The British seem less likely to get cancer than Americans but are also less likely to survive. But even though people in England, where the UK’s largest population is, are less likely to get cancer, five years after diagnosis, only 56% of English cancer patients survive, compared to 65% of American patients.
This difference raises many interesting questions about the difference between the two countries’ healthcare systems. In England and Wales, data from the Office for National Statistics show that survival rates varied by age—from 82% for females between 15 and 49 years of age, to 37% for males over 80.
The trend for variation by age was similar in the US—from 84% for females under 44 years of age to 52% for males over 75. Margaret Gates, an assistant professor of epidemiology at State University of New York at Albany, was a little surprised by the differences, too. But the biggest contributing factor to the difference in survival rates might be over-diagnosis. However, if American healthcare was indeed better than Britain’s National Health Service, then the number of deaths from cancers should be fewer in the US than in England and Wales. The cancer mortality rate for the US in 2010 was 172 per 100,000, and for the UK in 2010 was 178 per 100,000. Gates told Quartz that over-diagnosis related to screening in the US may likely drive the large difference in survival rates and incidence rates, especially in the common cancers of the prostate and breast. In other words, the American medical system seems to catch the existence of cancer earlier and in more people than the UK system does.
So it might appear that it is better to live in US, especially if you are at a higher risk of suffering from cancer. This story is part of our yearlong series "In Pursuit of Health," covering medical news and research happening across the university. Faculty at The University of Texas at Austin are tackling the challenge from many fronts, spending years in the lab, exploring new treatments with patients and working for funding to give people access to more effective diagnostic tools, less toxic medicine, less expensive care and more emotional support. From examining nanoparticles and cell biology to rethinking massive health care administration systems, these researchers are working to more deeply understand cancer in order to defeat it.
Suggs sees the most productive work coming from groups of inter-disciplinary researchers working together, rather than the now-common single-investigator-driven approach.
It's why she formed a cancer-focused working group with fellow UT researchers Amy Brock (biomedical engineering), Carla Van Den Berg (pharmacy) and Vernita Gordon (physics).
6. Edward Marcotte, professor of molecular biosciences is developing a large-scale rapid method for diagnosing and characterizing cancers noninvasively using fluids such as saliva, blood and urine, identifying and quantifying individual peptides or proteins that point to the presence of cancer in the body. 8. John DiGiovanni, professor of pharmacy and nutritional sciences, has identified a gene that plays a role in susceptibility to nonmelanoma skin cancer a discovery that could lead to novel strategies for prevention of that form of cancer. 10. Debbie Volker, associate professor of nursing, researches ethical issues and end-of-life care for adults with a cancer diagnosis, their families and nurses. 11. Barbara Jones, associate professor of social work, researches how to improve care for children, adolescents and young adults with cancer or recovering from cancer, including understanding the long-term needs of children who survive.
12. Mary Lou Adams, associate professor of nursing, led the five-year-long African-American Breast Cancer Outreach project, screening 8,000 Texas women, resulting in 100 diagnoses.
13. Erin Donovan-Kicken, assistant professor of communication studies, examines the ways in which cancer patients interact with families and health care providers and how that can lead to beneficial changes in their overall health.
16. Rong Cui, associate professor of pharmaceutics, examines anticancer drug delivery using nanoparticles in an effort to develop cancer treatments that are less toxic to the body.
Kevin Dalby, professor of medicinal chemistry, and Scarlett Ferguson, a recent postdoctoral fellow in the College of Pharmacy, at work in Dalby's lab. 18. George Georgiou, professor of molecular biosciences, chemical engineering and biomedical engineering, is in preclinical development of highly promising new proteins he developed for treating liver cancer, which has a median survival rate of only eight months.
3. Texas 4000 is a UT student organization that runs the longest annual charity bike ride in the world, pedaling more than 4,000 miles from Austin to Anchorage, Alaska, to raise funds for cancer research and raise awareness about cancer prevention and treatment.
That compares favorably with the rate of cancer in the US—396 per 100,000 people in the UK vs.
But before we try to understand why there is such a difference, let’s look at the data. There may also be lifestyle differences, associated with the culture and racial make-up of the two countries.
Survival rates measure the likelihood that a patient survives for a certain period of time after diagnosis.
This is a much smaller difference, especially when compared to the side-by-side cancer incidence rates (451 per 100,000 vs 396 per 100,000).
For instance, in the UK, every death is registered nationally but the US dataset is not so complete. In the US and the UK, the number of total deaths from cancer has fallen by more than 20% in the last two decades—and it continues to fall.
They are meeting to learn more about each other's work and review other research and hope to start collaborating on projects soon.
James Tunnell, associate professor of biomedical engineering, created a pen-sized instrument that can detect skin cancer within seconds using light pulses. Nutrition researcher Linda deGraffenried is working to identify the optimal combination of diet and chemotherapy to treat the most aggressive cancers that begin in the breast or the prostate and rapidly spread to other parts of the body. Doctors treating brain tumors can't choose a treatment plan without sufficiently understanding the extent of the tumor's invasion into normal tissue.

Molecular biosciences professor Tanya Paull studies how double-stranded DNA is repaired after it breaks and how pathways to DNA repair affect the development of tumors. Catherine Cubbin, associate professor of social work, is part of a team developing a program that helps low-income women living in Texas rural areas get access to breast cancer screening services and, if cancer is found, resources to help pay for treatment. In partnership with Marcotte, developmental biologist John Wallingford discovered that the inexpensive antifungal drug thiabendazole slows tumor growth.
Biomedical engineering professor Stanislav Emelianov is engineering nanoparticles that can extract information from cancer cells and relay the information to physicians in real time, allowing for more effective treatment. Adams discovered that fear of diagnosis and therefore avoidance of mammograms was a key reason why African-American women have a 32 percent higher death rate from breast cancer than white women. Psychology professor James Pennebaker is a pioneer in the study of using expressive writing as a route to healing, including surviving cancer. Assistant Professor of nutritional sciences Stefano Tiziani studies childhood leukemia and is working with Dell Children's Medical Center to identify new metabolic biomarkers that will better predict patients' responses to cancer treatment drugs, potentially resulting in higher survival rates, less chance of relapse and fewer side effects. Pharmacotheraphy professor Jim Koeller looks at the economics of standardized cancer disease treatment strategies and has performed numerous disease treatment maps for advanced lung, colon and breast cancer. The TherapeUTex Preclinical Core Lab, under the direction of College of Pharmacy faculty member Janet Walkow, prepares drugs for clinical trials, testing safety, effectiveness and delivery method. College of Pharmacy professor Kevin Dalby is working toward creating inhibitors of pathways that go awry in cancer cells.
Chemical engineering senior Sai Gourisankar has worked with professor Keith Johnston to design gold nanoclusters for biomedical imaging and therapy to treat cancer and other diseases.
Biomedical engineering senior Nishu Mehta worked in professor George Georgiou's lab for three years, creating a hybrid antibody that binds with combined immune cells, thus having the potential to be a much more potent cancer therapeutic. And, of course, the countries have vastly different systems of healthcare—the US has a system based on private insurance while the UK has a comprehensive national healthcare system. So if a patient is diagnosed (or misdiagnosed) earlier, his or her chance of survival increases. But such diagnoses mean that, among those diagnosed, fewer people die in the timeframe used for calculating survival rates.
Over the course of her career, Suggs has seen research funding decline, and thinks larger group projects might be able to advance the science further than solo researchers working on smaller projects independently. The quick, non-invasive tool could help save billions of dollars and ease patients' pain by eliminating the need for biopsies of benign lesions.
So George Biros, professor at the Institute for Computational Engineering and Sciences, is using UT's Stampede supercomputer at the Texas Advanced Computing Center to improve the quality of brain tumor imaging. His research could help identify malignant cell clusters within a healthy body and allow for pinpoint treatment that would limit damage to the surrounding cells. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.AbstractTurcot syndrome (TS) is a rare hereditary disorder clinically characterized by the occurrence of primary tumors of the colon and the central nervous system (CNS).
Here we present the case of an 11-year-old boy with a synchronous clinical presentation of both glioblastoma multiforme (GBM) and colonic adenocarcinoma. A molecular genetic study revealed microsatellite instability in the DNA mismatch repair (MMR) gene.
St Pierre, “Malignant tumors of the central nervous system associated with familial,” Diseases of the Colon and Rectum, vol.
Based on this case study, the synchronous presentation of glioblastoma multiforme and adenocarcinoma of the colon might suggest a shorter survival rate for patients with Turcot syndrome. It is characterized by the development of primary tumors of the central nervous system (CNS), such as glioblastoma multiforme (GBM) and medulloblastoma, along with numerous adenomatous colorectal polyps and colonic adenocarcinoma. TS usually develops in the patient’s teens and can be genetically distinguished as either familial adenomatous polyposis (FAP) or hereditary nonpolyposis colon carcinoma (HNPCC) [4]. TS type I is characterized by the presence of glial tumors, relatively few colonic polyps, and cancer. TS type II is characterized by thousands of colonic polyps and increased risk of medulloblastoma.Since the time when this syndrome was first identified, there have only been isolated case reports or case series with a limited number of patients being discussed in the literature. The synchronous clinical presentation of CNS tumors and colonic adenocarcinoma in this syndrome is extremely rare. In this paper, we present a case of TS with simultaneous clinical presentation of GBM and colonic adenocarcinoma.2. Case ReportAn 11-year-old boy presented with headache for the past 5 days, vomiting, and history of a single tonic clonic seizure. He was also suffering from vague abdominal pain and loose motion over a period of one month prior to presentation. Horii et al., “Germ-line and somatic mutations of the APC gene in patients with Turcot syndrome and analysis of APC mutations in brain tumors,” Genes Chromosomes and Cancer, vol. On his skin there were multiple café-au-lait spots and areas of hypopigmentation (Figure 1). Konishi et al., “Drastic genetic instability of tumors and normal tissues in Turcot syndrome,” Oncogene, vol. Hematoxylin and eosin stain 5 400.He continued to have abdominal pain and diarrhea and developed melena and intermittent frank bleeding from the rectum.
His blood cell count, platelets, and renal and coagulation profiles were within the normal range.
Upper GI endoscopy was normal; however, colonoscopy showed multiple colonic polyps of various sizes with ulceration and active bleeding (Figure 2).

A molecular genetic workup of the patient showed mutation in the DNA mismatch repair (MMR) gene with microsatellite instability. Van Meir, “Brain tumor-polyposis syndrome: two genetic diseases?” Journal of Clinical Oncology, vol. For adenocarcinoma of the colon, he underwent laparoscopic total colectomy and ileocolic anastomosis. Lucci-Cordisco et al., “Two PMS2 mutations in a Turcot syndrome family with small bowel cancers,” American Journal of Gastroenterology, vol. Three months later, he had multiple recurrences and dissemination of the cerebral tumors on the left temporal, multifocal frontal, and parietal areas. From a genetic standpoint, TS can be divided into two subtypes: the first is manifested by the MMR gene and PMS2 with a high risk of developing GBM, and the second type is manifested by the adenomatous polyposis coli gene germline mutation with a high risk of developing medulloblastoma [5, 16].
There are reports of cases with the occurrence of both GBM and medulloblastoma, as in the report from McLaughlin and colleagues [12]. Nevertheless, their patient was treated for medulloblastoma and received whole-brain radiation therapy 10 years prior to the diagnosis of GBM. Moreover, the occurrence of tumors other than GBM and medulloblastoma has been reported [17]. Based on TS classification, our patient fit the clinical and molecular genetic features of TS type I. The pathological differentiation between sporadic GBM and TS-associated GBM has not been adequately addressed in the literature.
Recently, Lusis and colleagues reported on three cases involving patients with TS-associated GBM [11].
The histopathological and molecular genetic features in all three cases consisted of giant-cell GBM, and the patients in two of the cases had sarcomatous changes. Kang, “Turcot syndrome: a case report in an unsuspected setting,” Journal of Gastrointestinal Surgery, vol. The first two patients survived 44 and 55 months, respectively, and the last patient survived 29 months and was still alive when the report was published.
The average survival rate of patients with TS and GBM was found to be 27 months; however, when the investigators excluded the two patients with the longest-term survival, the average survival rate dropped to 16 months [18, 19]. GBM and anaplastic astrocytoma are the most commonly reported CNS tumor associated with TS. In a review of 33 reported cases, 21 reports were for GBM and anaplastic astrocytoma [21].Most of the reported TS cases in the literature are characterized by different time intervals between the clinical presentation of CNS tumors and the colonic adenocarcinoma [18, 22]. The presence of symptomatic CNS GBM and colorectal cancers at the same time carries more management difficulties and, more important, might shorten the survival rate. We elected to treat the CNS tumor first due to the presence of mass effects that were causing increased intracranial pressure. He was operated on for the GBM recurrence; however, a few months later he had a disseminated GBM involving almost the entire left cerebrum that was not amenable to further surgical intervention.
The presence of GBM in TS may suggest a lower survival rate in contrast to other CNS tumors in most reported cases. ConclusionSimultaneous clinical presentation of CNS GBM and adenocarcinoma of the colon in TS might be an indicator of a shorter survival rate. A patient with sebaceous carcinoma, colon cancer, and a malignant astrocytoma,” Dermatology Online Journal, vol. Perry, “Glioblastomas with giant cell and sarcomatous features in patients with turcot syndrome type 1: a clinicopathological study of 3 cases,” Neurosurgery, vol.
Albright, “Medulloblastoma and glioblastoma multiforme in a patient with Turcot syndrome: a case report,” Surgical Neurology, vol. Halls, “Turcot syndrome: a case with spinal cord and colonic neoplasms,” American Journal of Roentgenology, vol. Report of an additional case and review of the literature,” Diseases of the Colon and Rectum, vol.
Paraf, “Turcot syndrome: evolution of knowledges,” Gastroenterologie Clinique et Biologique, vol. Ono et al., “Ganglioglioma in a patient with Turcot syndrome,” Journal of Neurosurgery, vol. Parsons, et al., “The molecular basis of Turcot's syndrome,” The New England Journal of Medicine, vol.
Scott, “Survival of patients with Turcot's syndrome and glioblastoma,” The New England Journal of Medicine, vol. Ajarim, “Turcot syndrome: report of a case and review of the literature,” International Surgery, vol. Chung et al., “Germline hMSH2 and differential somatic mutations in patients with Turcot's syndrome,” Genes Chromosomes Cancer, vol.

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