Papers by Carolyn Compton
Journal of Clinical Oncology, Aug 10, 2011
Colorectal cancer (CRC) develops as a result of a series of accumulated genomic changes that prod... more Colorectal cancer (CRC) develops as a result of a series of accumulated genomic changes that produce oncogene activation and tumor suppressor gene loss. These characteristics may classify CRC into subsets of distinct clinical behaviors. We studied two of these genomic defects-mismatch repair deficiency (MMR-D) and loss of heterozygosity at chromosomal location 18q (18qLOH)-in patients enrolled onto two phase III cooperative group trials for treatment of potentially curable colon cancer. These trials included prospective secondary analyses to determine the relationship between these markers and treatment outcome. A total of 1,852 patients were tested for MMR status and 955 (excluding patients with MMR-D tumors) for 18qLOH. Compared with stage III, more stage II tumors were MMR-D (21.3% v 14.4%; P Ͻ .001) and were intact at 18q (24.2% v 15.1%; P ϭ .001). For the combined cohort, patients with MMR-D tumors had better 5-year disease-free survival (DFS; 0.76 v 0.67; P Ͻ .001) and overall survival (OS; 0.81 v 0.78; P ϭ .029) than those with MMR intact (MMR-I) tumors. Among patients with MMR-I tumors, the status of 18q did not affect outcome, with 5-year values for patients with 18q intact versus 18qLOH tumors of 0.74 versus 0.65 (P ϭ .18) for DFS and 0.81 versus 0.77 (P ϭ .18) for OS. We conclude that MMR-D tumor status, but not the presence of 18qLOH, has prognostic value for stages II and III colon cancer.
Springer eBooks, 2020
The development of cancer is a slow, stepwise process, typically taking many years to several dec... more The development of cancer is a slow, stepwise process, typically taking many years to several decades. The process starts with an initiation mutation in a driver gene in an adult stem cell. The initiated cell becomes a clone when it is stimulated to divide, a step in the process called promotion. The initiating mutation typically makes the cell more susceptible to mutation. Therefore, as the initiated clone expands, random cells within it acquire additional mutations, forming unique subclones. This continues again and again over time as the nascent cancer grows, a protracted phase of cancer development called progression. The acquisition of new mutations accelerates as elements of mutation repair machinery themselves become mutated and dysfunctional. The rate of growth is also accelerated due to mutations in the cell division signaling systems of the cells. During its early development, a cancer is invisible and acquisition undetectable, unless cells or tissues are acquired and examined microscopically. As the cancer grows, it acquires mutation-driven changes in both form and function. For developing carcinomas, by far the most common type of human cancer, the changes in form manifest themselves as deviations from normal cell size, shape, and orientation. The early changes in cell morphology are known as dysplasia. The aberration become progressively more pronounced, from mild to severe dysplasia, until they have all of morphological characteristics of a malignant neoplasm, the most common characteristic of which is cell-to-cell heterogeneity. At this stage, the neoplasm confined to its anatomical niche of origin in the epithelium and is called carcinoma in situ. With further progression, the neoplasm acquires new traits and capabilities that allow the neoplasm to overtake and destroy normal tissue. It invades the tissue beneath the epithelium of origin, invades into lymphatic and/or blood vessels, and survives in either the low-pressure lymphatic or the high-pressure blood circulatory system or both. These circulatory systems carry the malignant cells to other sites in the body, either the regional draining lymph nodes via the lymphatics or distant organs and tissues via the blood. The cells then exit the vessel and establish new colonies of neoplastic cells that proceed to invade and destroy the tissue in the new site. This process is called metastasis. By the time the cancer has succeeded in metastasizing to distant body sites, it is highly heterogeneous, resistant to treatment, and highly likely to be lethal. This chapter describes the process of cancer development in detail, explaining the changes that occur on a molecular, morphological, and behavioral level.
Springer eBooks, Oct 26, 2016
The New England Journal of Medicine, Oct 27, 1988
Presentation of Case A 52-year-old man was admitted to the hospital because of severe diarrhea an... more Presentation of Case A 52-year-old man was admitted to the hospital because of severe diarrhea and weight loss. He was well until nine weeks earlier, when there was the abrupt onset of explosive, watery diarrhea one day after he ate raw clams and oysters in a restaurant; a friend ate the same food and remained well. The patient passed approximately 15 watery stools daily, without blood or abdominal pain; diarrhea occurred at all hours of the day and night, and he experienced occasional abdominal discomfort and bloating, nausea, and vomiting. Six weeks before admission he consulted a gastroenterologist because of . . .
Archives of Pathology & Laboratory Medicine, May 1, 2001
A number of articles on the subject of error in anatomic pathology have recently been published, ... more A number of articles on the subject of error in anatomic pathology have recently been published, stimulated in part by the Institute of Medicine's report on patient safety. 1 Many of these articles discuss histologic slide review as a means of reducing diagnostic variation, some including explicit recommendations for routine review of histologic or cytologic slides by a second pathologist. 2,3 However, most of these articles have not addressed the scope of routine slide review in the context of error reduction or how it fits into the practice of medicine. Articles reporting high rates of diagnostic variation in surgical pathology are often from referral centers where the case mix includes significantly more complex clinical presentations or difficult histologic diagnoses than that seen in an ordinary practice. A more accurate measure of the overall frequency of diagnostic variation in normal practice settings would be obtained by examining all cases, not those preselected because of diagnostic difficulty or adverse outcome. In contrast to studies reporting high error rates for selected cases, clinically significant disagreements are found in only 0.26% to 1.2% of cases following comprehensive review by a second pathologist. These lower rates reflect the inclusion of specimen types unlikely
The Canadian journal of gastroenterology, 1990
Chronic inflammatory bowel disease (IBO) predisposes affected individuals to the development of i... more Chronic inflammatory bowel disease (IBO) predisposes affected individuals to the development of invasive colon cancer. Increased cancer risk has been seen in ulcerative colitis and Crohn's disease in Western societies as well as in schistosomal colitis in China. In this study it was found that the frequency of the 12th codon of c-Ki-ras, as well as the specific amino acid substitutions, were similar in sporadic colon cancers, cancers associated with ulcerative colitis in the United States, and colon cancers found in patients with schistosomal colitis in Jiangsu province in China. Further, activating mutations of codon 12 of e-Ki-ras were found in high grade dysplastic lesions in chronic ulcerative colitis. The latter finding indicates that some dysplasias are clonal proliferative lesions with genetic characteristics associated with invasive cancer.
The New England Journal of Medicine, Jul 12, 1990
Presentation of Case A 72-year-old woman was admitted to the hospital because of severe abdominal... more Presentation of Case A 72-year-old woman was admitted to the hospital because of severe abdominal pain. The patient was well and active until five days earlier, when there was the onset of severe band-like pain about the level of the umbilicus, without radiation elsewhere, accompanied by a sensation of abdominal bloating; the pain was constant and was not affected by position or antacids but increased in severity about half an hour after meals. The patient's stools became soft, with a single episode of hematochezia; after two or three days she stopped passing stools. Several days before admission the pain became . . .
Springer eBooks, Jun 30, 2006
Springer eBooks, Jun 30, 2006
Journal of Clinical Oncology, Apr 1, 2023
PURPOSE The College of American Pathologists (CAP) has developed a guideline on testing for misma... more PURPOSE The College of American Pathologists (CAP) has developed a guideline on testing for mismatch repair (MMR) and microsatellite instability (MSI) for patients considered for immune checkpoint inhibitor therapy. ASCO has a policy and set of procedures for endorsing clinical practice guidelines that have been developed by other professional organizations. METHODS The CAP guideline was reviewed for developmental rigor by methodologists. An ASCO Endorsement Panel subsequently reviewed the content and the recommendations. The ASCO Endorsement Panel determined that the recommendations from the CAP guideline, published on August 3, 2022, are clear, thorough, and based on the most relevant scientific evidence. ASCO endorses Mismatch Repair and Microsatellite Instability Testing for Immune Checkpoint Inhibitor Therapy: Guideline From the College of American Pathologists in Collaboration With the Association for Molecular Pathology and Fight Colorectal Cancer. RECOMMENDATIONS Within the guideline, MMR immunohistochemistry (IHC), MSI polymerase chain reaction, and MSI next-generation sequencing are all recommended testing options for colorectal cancer, MMR-IHC and MSI-polymerase chain reaction for gastroesophageal and small bowel cancer, and only MMR-IHC for endometrial cancer. No recommendation in favor of any testing method over another could be made for any other cancer. Tumor mutational burden was not recommended as a surrogate for DNA MMR deficiency. If MMR deficiency consistent with Lynch syndrome is detected, it should be communicated to the treating physician.
Archives of Dermatology, May 1, 1992
BACKGROUND Continuous-wave carbon dioxide lasers are not widely used for the surgical removal of ... more BACKGROUND Continuous-wave carbon dioxide lasers are not widely used for the surgical removal of most skin lesions because it is difficult to control laser ablation and the extensive laser-induced thermal damage slows healing. Pulsed lasers provide means to reduce thermal damage produced during laser ablation and permit precise control of tissue removed during ablation. Using a swine model, we compared on a gross and microscopic level the healing of middermal wounds of similar depth and area created by a dermatome and a focused pulsed CO2 laser. RESULTS Pulsed CO2 laser ablation removed skin precisely and bloodlessly with 85 +/- 15 microns (mean +/- SD) of residual thermal damage covering the surface of the wound. Compared with the dermatome, tissue reepithelialization was delayed in the laser wounds at day 3. By day 7, epithelial coverage of the laser-created wounds was not significantly different from the dermatome-created wounds. No significant difference in the appearance of the two wounds was noted at 42 days. CONCLUSIONS We conclude that the focused pulsed CO2 laser is capable of precisely and bloodlessly ablating skin with conservation of residual subjacent adnexal elements, minimal early interference with epibolic epithelial outgrowth, and no pathologic effects on the wound healing process. Pulsed CO2 lasers may be a valuable instrument for the conservative ablation of skin and skin lesions.
American Journal of Roentgenology, Feb 1, 1989
Atlante Per La Stadiazione Dei Tumori Maligni
Atlante Per La Stadiazione Dei Tumori Maligni
Atlante Per La Stadiazione Dei Tumori Maligni
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Papers by Carolyn Compton