https://crimsonpublishers.com
For More Articles on Medical research
Please click on: https://crimsonpublishers.com/gjem/
ABSTRACT- Thrombocytosis has been reported in association with ovarian tumors and is often a poor prognostic
factor. The present study aims to study the incidence of pre-operative thrombocytosis in epithelial ovarian tumors and to
correlate it with anemia, serum CA-125 levels, presence or ascites, FIGO staging and tumor histology. Total 160 cases
of resected specimens of surface epithelial ovarian tumors (SEOT) received in department of Pathology, Kasturba
Medical College Mangalore were studied. The preoperative platelet count, haemoglobin levels and serum CA-125
levels were collected. The presence and degree of ascites was assessed. International Federation of Obstetrics and
Gynaecology (FIGO) staging was done. The incidence of thrombocytosis and its correlation with the presence of
anaemia, elevated CA-125 levels, FIGO stage and presence and degree of ascites among malignant cases were
statistically analysed. The incidence of pre-operative thrombocytosis was noted more in malignant SEOTs 80%
(40/160). The mean pre-operative platelet count in the present study was 321X109 /L. It was more prevalent in serous
epithelial ovarian tumors (83.3%) and these findings were statistically significant (p=0.0001). There was a statistically
significant association of pre-operative thrombocytosis with the presence and degree of ascites and advanced FIGO
staging (p=0.0001). Pre-operative thrombocytosis is a frequent finding in malignant SEOTs and is associated with other
prognostic markers. This implies that thrombocytosis is probably a marker of tumor aggressiveness, and that platelet
may have a role in cancer growth and progression. Thus, presence of pre-operative thrombocytosis has significance as a
poor prognosticator in epithelial ovarian tumors.
Key-words- Thrombocytosis, Surface Epithelial Ovarian Tumors (SEOT), CA 125, FIGO staging
The KRAS-Variant and miRNA Expression in RTOG Endometrial Cancer Clinical Tri...UCLA
The KRAS-variant may be a genetic marker of risk for type 2 endometrial cancers. In addition, tumor miRNA expression appears to be associated with patient age, lymphovascular invasion and the KRAS-variant, supporting the hypothesis that altered tumor biology can be measured by miRNA expression, and that the KRAS-variant likely impacts endometrial tumor biology.
Awareness about Intestinal Cancer in University Student_Crimson PublishersCrimsonpublishersCancer
Cancer is a disease which is caused by the uncontrolled growth of cells. The cancer stem cells suggest that the clones are obtained by the sub population of cells showing diverse cancer cells phenotypically. First possible cancer stem cells are seen in leukemia, brain tumors and breast cancer. The gastrointestinal cancer becoming the major causes of deaths in the world. A questionnaire was developed and it is distributed among the students of class to determine the ideas and awareness of this disease. Questionnaires contain 15 different types of question regarding the disease. 39 students taken from the Bahauddin Zakariya University Multan, Pakistan. All the students are post graduated and the results show that all of them have awareness from this disease.
Adjuvant therapy protocols for liver cancer in patients undergoing liver tran...hr77
Many patients undergo liver transplantation for a liver cancer in a setting of liver cirrhosis. When is it possible to consider chemotherapy in such patients? Is it even possible? Is there a role?
Characteristics of cases with unknown stage prostate cancerCancer Council NSW
Stage of cancer at diagnosis (e.g. localised, regional involvement, metastatic) is an important predictor of survival. This paper identifies there is cause for concern surrounding the 40% of "unknown" or unrecorded stage of diagnosis on prostate cancer patient records in NSW. This means crucial information is missing from their records. The second stage of this project, scheduled for completion in late 2014, is to identify the reasons for these missing data. Once this has been completed we can inform policy makers to ensure the data completeness can be improved. Studies using cancer staging data can then increase in quality and quantity.
Introduction to Cancer Epidemiology and CarcinogenesisPUBH 6.docxbagotjesusa
Introduction to Cancer Epidemiology and Carcinogenesis
PUBH 6550/8550
Chronic Disease Epidemiology
1
Cancer is a term describing malignant diseases. Cancer should not be thought of as a single disease but rather a group of diseases which may have many characteristics in common but not necessarily the same causative agents, etiology or molecular profiles. In general, cancer defines diseases that have the capacity to invade surrounding normal tissue, metastasize (spread to distant sites) and kill the host in which it originates.
Objectives
What is the definition of cancer?
Benign vs. Malignant
Most common cancer types in men and women
Learn how to obtain cancer-related data using Internet sources
Understand cancer staging
Understand the basics of how carcinogenesis occurs
Describe inherited cancer syndromes
2
Causation and Cancer
Examples of Identified Causes and
Future Efforts in Cancer Prevention
Tobacco use and lung cancer
Infectious agents (e.g., HPV) and cervical cancer
Ionizing radiation and leukemia
Designation of a risk factor as “causal” has been the starting point for initiating cancer prevention programs based on reducing exposure to the risk factor
4
4
The concept of causation has long had a central role in the application of epidemiologic evidence for controlling cancer. Designation of a risk factor as “causal” has been the starting point for initiating cancer prevention programs based on reducing exposure to the risk factor. Though the concept of causation remains a matter of continuing discussion, use of the term in public health implies that the evidence supporting causality of association has reached a critical threshold of certainty and that reduced exposure can be expected to be followed by reduced disease occurrence. In other words, if there is “enough” evidence supporting a particular risk factor (or a preventive or prognostic factor), it seems to be considered ‘causal’. Keep in mind, though, that risk factor is the most proper term.
What is cancer?
Cancer is a group of diseases characterized by uncontrolled growth and spread of abnormal cells. If the spread is not controlled, it can result in death.
Characteristics: Abnormality, Uncontrollability, invasiveness
5
5
According to the American Cancer Society (ACS), cancer is a group of diseases characterized by uncontrolled growth and spread of abnormal cells. If the spread is not controlled, it can result in death. Although cancer is often referred to as a single condition, it actually consists of more than 100 different diseases. These diseases are characterized by uncontrolled growth and spread of abnormal cells. Cancer can arise in many sites and behave differently depending on its organ of origin. Breast cancer, for example, has different characteristics than lung cancer. It is important to understand that cancer originating in one body organ takes its characteristics with it even if it spreads to another part of the body. For example, metastatic br.
Сулаєва О.М. - Молекулярна діагностика в менеджменті пацієнтів з рмзAlinaPokhilko
Навчальний курс: «Молекулярна онкологія, патологія та генетика»
Медична лабораторія CSD спільно з Center for research and education of translational biology and medicine (www.tbm.center ) пропонує безкоштовний курс навчальних лекцій для усіх бажаючих.
Thyroid Papillary Carcinoma and Noninvasive Follicular Thyroid Neoplasm with ...CrimsonPublishersGJEM
Papillary thyroid carcinomas (PTC) are well differentiated malignante pithelial tumors with characteristic nuclear features and they originate from epithelial cells of thyroid follicle. Papillary thyroid carcinoma is the most common type of thyroid cancers, which composes 85-90% of all thyroid carcinomas. Number of patients diagnosed with thyroid cancer has significantly increased during the last two decades due to increased awareness of nodular thyroid diseases, developments in diagnostic methods, wide applicability of thyroid fine needle aspiration, new descriptions of histopathology criteria and increased radiation exposure. It is more common in males than females with some ethnic variations. Although it is very rare during early childhood, it is the most common thyroid cancer of this age group. The mean age is 46 years at the time of diagnosis. Tumor has some histologic variants, the most common ones are being classical and follicular variants
https://crimsonpublishers.com/gjem/fulltext/GJEM.000505.php
For more open access journals in Crimson Publishers
Please click on link: https://crimsonpublishers.com
For More Articles on Medical research
Please click on: https://crimsonpublishers.com/gjem/
ABSTRACT- Thrombocytosis has been reported in association with ovarian tumors and is often a poor prognostic
factor. The present study aims to study the incidence of pre-operative thrombocytosis in epithelial ovarian tumors and to
correlate it with anemia, serum CA-125 levels, presence or ascites, FIGO staging and tumor histology. Total 160 cases
of resected specimens of surface epithelial ovarian tumors (SEOT) received in department of Pathology, Kasturba
Medical College Mangalore were studied. The preoperative platelet count, haemoglobin levels and serum CA-125
levels were collected. The presence and degree of ascites was assessed. International Federation of Obstetrics and
Gynaecology (FIGO) staging was done. The incidence of thrombocytosis and its correlation with the presence of
anaemia, elevated CA-125 levels, FIGO stage and presence and degree of ascites among malignant cases were
statistically analysed. The incidence of pre-operative thrombocytosis was noted more in malignant SEOTs 80%
(40/160). The mean pre-operative platelet count in the present study was 321X109 /L. It was more prevalent in serous
epithelial ovarian tumors (83.3%) and these findings were statistically significant (p=0.0001). There was a statistically
significant association of pre-operative thrombocytosis with the presence and degree of ascites and advanced FIGO
staging (p=0.0001). Pre-operative thrombocytosis is a frequent finding in malignant SEOTs and is associated with other
prognostic markers. This implies that thrombocytosis is probably a marker of tumor aggressiveness, and that platelet
may have a role in cancer growth and progression. Thus, presence of pre-operative thrombocytosis has significance as a
poor prognosticator in epithelial ovarian tumors.
Key-words- Thrombocytosis, Surface Epithelial Ovarian Tumors (SEOT), CA 125, FIGO staging
The KRAS-Variant and miRNA Expression in RTOG Endometrial Cancer Clinical Tri...UCLA
The KRAS-variant may be a genetic marker of risk for type 2 endometrial cancers. In addition, tumor miRNA expression appears to be associated with patient age, lymphovascular invasion and the KRAS-variant, supporting the hypothesis that altered tumor biology can be measured by miRNA expression, and that the KRAS-variant likely impacts endometrial tumor biology.
Awareness about Intestinal Cancer in University Student_Crimson PublishersCrimsonpublishersCancer
Cancer is a disease which is caused by the uncontrolled growth of cells. The cancer stem cells suggest that the clones are obtained by the sub population of cells showing diverse cancer cells phenotypically. First possible cancer stem cells are seen in leukemia, brain tumors and breast cancer. The gastrointestinal cancer becoming the major causes of deaths in the world. A questionnaire was developed and it is distributed among the students of class to determine the ideas and awareness of this disease. Questionnaires contain 15 different types of question regarding the disease. 39 students taken from the Bahauddin Zakariya University Multan, Pakistan. All the students are post graduated and the results show that all of them have awareness from this disease.
Adjuvant therapy protocols for liver cancer in patients undergoing liver tran...hr77
Many patients undergo liver transplantation for a liver cancer in a setting of liver cirrhosis. When is it possible to consider chemotherapy in such patients? Is it even possible? Is there a role?
Characteristics of cases with unknown stage prostate cancerCancer Council NSW
Stage of cancer at diagnosis (e.g. localised, regional involvement, metastatic) is an important predictor of survival. This paper identifies there is cause for concern surrounding the 40% of "unknown" or unrecorded stage of diagnosis on prostate cancer patient records in NSW. This means crucial information is missing from their records. The second stage of this project, scheduled for completion in late 2014, is to identify the reasons for these missing data. Once this has been completed we can inform policy makers to ensure the data completeness can be improved. Studies using cancer staging data can then increase in quality and quantity.
Introduction to Cancer Epidemiology and CarcinogenesisPUBH 6.docxbagotjesusa
Introduction to Cancer Epidemiology and Carcinogenesis
PUBH 6550/8550
Chronic Disease Epidemiology
1
Cancer is a term describing malignant diseases. Cancer should not be thought of as a single disease but rather a group of diseases which may have many characteristics in common but not necessarily the same causative agents, etiology or molecular profiles. In general, cancer defines diseases that have the capacity to invade surrounding normal tissue, metastasize (spread to distant sites) and kill the host in which it originates.
Objectives
What is the definition of cancer?
Benign vs. Malignant
Most common cancer types in men and women
Learn how to obtain cancer-related data using Internet sources
Understand cancer staging
Understand the basics of how carcinogenesis occurs
Describe inherited cancer syndromes
2
Causation and Cancer
Examples of Identified Causes and
Future Efforts in Cancer Prevention
Tobacco use and lung cancer
Infectious agents (e.g., HPV) and cervical cancer
Ionizing radiation and leukemia
Designation of a risk factor as “causal” has been the starting point for initiating cancer prevention programs based on reducing exposure to the risk factor
4
4
The concept of causation has long had a central role in the application of epidemiologic evidence for controlling cancer. Designation of a risk factor as “causal” has been the starting point for initiating cancer prevention programs based on reducing exposure to the risk factor. Though the concept of causation remains a matter of continuing discussion, use of the term in public health implies that the evidence supporting causality of association has reached a critical threshold of certainty and that reduced exposure can be expected to be followed by reduced disease occurrence. In other words, if there is “enough” evidence supporting a particular risk factor (or a preventive or prognostic factor), it seems to be considered ‘causal’. Keep in mind, though, that risk factor is the most proper term.
What is cancer?
Cancer is a group of diseases characterized by uncontrolled growth and spread of abnormal cells. If the spread is not controlled, it can result in death.
Characteristics: Abnormality, Uncontrollability, invasiveness
5
5
According to the American Cancer Society (ACS), cancer is a group of diseases characterized by uncontrolled growth and spread of abnormal cells. If the spread is not controlled, it can result in death. Although cancer is often referred to as a single condition, it actually consists of more than 100 different diseases. These diseases are characterized by uncontrolled growth and spread of abnormal cells. Cancer can arise in many sites and behave differently depending on its organ of origin. Breast cancer, for example, has different characteristics than lung cancer. It is important to understand that cancer originating in one body organ takes its characteristics with it even if it spreads to another part of the body. For example, metastatic br.
Running head YOU ARE WHAT YOU EAT1YOU ARE WHAT YOU EAT2.docxtoltonkendal
Running head: YOU ARE WHAT YOU EAT 1
YOU ARE WHAT YOU EAT 2
You Are What You Eat
Awesome Doctor
West Coast University
Abstract
Scientist have found evidence that life with cancer can be extended and certain cancers can be prevented by changing dietary habits. People who are influenced by western society and maintain a western diet are in great danger if nothing is done to limit the intake of meat and consumption of process meats. New dietary guidelines are released every 5 years by the U.S. Department of Agriculture and the department of Health and Human Services. Both organizations are responsible for reviewing clinical evidence and reports from research, and creating new dietary guidelines for consumers to follow. Critics of the new guidelines argue that the USDA has censored the recommendations to eat less red meat in such a way that only the food corporations funding the research receive benefits. Cancer is caused by multiple factors but mainly from exposure to carcinogens and mutations in DNA. Carcinogens either promote cancer growth or initiate cancer growth. Certain risk factors have been associated with the development of cancers. Air pollution, tobacco use, excessive alcohol consumption, occupational hazards, exposure to radiation, and certain aspects of diet are all risk factors liked to be carcinogenic. The carcinogenic links in diet have been attracting a lot of attention in the scientific community. Scientist working with the national cancer institute, under the national institute of health, have been working together to verify the relationship between consuming meat and processed foods, and the development or progression of cancer. The national cancer institute’s division of cancer prevention, conducted a two-year study that divided 200 people into 2 groups that were diagnosed with colorectal cancer within 3 to 6 months of the study. The control group maintained their normal diet that included eating meat and processed foods while the experimental group eliminated meat and processed foods and maintained a strict vegetarian diet for the life of the experiment. The experiments objective was to test the correlation between meat consumption and the effects of colorectal cancer. The funding assisted with the research needed to find subjects for the study and to transport them to and from facilities rented out to perform colonoscopy or CT scan procedures. Graphs were made to measure the rates of reoccurrence or metastasis. 72 of the 200 participants died during the 24-month long experiment. The participants from the control group suffered a loss of 42%, while the experimental group only lost 30% of its participants before the trial was over. Those who maintained a vegetarian diet displayed an additional 25% chance of not developing metastasis and 26% decrease in polyp reoccurrence. Participants in the study who maintained a vegetarian diet developed end stage cancer or metastasis at slower rates. The informatio ...
3 hours agoTiffany Jones WEEK 1 Main PostCOLLAPSETop of .docxrhetttrevannion
3 hours ago
Tiffany Jones
WEEK 1 Main Post
COLLAPSE
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Week 1 Main Post
I chose to focus this post on colon cancer with the factor, genetics. Genetics plays a larger role in cancer diagnoses than a lot of people are aware of. Some genetics testing and syndromes are still not even well known to a lot of practitioners, but hopefully, with more research and education this will become something that is used when testing for certain types of cancers or for being proactive to help prevent it.
The patient scenario I chose is a personal one. My Aunt was diagnosed with colon and gastric cancer. When another of my paternal aunts was diagnosed with colon cancer their oncologist realized that there could be a genetic factor in play. After doing some genetic testing, it was discovered that my aunts had Lynch Syndrome. “Lynch syndrome is an inherited condition that increases your risk of colon cancer, endometrial cancer, and several other cancers. Lynch syndrome has historically been known as hereditary nonpolyposis colorectal cancer (HNPCC)” (Mayo Clinic, 2018). People with Lynch syndrome typically have a higher chance of getting colon, gastric, and endometrial cancers, along with several others. Lynch syndrome also causes people to get cancer at much younger ages than someone without it; For instance, colon cancer before the age of 50. If a family has a history of Lynch syndrome there is a 50/50 chance that their children and grandchildren will have it also.
Colon cancer will typically start as small polyps that are not benign (cancerous), but then become cancerous over time. “It is a multifactorial disease process, with etiology encompassing genetic factors, environmental exposures (including diet), and inflammatory conditions of the digestive tract” (Dragovich, T. 2019). There are many signs and symptoms of colon cancer so it can be difficult to diagnose sometimes, especially since most signs and symptoms do not present early on in the disease process. This is why it is so important to get yearly colonoscopies, especially in people who have Lynch Syndrome. Some of the signs and symptoms patients can experience include changes in bowel habits, blood in the stool, abdominal pain that is persistent, not feeling like your bowels are emptying enough when you go, unexplained weight loss, and weakness or fatigue with no known cause (Mayo Clinic, 2019).
A large percentage of colorectal cancer develops from preexisting adenomas. However, this does not mean that every adenoma will become malignant. “The earliest phases of colorectal tumourigenesis initiate in the normal mucosa, with a generalized disorder of cell replication, and with the appearance of clusters of enlarged crypts (aberrant crypts) showing proliferative, biochemical and biomolecular abnormalities” (Leon, P., Gregorio, D., 2001). MicroRNA are small, single-stranded RNA that are noncoding and that can interfere with translation within a cell or cause degradation of the target miRNA. (Y.
An Adrenal Mass in a Patient with Lynch Syndromedaranisaha
Adrenocortical cancer (ACC) is a rare malignancy (estimated annual incidence 0.7 to 2.0 cases per million individuals worldwide) with a poor prognosis. In contrast, Lynch Syndrome (LS) is a much more commonly encountered hereditary syndrome that predisposes individuals to colon cancer and multiple other malignancies...
An Adrenal Mass in a Patient with Lynch SyndromeJohnJulie1
Adrenocortical cancer (ACC) is a rare malignancy (estimated annual incidence 0.7 to 2.0 cases per million individuals worldwide) with a poor prognosis. In contrast, Lynch Syndrome (LS) is a much more commonly encountered hereditary syndrome that predisposes individuals to colon cancer and multiple other malignancies...
An Adrenal Mass in a Patient with Lynch SyndromeAnonIshanvi
Adrenocortical cancer (ACC) is a rare malignancy (estimated annual incidence 0.7 to 2.0 cases per million individuals worldwide) with a poor prognosis. In contrast, Lynch Syndrome (LS) is a much more commonly encountered hereditary syndrome that predisposes individuals to colon cancer and multiple other malignancies...
An Adrenal Mass in a Patient with Lynch SyndromeNainaAnon
Adrenocortical cancer (ACC) is a rare malignancy (estimated annual incidence 0.7 to 2.0 cases per million individuals worldwide) with a poor prognosis. In contrast, Lynch Syndrome (LS) is a much more commonly encountered hereditary syndrome that predisposes individuals to colon cancer and multiple other malignancies...
An Adrenal Mass in a Patient with Lynch Syndromesemualkaira
Adrenocortical cancer (ACC) is a rare malignancy (estimated annual incidence 0.7 to 2.0 cases per million individuals worldwide) with a poor prognosis. In contrast, Lynch Syndrome (LS) is a much more commonly encountered hereditary syndrome that predisposes individuals to colon cancer and multiple other malignancies
An Adrenal Mass in a Patient with Lynch SyndromeEditorSara
Adrenocortical cancer (ACC) is a rare malignancy (estimated annual incidence 0.7 to 2.0 cases per million individuals worldwide) with a poor prognosis. In contrast, Lynch Syndrome (LS) is a much more commonly encountered hereditary syndrome that predisposes individuals to colon cancer and multiple other malignancies.
Lynch syndrome (LS) describes a subset of patients with germline mutations in DNA mismatch repair (MMR) genes (most
commonly MLH1, MSH2, MSH6, and PMS2) that account for
2-4% of all colorectal cancers [1, 2] with varying phenotypes
de-pending on specific mutation. Patients with LS have an
estimated lifetime risk of 80% for developing colorectal cancer
and an in-creased risk for other extracolonic malignancies,
including endo-metrial, gastric, ovarian, pancreas, ureter and
renal pelvis, biliary tract, brain, and small intestinal cancers.2
Recently adrenocor-tical cancer (ACC), a rare and aggressive
malignancy, has been associated with LS [3-7], although the
low prevalence of ACC makes it difficult to attribute causality.
Adrenocortical cancer (ACC) is a rare malignancy (estimated annual incidence 0.7 to 2.0 cases per million individuals worldwide) with a poor prognosis. In contrast, Lynch Syndrome (LS) is a much more commonly encountered hereditary syndrome that predisposes individuals to colon cancer and multiple other malignancies..
An Adrenal Mass in a Patient with Lynch Syndromesemualkaira
Adrenocortical cancer (ACC) is a rare malignancy (estimated annual incidence 0.7 to 2.0 cases per million individuals worldwide) with a poor prognosis. In contrast, Lynch Syndrome (LS) is a much more commonly encountered hereditary syndrome that predisposes individuals to colon cancer and multiple other malignancies..
I have no doubt that the period we are living through will be looked at as the single biggest inflection point of our lifetimes. Every community will make an explicit decision to move forward or move further backwards.
2016: Do any of you remember what happened on March 9, 2016? Bernie/Trump; populism; economic depression; Draw on “Gone to War for Less” chapter (78% living paycheck to paycheck with most being functionally uninsured; opioid crisis; undisputed world leader’s in bankruptcy - 70% had so-called insurance). The fact is we’re already investing more than enough money to not only fund a world class hc system but fund what drives 80% of health outcomes -- what are broadly referred to as the SDoH. Today, there is a $1 trillion “tax” on the American Dream that isn’t a law...it’s a choice to accept wasted spending in hc. That “tax” would be the 15th largest economy in the world. Healthcare isn’t expensive. After all, clinicians only receive $0.27 of every $1 ostensibly spent on hc. What’s expensive is administrative bloat, price-gouging, fraud and profiteering. The result is what I’d call “hellth.”
2031: Let’s fast forward imagine a future together every community whether it’s an employer community or place-based community can focus on building what I call “wellth” that focuses on the totality of well-being. Things like a good, well-paying job, educational opportunities independent of your family history and the ability to live in a nice home in a safe neighborhood are central and are actually what drives 80% of health outcomes. The great news is you don’t have to imagine this future. You can see it with your own eyes from Florida to Alaska.
You would be hard-pressed to find more challenging pre-existing community conditions when a small group of forward-looking community members became true stewards of their community. Most didn’t have an official capacity or specific training. Rather, they simply had will...a will that is based in love for their community and can endure the inevitable challenges any time one tackles a meaningful problem.
Collection of graphics from the havoc that status quo healthcare has wreaked on the American Dream. Impacts of price gouging and profiteering. Includes comparison between U.S. hospital prices vs international prices.
Updated collection with more slides at https://www.slideshare.net/dchase/health-care-status-quo-results-gallery-234289014
Collection of graphics from the havoc that status quo healthcare has wreaked on the American Dream. Impacts of price gouging and profiteering.
HR Digest interview on opioids in the workplaceDave Chase
How employers can effectively prevent addiction by going upstream with proper primary care and ensuring employees only go to high quality healthcare providers.
The follow-on edition to the CEO's Guide to Restoring the American Dream. Picks up where CEO's Guide left off (on Opioid Crisis). Book designed for civic leaders (mayors, school board members, union leaders, faith & social service leaders, police/fire chiefs & civic-minded business people). For more, check out www.healthrosetta.org/wakeup-call.
Health Rosetta Case Study - City of Kirkland, WashingtonDave Chase
City of Kirkland, WA is a suburb of Seattle that was, like municipalities, struggling with healthcare costs and feared the coming Cadillac Tax. Their "moonshot" goal was to improve health benefits while eliminating healthcare cost inflation
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Integrating Ayurveda into Parkinson’s Management: A Holistic Approach
Overdiagnosis in cancer
1. jnci.oxfordjournals.org JNCI | Review 605
DOI: 10.1093/jnci/djq099 Published by Oxford University Press 2010.
Advance Access publication on April 22, 2010.
Early detection has forced clinicians and researchers to contem-
plate a more expansive and, to many, counterintuitive definition of
the word “cancer.” What most of us were taught in medical school
is captured by the terse definition contained in the medical
dictionary—“a neoplastic disease the natural course of which is
fatal” (1). It was a simple definition that was largely accurate in an
era when patients were diagnosed with cancer because they had
signs and symptoms of the disease.
But that all changed after we became technologically able to
advance the time of diagnosis and detect cancer early—before it
produces signs and symptoms. Now it has become evident that the
word “cancer” encompasses cellular abnormalities with widely
variable natural courses: Some grow extremely rapidly, others do
so more slowly, others stop growing completely, and some even
regress. Clinicians are left with the realization that the word
“cancer” is less a prediction about disease dynamics and more a
pathological description made at a single point in time. Continued
adherence to the dictionary definition of cancer, however, can lead
to harm—including overuse of anticancer therapies.
Although not yet contained in medical dictionaries, recently, a
new word has appeared in the medical literature to describe a side
effect of our technological progress: “overdiagnosis.” This article
is intended to summarize the phenomenon.
What Is Cancer Overdiagnosis?
Overdiagnosis is the term used when a condition is diagnosed that
would otherwise not go on to cause symptoms or death. Cancer
overdiagnosis may have of one of two explanations: 1) The cancer
never progresses (or, in fact, regresses) or 2) the cancer progresses
slowly enough that the patient dies of other causes before the cancer
becomes symptomatic. Note that this second explanation incorpo-
Review
Overdiagnosis in Cancer
H. Gilbert Welch, William C. Black
Manuscript received September 3, 2009; revised March 1, 2010; accepted March 5, 2010.
Correspondence to: H. Gilbert Welch, MD, MPH, Veterans Affairs Outcomes Group (111B), Department of Veterans Affairs Medical Center, White River
Junction, VT 05009 (e-mail: h.gilbert.welch@dartmouth.edu).
This article summarizes the phenomenon of cancer overdiagnosis—the diagnosis of a “cancer” that would otherwise not go on
to cause symptoms or death. We describe the two prerequisites for cancer overdiagnosis to occur: the existence of a silent
disease reservoir and activities leading to its detection (particularly cancer screening). We estimated the magnitude of overdiag-
nosis from randomized trials: about 25% of mammographically detected breast cancers, 50% of chest x-ray and/or sputum-detected
lung cancers, and 60% of prostate-specific antigen–detected prostate cancers. We also review data from observational studies
and population-based cancer statistics suggesting overdiagnosis in computed tomography–detected lung cancer, neuroblas-
toma, thyroid cancer, melanoma, and kidney cancer. To address the problem, patients must be adequately informed of the
nature and the magnitude of the trade-off involved with early cancer detection. Equally important, researchers need to work to
develop better estimates of the magnitude of overdiagnosis and develop clinical strategies to help minimize it.
J Natl Cancer Inst 2010;102:605–613
rates the interaction of three variables: the cancer size at detection,
its growth rate, and the patient’s competing risks for mortality.
Thus, even a rapidly growing cancer may still represent overdiag-
nosis if detected when it is very small or in a patient with limited life
expectancy. Overdiagnosis should not be confused with false-positive
results, that is, a positive test in an individual who is subsequently
recognized not to have cancer. By contrast, an overdiagnosed
patient has a tumor that fulfills the pathological criteria for cancer.
To understand overdiagnosis, one must first understand the
heterogeneity of cancer progression, which can be diagrammed
using arrows to represent different rates of cancer progression
(Figure 1). The arrow labeled “fast” represents a fast-growing can-
cer, which is defined as one that quickly leads to symptoms and to
death. The arrow labeled “slow” represents a slow-growing cancer,
which is defined as one that leads to symptoms and death but only
after many years. The arrow labeled “very slow” represents a
cancer that never causes problems because the patient will die of
some other cause before the cancer is large enough to produce
symptoms. The most familiar clinical example is likely a small low-
grade prostate cancer in an elderly male. The arrow labeled “nonpro-
gressive”representscellularabnormalitiesthatmeetthepathological
definition of cancer but never grow to cause symptoms—
alternatively, they may grow and then regress. Although the concept
of nonprogressive cancers may seem implausible, basic scientists have
begun to uncover biological mechanisms that halt the progression of
cancer (2–4). Some cancers outgrow their blood supply (and are
starved), others may be recognized by the host’s immune system or
other defense mechanisms (and are successfully contained), and some
are simply not that aggressive in the first place.
Overdiagnosis occurs when either nonprogressive cancers or
very slow–growing cancers (more precisely, at a slow enough pace
that individuals die from something else before the cancer ever
2. 606 Review | JNCI Vol. 102, Issue 9 | May 5, 2010
causes symptoms) are detected. These two forms of cancer
have been collectively referred to as pseudodisease—literally
false disease. Although we will not use the term subsequently,
another definition of overdiagnosis is simply the detection of
pseudodisease.
The conundrum in overdiagnosis is that clinicians can never
know who is overdiagnosed at the time of cancer diagnosis.
Instead, overdiagnosis can only be identified in an individual if
that individual 1) is never treated and 2) goes on to die from
some other cause. Because clinicians do not know which patients
have been overdiagnosed at the time of diagnosis, we tend to
treat all of them. Thus, overdiagnosis contributes to the problem
of escalating health-care costs. But even where there no money
involved, overdiagnosis would be a major concern: Although
such patients cannot benefit from unnecessary treatment, they
can be harmed.
Prerequisites for Overdiagnosis
The Existence of a Disease Reservoir
The first prerequisite for overdiagnosis is the existence a substan-
tial number of subclinical cancers—in other words, a disease reser-
voir of detectable cancer. Inferences about the size of this disease
reservoir come from the methodical inspection of tissues at au-
topsy in a series of individuals who died from causes other than
cancer. This reservoir is most easily investigated in prostate and
thyroid cancers because the glands are small enough to allow an
exhaustive examination of thin sections of the entire organ. In ad-
dition, there have been multiple investigations of the reservoir in
breast cancer.
Let us consider the data of two investigators who made age-
specific estimates of the reservoir of prostate cancer from autopsies
(Figure 2). Sakr et al. (5) examined the prostate glands of 525
American men who died in an accident; Stamatiou et al. (6) exam-
ined 212 Greek men who died of other causes and were not found
to have palpable prostate cancer. Because additional estimates
based on specimens obtained by radical cystectomy are similarly
variable (7), it is clear that the reservoir of potentially detectable
prostate cancer is highly age dependent and is probably in the
range of 30%–70% in men older than 60 years.
Harach et al. (8) systematically examined the thyroid gland in
101 autopsies. They examined slices of thyroid tissue taken every
2.5 mm and found at least one papillary carcinoma in 36% of
Finnish adults. Because many of the cancers were smaller than the
width of the slices, they reasoned that they were missing some.
Given the number of small cancers they did find and the number
that they estimated they had missed (which was a function of size),
Harach et al. concluded that the prevalence of histologically veri-
fiable papillary carcinoma would be close to, if not equal to, 100%
if one could look at thin enough slices of the gland.
Seven autopsy series have been directed at determining the
disease reservoir of breast cancer (9). The four series that included
age-specific data suggested that the proportion of middle-aged
women who harbored undetected breast cancer ranged from 7% to
39%. Two explanations for this variability are possible that are
germane to pathological estimates of the disease reservoir for any
cancer. First, different series involve different pathologists, who
may have different thresholds about whether to label a small ab-
normality as “cancer.” Second, different studies have different
degrees of scrutiny, that is, some investigators did not look as hard
as others. Among the seven series, for example, at one extreme, the
investigators examined fewer than 10 slices per breast and at the
other extreme, the investigators examined more than 200.
We have summarized the above data in the context of the life-
time risk of death or metastatic disease (Table 1). The lifetime risk
of death or metastatic disease is perhaps the least ambiguous
measure of the true disease burden for each cancer. The extent to
which the disease reservoir exceeds this lifetime risk provides a
crude estimate of the amount of overdiagnosis possible.
Activities Leading to Detection of the Disease Reservoir
But the existence of a disease reservoir of detectable cancer, by
itself, will not lead to overdiagnosis. There must also be actions
that tap it. Thus, the second prerequisite for overdiagnosis is activ-
ities leading to early cancer detection.
By far, the most obvious of these is cancer screening. The most
familiar efforts involve cancer screening programs organized
around a single test, such as mammography or prostate-specific
antigen (PSA) testing. But cancer screening should be conceived
Figure 2. Prostate cancer reservoir in men dying from causes other than
prostate cancer (and who were not known to have prostate cancer
during life).
Figure 1. Heterogeneity of cancer progression. The arrow labeled “fast”
represents a fast-growing cancer, one that quickly leads to symptoms
and to death. The arrow labeled “slow” represents a slow-growing cancer,
one that leads to symptoms and death but only after many years. The
arrow labeled “very slow” represents a cancer that never causes prob-
lems because the patient will die of some other cause before the cancer
is large enough to produce symptoms. The arrow labeled “nonprogres-
sive” represents cellular abnormalities that meet the pathological defi-
nition of cancer but never grow to cause symptoms—Alternatively, they
may grow and then regress (dotted line). (Figure 1 was previously sup-
plied by the authors to Wikipedia.)
3. jnci.oxfordjournals.org JNCI | Review 607
more broadly as any effort to detect cancer in those who have no
symptoms of the disease. Thus, components of general periodic
physical examination, such as searching for moles by closely
inspecting the skin or seeking masses by palpating the neck, are
also a form of screening.
Furthermore, interventions unrelated to screening can lead to
early cancer detection. Pathological inspection of tissues removed
in surgeries performed for reasons other than cancer may nonethe-
less find cancer. The most familiar example is prostate cancer de-
tection following transurethral resection of the prostate for benign
prostatic hyperplasia (11). However, the most important activity
leading to unintended cancer detection undoubtedly involves the
increased use of diagnostic imaging. Detailed imaging of the brain,
thorax, abdomen, and pelvis intended to evaluate symptoms not
suggestive of cancer nonetheless frequently detect abnormalities
worrisome for cancer. Clinicians are familiar with this phenom-
enon, which is sometimes referred to as the detection of “inciden-
talomas.” For example, screening for colon cancer with computed
tomography (CT) colonography detects extracolonic abnormal-
ities in up to 50% of examinations (12).
The growth of early cancer detection activities is easiest to
measure in organized cancer screening efforts, many of which did
not exist two decades ago. Some of the growth is not simply in
terms of the number of examinations but also in terms of the in-
creasing sensitivity of the examination itself. It is very difficult to
gauge the increase in screening physical examinations because
these are not systematically recorded. However, increased use of
diagnostic imaging in general is well documented, particularly in
the Medicare program (Figure 3) (13).
Evidence That Early Detection Has Led to
Overdiagnosis
Randomized Trials of Screening
The strongest evidence for overdiagnosis comes from long-term
follow-up after a randomized trial of screening. At the end of the
trial, it is expected that the screening group will have a greater
number of cancers detected than the control group, simply because
screening advances the time of diagnosis and moves the detection
of some cancers forward in time. If all of the excess of detected
disease represents cancers that were destined to progress to clinical
disease (ie, there is no overdiagnosis), the excess should disappear
over time when both groups receive similar diagnostic scrutiny. In
other words, the control group would be expected to “catch-up” to
the screening group—because cancers appear clinically because of
signs and symptoms. Although the duration of follow-up necessary
to completely catch-up is equal to the lead time of the slowest
growing cancer, a shorter interval may be sufficient to confirm
overdiagnosis given the existence of competing mortality. A persis-
tent excess in the screening group years after the trial is completed
constitutes the best evidence that overdiagnosis has occurred.
Breast Cancer. Of the nine randomized trials of mammography,
only one has reported long-term follow-up data on incident
Table 1. Estimated size of the disease reservoir for three cancers, the lifetime risk of death or metastatic disease, and the probability of
overdiagnosis where the entire disease reservoir detected
Cancer Population
% With cancer
(disease reservoir) (a)
Lifetime risk of death or
metastatic disease* (b), %
Probability of overdiagnosis where entire
disease reservoir detected† (c = [a 2 b]/a), %
Prostate Men older than 60 y 30–70 4 87–94
Thyroid Adults aged 50–70 y 36–100 0.1 99.7–99.9
Breast Women aged 40–70 y 7–39 4 43–90
* The lifetime risk of death or metastatic disease was estimated by multiplying the lifetime risk of death reported by the Surveillance, Epidemiology, and End
Results program (10) by 1.33, which more than accounts for the small proportion of patients diagnosed with metastatic disease who die from other causes
(approximately 20%, 15%, and 10% of those with metastatic cancer of the prostate, thyroid, and breast cancer, respectively).
† This estimate is a lower-bound estimate because lethal and/or metastatic cancers do not always arise from prevalent cancers (those contained in the disease
reservoir) but also from incident cancers (those not contained in the disease reservoir).
Figure 3. Trends in the number of various scans
used in the Medicare population in the United
States, 1991–2006. CT = computerized tomography;
MRI = magnetic resonance imaging.
4. 608 Review | JNCI Vol. 102, Issue 9 | May 5, 2010
cancers. The report on 15 years of extended follow-up after the
end of Malmö mammographic screening trial provided evidence
for breast cancer overdiagnosis (14). At the end of the 10-year trial,
741 breast cancers were detected in the screening group as com-
pared with 591 in the control group. Over the subsequent 15 years,
this difference of 150 cancers narrowed to 115, suggesting 35
catch-up cancers. The persistent excess of 115 cancers, however,
suggests overdiagnosis.
The findings at the end of the trial, with the 35 catch-up can-
cers added, highlight a complexity in the estimation of overdiagno-
sis (Figure 4). One could say that 16% (115 in 741) of cancers
detected in the screening group were overdiagnosis. Alternatively,
one could restrict the denominator to screen-detected cancers
because overdiagnosis can only occur in this subset (a clinically
detected symptomatic cancer does not represent overdiagnosis).
An earlier publication from the trial showed that 64.4% of cancers
detected in the screened group were a consequence of screening,
which suggested that about 477 were screen detected. Using this
denominator, the risk that a mammographically detected cancer
represents overdiagnosis is about 24% (115 in 477) (15).
Lung Cancer. Screening can result in overdiagnosis even among
cancers that are traditionally viewed as the most rapidly growing
and lethal. The Mayo trial of chest x-ray and sputum cytology
screening (16) provided strong evidence for lung cancer overdiag-
nosis. At the end of the 6-year screening phase, 143 lung cancers
were detected in the screening group as compared with 87 in the
control group. In follow-up over the subsequent 5 years, 10
catch-up cancers appeared. Extended follow-up over the next 16
years identified no further catch-up cancers (17). Thus, the persis-
tent excess of 46 cancers reflected overdiagnosis (Figure 5). The 46
extra cancers arose among the 90 screen-detected cases in the
screening group. Using this denominator, the risk that a chest
x-ray– and/or sputum cytology–detected cancer represents over-
diagnosis is about 51% (46 in 90).
Prostate Cancer. Although there has been no long-term fol-
low-up, the recently reported randomized trials of PSA screening
for prostate cancer also provide some insight into overdiagnosis.
The Prostate, Lung, Colorectal, and Ovarian Cancer (PLCO) trial
(18) suffered from substantial contamination (ie, screening in the
control group) and found no difference in prostate cancer mor-
tality, nonetheless there was a 22% increase in prostate cancer
detection in the screening group. It is not known whether this
excess will ultimately be diminished by the appearance of catch-up
cancers in the control group.
The European Randomized Study of Prostate Cancer (ERSPC)
trial (19) used a lower PSA threshold for biopsy (3 vs 4 ng/mL) and
a longer screening interval (every 4 years vs annually) and is
believed to have had less contamination than the PLCO trial. It
found that PSA screening was associated with a 20% reduction in
prostate cancer mortality. There was a 70% increase in prostate
cancer detection in the screening group—an extra 34 prostate
cancers per 1000 men screened. This excess arose from the 58
screen-detected prostate cancers per 1000 men. If this excess rep-
resents overdiagnosis, the risk that a PSA-detected cancer repre-
sents overdiagnosis would be about 60% (0.034 in 0.058). However,
it could be argued that there has been insufficient follow-up for
catch-up cancers to become evident and that, therefore, this risk
could be an overestimate.
A prior publication by the European group (20) suggested
that the risk of overdiagnosis is, in fact, about this magnitude.
The investigators estimated that 48% of all patients diagnosed
in the screened group (which included both PSA- and clinically
detected cancers) had been overdiagnosed (20). Application of
that estimate to 82 per 1000 men diagnosed in the screening
group during the trial would suggest that overdiagnosis had
occurred in about 39 per 1000 men. Using this estimate, the
risk that a PSA-detected cancer represents overdiagnosis is
about 67% (0.039 in 0.058).
Observational Studies
Observational studies can also provide good evidence for overdiag-
nosis. In one striking example, investigators in Japan reported,
after a first round of spiral CT screening (ie, prevalence screen),
finding almost 10 times as much lung cancer as they had previously
found in the same population using chest x-rays (21). At the com-
pletion of the 3-year screening program, lung cancer detection was
virtually the same in smokers as that in never-smokers (22), pro-
ducing a relative risk that approached 1:
Figure 4. Number of breast cancers detected after 10 years in the
Malmö randomized trial of mammography with the 35 additional
“catch-up” cancers that appeared in the control group in the subse-
quent 15 years. “Extra cancers” refer to the difference between the
mammography and control groups (after adding the catch-up cancers
to the control group). They likely represent overdiagnosed cancers (see
Supplementary Technical Appendix, available online).
Figure 5. Number of lung cancers detected after 6 years in the Mayo clinic
randomized trial of chest x-ray and sputum cytology screening with the
10 additional “catch-up” cancers that appeared in the control group in
the subsequent 5 years. “Extra cancers” refer to the difference between
the screening group and control group (after adding the catch-up cancers
to the control group). They likely represent overdiagnosed cancers (see
Supplementary Technical Appendix, available online).
5. jnci.oxfordjournals.org JNCI | Review 609
smokers
smokers
smokers
never smokersnever smokers
never smokers
Lung Cancers Detected
Number Screened
Relative Risk
Lung Cancers Detected
Number Screened
29
11.5/10002529 1.1
31 10.5/1000
2954
Because a wealth of epidemiological investigation has demon-
strated that the risk of smokers dying from lung cancer is at least
15 times higher than that of never-smokers (23), the Japanese data
(the only large-scale CT screening study to include a similar pro-
portion of smokers and nonsmokers) provide evidence that over-
diagnosis can be a substantial problem with spiral CT screening.
Japanese investigators have also studied screening for a rare
neuroendocrine cancer in children: neuroblastoma (24). Following
the initiation of a national screening program, the number of chil-
dren diagnosed with neuroblastoma more than doubled, and it
went up almost fivefold in the group being screened—children
younger than 1 year of age. Because some Japanese physicians were
concerned about this trend (25), a group of pediatric oncologists
decided to offer a “watchful waiting” strategy to the parents of
infants with small cancers that were not obviously doing damage
(26). Of the 17 couples offered the strategy, 11 accepted, and in
each infant, the cancer regressed. Thus, these 11 cancers repre-
sented overdiagnosis. Subsequent studies of large-scale screening
in Germany and Quebec found that screening detected about
twice as many cancers as expected (suggesting overdiagnosis) but
no change in neuroblastoma mortality (27,28).
Evidence That Overdiagnosis Is Happening
in Populations
Although it is extremely difficult to assess when overdiagnosis has
occurred in an individual, it is relatively easy to assess when over-
diagnosis has occurred in a population. Rapidly rising rates of
testing and disease diagnosis in the setting of stable death rates are
suggestive of overdiagnosis. Let us now consider two hypothetical
examples of rapid rises in the rate of diagnosis, one of which is
suggestive of overdiagnosis and the other is not (Figure 6).
In the left panel of Figure 6, the rapid rise in cancer diagnosis
is accompanied by a rapid rise in death from cancer. This pattern
suggests that the new diagnoses are life threatening and clinically
important. This is the pattern that has been reported in esophageal
adenocarcinoma (29).
In the right panel of Figure 6, the rapid rise in cancer diagnosis
is not accompanied by a rise in cancer death. This suggests that
there is more diagnosis, but no change in the underlying amount
of cancer destined to affect patients. It suggests overdiagnosis—the
detection of very slow or nonprogressive cancers.
An alternative explanation is that there is a true increase in
underlying amount of cancer destined to affect patients but that
improvements in diagnosis and treatment coincidentally (and pre-
cisely) counterbalance the increase in new cancers—to leave cancer
deaths unchanged. Although possible, this explanation is less
likely. Not only is it not the most parsimonious explanation (it
requires two assumptions instead of one) but also it requires that
the rate of diagnosis and/or treatment improvement exactly match
the increase in true disease burden (not too fast or mortality would
fall, not too slow or mortality would rise).
The most credible population-based evidence for overdiagnosis
comes from 30-year incidence and mortality data reported by
Surveillance, Epidemiology, and End Results. For five cancers, the
trends show increased rates of new diagnoses but not of deaths
(Figure 7). In each case, increased screening activity or increased
use of imaging tests capable of detecting incidentalomas is tempo-
rally associated with the increased rate of new diagnoses.
For thyroid cancer, the rate of diagnosis has more than doubled
(from 4.9 per 100 000 to 10.6 per 100 000). Yet the rate of thyroid
cancer death has been among the most stable of all cancers in the
United States. The increase in new diagnosis has been confined to
the histology with the most favorable prognosis (papillary thyroid
cancer) and almost entirely consists of tumors less than 2 cm in
diameter (30). The overdiagnosis of thyroid cancer likely reflects
some combination of the increasing tendency of physicians to pal-
pate the neck for masses (then refer for thyroid ultrasound) and
incidental detection on ultrasounds and CT scans ordered for
other reasons.
For melanoma, the rate of diagnosis has almost tripled (from
7.9 per 100 000 to 21.5 per 100 000). Again, the rate of death
is generally stable (little change in the past 15 years). Although
there may be an element of a true increase in clinically significant
melanoma, these data suggest that most of the increase in diagno-
sis reflects overdiagnosis. The issue of overdiagnosis is well known
to dermatologists (31–33). Because almost all the new diagnoses
are localized (or in situ) melanomas and because their appearance
Figure 6. Two distinct patterns of rapid rises in the
rate of diagnosis. A) Population data that suggest a
true increase in the amount of cancer; B) popula-
tion data that suggest overdiagnosis of cancer.
6. 610 Review | JNCI Vol. 102, Issue 9 | May 5, 2010
almost perfectly tracks the increase in population skin biopsy
rates, overdiagnosis is likely the predominant explanation for the
rise (34).
For cancers of the kidney and renal pelvis, rate of diagnosis has
almost doubled over the past 30 years (from 7.1 per 100 000 to 13.4
per 100 000). However, the rate of death has been stable, with little
change in the past 15 years. A recent investigation on the growth
rate of 53 solid renal tumors, in which each tumor had at least two
CT volumetric measurements 3 months apart before nephrec-
tomy, demonstrated their variable natural history and the potential
for overdiagnosis (35). Twenty-one (40%) had a volumetric dou-
bling time of more than 2 years and seven (14%) regressed.
Furthermore, slow-growing tumors were more common in the
elderly. Thus, it is likely that a substantial proportion of renal
tumors represent overdiagnosis either because they do not grow at
all or because their growth is too slow for the tumor to cause
symptoms before the patient dies of other causes. Because there
has been no systematic screening for these renal cancers, the
increased rate of diagnosis is most likely because of incidental
detection by the increasing use of abdominal ultrasound and CT.
Rising rates of diagnosis have occurred for both prostate and
breast cancers. In both types of cancer, however, the story is more
complex because the death rates for each are falling. In the past
15 years, prostate cancer mortality has fallen by about a third
(from 38.6 per 100 000 to 24.6 per 100 000) and breast cancer
mortality by about a quarter (from 33.1 per 100 000 to 24.0 per
Figure 7. Rate of new diagnoses and death in five cancers in the Surveillance, Epidemiology, and End Results data from 1975 to 2005. A) Thyroid
cancer. B) Melanoma. C) Kidney cancer. D) Prostate cancer. E) Breast cancer.
7. jnci.oxfordjournals.org JNCI | Review 611
100 000). This decrease reflects the combined effect of screening
and improved therapy—and possibly, in the case of breast cancer,
declining hormone replacement therapy use and women with
new breast lumps presenting earlier for diagnostic mammog-
raphy. But in both diseases, the combination of the data from
randomized trials and from the population leaves little doubt that
overdiagnosis is occurring. Thus, in these two diseases, we are left
with the possibility that overdiagnosis because of early detection
coexists with a mortality benefit from early detection. By con-
trast, in the case of the first three panels in Figure 7, it is difficult
to identify a new and highly effective treatment capable of coun-
terbalancing any true increase in incidence, resulting in unchanged
mortality rates.
It is important to highlight those cancers for which there has
been widespread screening yet little evidence that overdiagnosis is
occurring in the population. There is little evidence of overdiag-
nosis of either cervical or colorectal cancer because the rate of
diagnosis of both is falling (see Supplementary Technical Appendix,
available online). If overdiagnosis is occurring as a consequence of
screening for these two cancers, it is less cancer overdiagnosis and
more overdiagnosis of the precursor lesions, for example, cervical
dysplasia or adenomatous polyps.
Addressing the Problem
Overdiagnosis—along with the subsequent unneeded treatment
with its attendant risks—is arguably the most important harm as-
sociated with early cancer detection. The impact of false-positive
test results is largely transitory, but the impact of overdiagnosis can
be life-long and affects patients’ sense of well-being, their ability to
get health insurance, their physical health, and even their life
expectancy.
For clinicians and patients, overdiagnosis adds complexity to
informed decision making: Whereas early detection may well help
some, it undoubtedly hurts others. In general, there is no right
answer for the resulting trade-off—between the potential to avert
a cancer death and the risk of overdiagnosis. Instead, the particular
situation and personal choice have to be considered. Often, the
decision about whether or not to pursue early cancer detection
involves a delicate balance between benefits and harms—different
individuals, even in the same situation, might reasonably make
different choices.
To address overdiagnosis, it is important to ensure that
patients are adequately informed of the nature and the magni-
tude of the trade-off involved with early detection. This kind of
discussion has been widely advocated as part of PSA screening
but is nevertheless challenging for patients. They must first
clearly understand the nature of the trade-off that although
early diagnosis may offer the opportunity to reduce the risk of
cancer death, it also can lead one to be diagnosed and treated for
a “cancer” that is not destined to cause problems. Then, they
must understand the magnitude of the trade-off. Each idea will
be foreign and difficult, so they must be presented very clearly.
We believe that this is best done through the construction of
simple one-page balance sheets that frame the trade-off. We
have provided one such example for screening mammography
(Table 2).
The exercise of drafting a balance sheet highlights another
important response: researchers need to work to develop reliable
estimates of the magnitude of overdiagnosis. Consider the mam-
mography example. In Malmo, there were 62 fewer breast cancer
deaths and 115 women overdiagnosed (14)—a ratio of one breast
cancer death avoided to two women overdiagnosed; yet others
have argued that the ratio is 1 to 10 (37).
Admittedly, quantifying overdiagnosis is challenging. There
are relatively few randomized trials of screening to start with, and
even fewer will provide the needed long-term follow-up data.
Nevertheless, even “best guess” estimates about the magnitude of
overdiagnosis may play an important role in decision making.
This effort will undoubtedly require modeling the natural history
of the cancer, the impact of early diagnosis, and competing mor-
tality. Although complex models may offer the highest degree of
precision, their complexity can make it difficult for outsiders to
review (or, in fact, even know) their structure and assumptions.
Thus, we believe that there is an important place for more
simple and transparent models in which all the assumptions, input
values, and calculations are explicit and can be contained in a
single spreadsheet.
A third response is to better understand patients’ values re-
garding overdiagnosis. But researchers cannot understand patient
values before patients understand the trade-off. Thus, efforts to
determine preferences will need to be preceded by efforts to edu-
cate patients. Learning how sensitive patient preferences are to
overdiagnosis (eg, whether changing the trade-off from 1:2 to
1:10 influences the decision to have mammography) will help
inform us about how precise the estimates of overdiagnosis need
to be.
A fourth response is to develop clinical strategies to help miti-
gate overdiagnosis. Overdiagnosis creates a powerful cycle of pos-
itive feedback for more overdiagnosis because an ever increasing
proportion of the population knows someone—a friend, a family
member, an acquaintance, or a celebrity—who “owes their life” to
early cancer detection. Some have labeled this the popularity par-
adox of screening: The more overdiagnosis screening causes, the
more people who feel they owe it their life and the more popular
screening becomes (38). The problem is compounded by messages
(in the media and elsewhere) about the dramatic improvements in
survival statistics, which may not reflect reduced mortality, but
instead be an artifact of overdiagnosis—diagnosing a lot of men
Table 2. Draft balance sheet for screening mammography in
50-year-old women*
Benefits Harms
One woman will avoid a
breast cancer death (36)
Between two and 10 women will be
overdiagnosed and treated needlessly
Between five and 15 women will be
told that they have breast cancer
earlier than they would otherwise
yet have no effect on their prognosis
Between 200 and 500 women will
have at least one “false alarm”
(50–200 will be biopsied)
* Among one thousand 50-year-old women undergoing annual mammography
for 10 years. See Supplementary Technical Appendix (available online).
8. 612 Review | JNCI Vol. 102, Issue 9 | May 5, 2010
and women with cancer who were not destined to die from the
disease (39).
It is possible that new insights from genomics will ultimately
allow us to more accurately predict tumor behavior at the indi-
vidual level. However, the field has not advanced to that point
yet. We must explore other clinical strategies. One potential
strategy to mitigate overdiagnosis is to raise the threshold to
label a test as “abnormal” or the threshold to intervene. The
diagnostic thresholds for common screening tests typically had
their origins in arbitrary decisions (eg, PSA > 4 ng/mL). And
the tendency over time has been for these thresholds to fall—-
either because we can see more (eg, microcalcifications on
a mammogram) or because we learn that individuals below
the threshold can still have cancer (leading some to argue for
biopsies for PSA > 2.5 ng/mL).
The problem of overdiagnosis provides the motivation to inves-
tigate the other direction—testing higher diagnostic thresholds for
labeling a screening test abnormal. One threshold to test is that of
size—It may be better to simply ignore small abnormalities. This
approach already has precedent in the use of size criteria to manage
small pulmonary nodules (40) and adrenal lesions (41,42) inciden-
tally detected on CT. There is an analogous threshold to test in
laboratory values (such as a PSA)—that of magnitude—where it
may be better to ignore what are now considered small
elevations.
But most important may be to add an additional threshold that
must be observed before labeling a screening test abnormal—that
of growth. In spiral CT screening for lung cancer, demonstrating
the growth of small lesions is now accepted as a prerequisite for
biopsy—even among ardent screening proponents (43). Testing
the effect of higher thresholds in randomized trials would offer the
opportunity reduce not only overdiagnosis but also false-positive
results.
Finally, there is much work to be done to incorporate the con-
cept of overdiagnosis into the medical curriculum. Enthusiasm for
new screening tests in the medical community is often based upon
preliminary studies with inadequate study designs. Consequently,
medical school curricula should incorporate formal coursework on
how to evaluate screening tests and how to recognize
overdiagnosis.
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Funding
Department of Veterans Affairs Medical Center (H.G.W.).
Notes
The opinions in this manuscript are those of the authors and should not be
interpreted as official positions of the Department of Veterans Affairs, the
Department of Health and Human Services, or the US Government. The
authors take sole responsibility for the study design, data collection and analysis,
interpretation of the data, and the preparation of the manuscript.
Affiliations of authors: Veterans Affairs Outcomes Group, Department
of Veterans Affairs Medical Center, White River Junction, VT (HGW);
Department of Medicine (HGW) and Department of Community and
Family Medicine (HGW, WCB), The Dartmouth Institute for Health Policy
and Clinical Practice, Dartmouth Medical School, Hanover, NH;
Department of Radiology, Dartmouth-Hitchcock Medical Center, Lebanon,
NH (WCB).