Disease Knowledge Centres

• Oncology - Disease Topic Overview

  Oncology is the medical specialty of study, diagnosis and treatment of cancer. A cancer is a group of cells (usually derived from a single cell) that has lost its normal control mechanisms and thus has unregulated growth ¹. Cancerous cells can develop from any tissue within any organ and can spread throughout the body (metastasize) ¹. Cancerous tissue can be divided into those of the blood and blood-forming tissue, and solid tumors, carcinomas or sarcomas ¹.

  Leukemias and lymphomas are cancers of the blood and blood-forming tissues. Cancerous cells often harm the body by crowding out normal blood cells in the bone marrow and bloodstream, so that normal functioning cells are gradually replaced by cancerous blood cells ¹. The non-Hodgkin's lymphoma is the most common but still a rare cancer, like chronic myeloid leukemia.

  Carcinomas are cancers of epithelial cells (skin, mucous membrane) ¹. Carcinomas are the most common form of cancers, including prostate, breast or lung cancer. Non-small cell lung cancer, which represents about 80% of lung cancers, is the most common cause of death by cancer among men and second among women ².

  Sarcomas are cancers of mesodermal cells, which are the cells that form muscles and connective tissue ¹. Examples of sarcomas are soft tissue sarcoma, gastrointestinal stromal tumours.

  Many genetic and environmental factors increase the risk of developing cancer: family history, pollution, exposure to radiation, diet and/or viral infections ¹. The papillomavirus is one of main cause of cervical cancer in women ³. In developed countries, the diet is also an important risk factor. Indeed, high consumers of cured meats and red meat are an increased risk of colorectal cancer ⁴.

  The recent discovery of signaling pathways and proteins expressed in the process of tumorigenesis has led to the development of new drugs called "targeted therapies" ⁵. Targeted therapy act specifically on a molecule that has a role in tumor growth. In the case of renal cell carcinoma, the tumor growth is highly dependent on VEGF and drugs targeting this factor have a significant anti-angiogenic effect ⁶.

  But, faced with the phenomenon of resistance and relapse, a better understanding will lead the development of new targeted molecules or more efficient combinations therapy ⁷.

  1 Beers M.H. et al. The Merck manual of medical information. Merck research laboratories. Second home edition. 2003, 1031-1047.
  2 Dempke W.C.M. et al. Targeted therapies for non-small cell lung cancer. Lung Cancer. 2010 ; 67 (3) : 257-274.
  3 Bosch X.F. et al. Prevalence of Human Papillomavirus in Cervical Cancer: a Worldwide Perspective. Journal of the National Cancer Institute. 1995 ; 87 (11) : 796-802.
  4 Corpet D.E. Red meat and colon cancer: Should we become vegetarians, or can we make meat safer? Meat Science, In Press, Corrected Proof, Available online 17 April 2011.
  5 Sawyers C. Targeted cancer therapy. Nature. November 2004 ; 432, 294-297.
  6 Motzer R.J. et al. Targeted Therapy for Metastatic Renal Cell Carcinoma. 7 Journal of Clinical Oncology. December 2006 ; 24 (35) : 5601-5608.
  8 Méjean A. et al. Targeted therapies. Progrès en Urologie. November 2008 ; 18 (7) : S228-S233.
  

• NSCLC

  

  The World Health Organisation estimates that globally there were 7.6 million deaths caused by cancer worldwide in 2008, and expects this figure to exceed 11 million by 2030 if the current trends continue. Lung cancer was the most common; accounting for 1.4 million deaths annually¹.

  Lung cancer can be divided into two forms; Non-Small Cell Lung Cancer (NSCLC) and Small Cell Lung Cancer. NSCLC is the most common form accounting for 80% of all cases². It is not one single type of cancer; instead it is a group of cancers that have been grouped together because approaches to diagnosis, staging, prognosis and treatment are similar. This group is composed of squamous cell carcinomas, adenocarcinomas and large cell carcinomas².

  During 2011, four symposia have been hosted by AstraZeneca to discuss the role of EGF Receptor Tyrosine Kinase Inhibitors on the treatment of EGFR+ tumours in people with advanced stage lung cancer. These symposia were held during four conferences; The 7th Asia Pacific International Academy of Pathology Congress (APIAP 2011), the 14th World Conference on Lung Cancer (WCLC 2011), the 23rd European Congress of Pathology of the European Society of Pathology (ECP 2011), and the 2011 European Multidisciplinary Cancer Congress (ECCO-ESMO 2011).

  Click here to view webinars from these symposia on our NSCLC symposia resource.

  EGFR mutation testing: guiding treatment for advanced non-small-cell lung cancer (NSCLC) was an AstraZeneca sponsored symposium held during APIAP 2011 in Taipei, Taiwan on 20th-24th May 2011. Webinars of the symposium presentations from two key speakers; Dr Kaoru Kubota and Dr Manuel Salto-Tellez can be viewed here.

  The symposia entitled “EGFR mutation-positive advanced NSCLC: optimising treatment sequences based on molecular biology” was held during WCLC 2011 in Amsterdam, The Netherlands on 3rd-7th July. Five presentations from the major speakers (Professor Egbert Smit, Professor Tony Mok, Dr Pasi Jänne, and Professor Jean-Yves Douillard) at this CME symposium are available to watch here.

  EGFR mutation testing in advanced NSCLC: best practice and future perspectives was held during ECP 2011 on 29th August 2011 in Helsinki, Finland. Webinars from this symposium were presented by Dr Nicola Normanno, Professor Keith Kerr, and Dr Marc Denis and can be viewed here.

  The symposium entitled ‘Advanced NSCLC: current concepts and future development of targeted treatment’ was held during ECCO-ESMO 2011 on 25th September 2011 in Stockholm, Sweden. Presentations from four key speakers; Dr Martin Reck, Professor Fabrice Barlesi, Dr James Yang and Dr Bruce Johnson, are available to view here.

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  References:

  1. WHO. Cancer Fact Sheet [http://www.who.int/en/]. Geneva: WHO; updated 2011 February; cited 2011 September 22]. Available from: http://www.who.int/mediacentre/factsheets/fs297/en/

  2. NICE. Clinical Guidelines 24. National Institute of Clinical Excellence. February 2005; All Pages

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  The World Health Organisation estimates that globally there were 7.6 million deaths caused by cancer worldwide in 2008, and expects this figure to exceed 11 million by 2030 if the current trends continue. Lung cancer was the most common; accounting for 1.4 million deaths annually¹.

  Lung cancer can be divided into two forms; Non-Small Cell Lung Cancer (NSCLC) and Small Cell Lung Cancer. NSCLC is the most common form accounting for 80% of all cases². It is not one single type of cancer; instead it is a group of cancers that have been grouped together because approaches to diagnosis, staging, prognosis and treatment are similar. This group is composed of squamous cell carcinomas, adenocarcinomas and large cell carcinomas².

  During 2011, four symposia have been hosted by AstraZeneca to discuss the role of EGF Receptor Tyrosine Kinase Inhibitors on the treatment of EGFR+ tumours in people with advanced stage lung cancer. These symposia were held during four conferences; The 7th Asia Pacific International Academy of Pathology Congress (APIAP 2011), the 14th World Conference on Lung Cancer (WCLC 2011), the 23rd European Congress of Pathology of the European Society of Pathology (ECP 2011), and the 2011 European Multidisciplinary Cancer Congress (ECCO-ESMO 2011).

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• Chronic Myeloid Leukemia

  

  Throughout life, the bone marrow continuously produces a variety of blood cell lineages in a tightly controlled, yet flexible process termed haematopoiesis1. The 2 main groups of mature blood cells are red blood cells (RBCs) and white blood cells (WBCs), or leukocytes...

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  The World Health Organization (WHO) classifies chronic myeloid leukaemia (CML) as a myeloproliferative disease characterised by the presence of the Philadelphia chromosome (Ph) or the BCR-ABL fusion oncogene¹. The diagnosis is generally easily made on the basis of morphological examination of a peripheral blood smear, but confirming genetic studies have become essential with the advent of molecularly targeted therapy.

  Leukaemias account for 300,000 new cases (~3% of all new cancer cases) each year and 220,000 deaths worldwide². CML accounts for about 15%-20% of all adult leukaemias and occurs slightly more frequently in men than in women (incidence ratio: 1.4 to 2.2:1)^3-6.

  Chronic myeloid leukemia typically progresses through 3 stages or phases. Most patients present in chronic phase, deteriorate during the subsequent accelerated phase, and finally progress to a brief terminal phase, blast crisis. Although the lengths of the phases were altered by previous therapies, the clinical course and natural history of CML had not been changed before the molecular era.

  Within the treatment section we examine the following treatment options:

  • Chemotherapy
  • Interferon Alfa
  • Stem-cell Transplantation

  Advances in the investigation of the molecular biology of cancer over several decades have made it possible to rationally design drugs to target oncogenic events with unprecedented specificity⁷.

  Enter the Chronic Myeloid Leukemia (CML) Knowledge Centre

  What’s in the Chronic Myeloid Leukemia (CML) Knowledge Centre?

  • CML Home
  • CML Management - Diagnosis
  • Current Treatment Options
  • ELN Recommendations
  • Historical Perspective - Chemotherapy
  • Historical Perspective - Interferon Alfa
  • Historical Perspective - Stem-Cell Transplantation
  • Ongoing Management
  • Other Therapeutic Approaches
  • Prognosis - Goals of Therapy
  • Prognosis
  • Treatment - historical perspective
  • Resources - Imatinib
  • Resources - Nilotinib
  • Useful Links (General)
  • Efficacy: Phase I
  • Efficacy: Phase II
  • Imatinib - Clinical Efficacy
  • Imatinib - Glivec
  • Imatinib - Indication
  • Imatinib - Mechanism of Action
  • Imatinib - Rationale
  • Imatinib - Safety Information
  • Nilotinib- Adverse Events
  • Nilotinib - Mechanism of Action
  • Nilotinib- Preclinical Studies
  • Nilotinib- Rationale
  • Nilotinib - Response Criteria
  • Nilotinib- Safety information
  • Nilotinib - Tasigna
  • Clinical Presentation
  • Epidemiology
  • Haematological Malignancy and Leukaemia
  • Pathophysiology
  • Phases of Disease
  • Understanding CML - Haematopoiesis

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  References:
  1. Vardiman JW, Harris NL, Brunning RD. The World Health Organization (WHO) classification of the myeloid neoplasms. Blood. 2002;100:2292-2302.
  2. Parkin DM, Bray F, Ferlay J, Pisani P. Global cancer statistics, 2002. CA Cancer J Clin. 2005;55:74-108.
  3. Druker BJ. Perspectives on the development of a molecularly targeted agent. Cancer Cell. 2002;1:31-36.
  4. Greenlee RT, Hill-Harmon MB , Murray T, Thun M. Cancer statistics, 2001. CA Cancer J Clin. 2001;51:15-36.
  5. Ries LAG, Eisner MP, Kosary CL, et al. SEER Cancer Statistics Review, 1975-2001. National Cancer Institute. Available at: http://seer.cancer.gov 11 November 2011
  6. Cortes J. Natural history and staging of chronic myelogenous leukemia. Hematol Oncol Clin North Am. 2004;18:569-584.
  7. Druker BJ. Perspectives on the development of a molecularly targeted agent. Cancer Cell. 2002;1:31-36.

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• Gastrointestinal Stromal Tumours

  

  Gastrointestinal stromal tumours (GISTs) are the most common mesenchymal tumours of the gastrointestinal (GI) tract. Before the current definition of GIST evolved, GISTs were classified as benign or malignant smooth muscle tumours including true smooth muscle tumours (leiomyomas, leiomyoblastomas, leiomyosarcomas) and neuronal tumours (schwannomas)

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  Gastrointestinal stromal tumours (GISTs) are the most common mesenchymal tumours of the gastrointestinal (GI) tract. Before the current definition of GIST evolved, GISTs were classified as benign or malignant smooth muscle tumours including true smooth muscle tumours (leiomyomas, leiomyoblastomas, leiomyosarcomas) and neuronal tumours (schwannomas)^1,2.

  Patients with GIST may be asymptomatic (31%) or symptomatic.³ Asymptomatic GISTs can be discovered incidentally during endoscopy or laparoscopy as well as during computed tomography (CT)⁴. Symptomatic GIST patients may present with a range of symptoms associated with the location of the tumour, growth pattern, and size.

  The diagnosis of GIST relies on standard histologic examination and immunohistochemical analysis of several markers, including KIT. Equivocal cases should be submitted to a central review by an expert in sarcoma pathology, experienced in the diagnosis of GIST.

  Before the availability of Glivec, the only treatments for GIST other than surgery were conventional chemotherapy and radiation therapy^5,6. The role of chemotherapy and radiation therapy has been limited by a lack of efficacy and intolerable toxicity, currently surgery is Standard of Care for Resectable Primary GIST.

  GIST is now recognised as having a much higher incidence than previously thought. Under the current, widely accepted definition of GIST as a distinct molecular and pathologic entity, the incidence of GIST is in the range of 10-20 cases per million persons per year ^7-11. The prevalence of GIST in a population-based study was estimated to be 129 cases per million persons¹¹. GIST tumours occur at a median age of 60 years and are slightly more predominant in men than women⁹. 

  Enter the Gastrointestinal Stromal Tumours (GIST) Knowledge Centre

  What’s in the Gastrointestinal Stromal Tumours (GIST) Knowledge Centre?

  • GIST Home
  • Current Options
  • Diagnosis- Histopathology
  • Diagnosis- Immunohistochemistry
  • Diagnosis
  • Differential Diagnosis
  • Goals of therapy
  • Historical perspective
  • Ongoing Management
  • Other Therapeutic Approaches
  • Prognosis
  • Treatment Guidelines
  • GIST Molecular Target animation
  • Resources
  • Useful Links
  • Imatinib - Clinical Investigation
  • Imatinib - Efficacy
  • Imatinib - Management of Adverse Events
  • Imatinib - Mechanism of Action
  • Imatinib - Monitoring
  • Imatinib - Progression
  • Imatinib - Rationale
  • Imatinib - Resistance
  • Imatinib - Safety and Tolerability
  • Definition
  • Epidemiology
  • Etiology
  • Pathophysiology
  • Symptoms

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  References

  1. Fletcher CDM, Berman JJ, Gorstein F, et al. Diagnosis of gastrointestinal stromal tumors: a consensus approach. Hum Pathol. 2002;33:459-465.
  2. Connolly EM, Gaffney E, Reynolds JV. Gastrointestinal stromal tumours,Br J Surg. 2003;90:1178-1186.
  3. Kindblom LG. Gastrointestinal stromal tumors: diagnosis, epidemiology, prognosis. Available at: www.asco.org. Accessed July 13, 2007.
  4. Joensuu H, Fletcher C, Dimitrijevic S, Silberman S, Roberts P, Demetri G. Management of malignant gastrointestinal stromal tumours. Lancet Oncol. 2002;3:655-664.
  5. Eisenberg BL, Judson I. Surgery and imatinib in the management of GIST: emerging approaches to adjuvant and neoadjuvant therapy. Ann Surg Oncol. 2004;11:464-475.
  6. Dematteo RP, Heinrich MC, El-Rifai WM, Demetri G. Clinical management of gastrointestinal stromal tumors: before and after STI-571. Hum Pathol. 2002;33:466-477.
  7. Goettsch WG, Bos SD, Breekveldt-Postma N, Casparie M, Herings RM, Hogendoorn PC. Incidence of gastrointestinal stromal tumours is underestimated: results of a nation-wide study. Eur J Cancer. 2005;41:2868-2872.
  8. Joensuu H. Current perspectives on the epidemiology of gastrointestinal stromal tumours. Eur J Cancer. 2006;4(suppl 1):4-9.
  9.  Blay JY, Bonvalot S, Casali P, et al. Consensus meeting for the management of gastrointestinal stromal tumors. Report of the GIST Consensus Conference of 20-21 March 2004, under the auspices of European Society for Medical Oncology. Ann Oncol. 2005;16:566-578.
  10. Miettinen M, Lasota J. Gastrointestinal stromal tumors--definition, clinical, histological, immunohistochemical, and molecular genetic features and differential diagnosis. Virchows Arch. 2001;438:1-12.
  11. Nilsson B, Bumming P, Meis-Kindblom JM, et al. Gastrointestinal stromal tumors: The incidence, prevalence, clinical course, and prognostication in the preimatinib mesylate era. Cancer. 2005;103:821-829

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• Prostate Cancer

  

  Prostate cancer is the most frequently diagnosed non-cutaneous malignancy in men, accounting for one in five male cancers.¹ The introduction of prostate-specific antigen (PSA) screening, has led to an increase in the detection of asymptomatic prostate cancer, and subsequently an increase in incidence and survival rates.^1,2

  There are only three well established risk factors for prostate cancer; age, family history and ethnicity.³ In contrast to many other types of tumour, smoking, alcohol and a sedentary lifestyle are not currently thought to be involved in the development of prostate cancer.⁴

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  Prostate cancer is the most frequently diagnosed non-cutaneous malignancy in men, accounting for one in five male cancers.¹ The introduction of prostate-specific antigen (PSA) screening, has led to an increase in the detection of asymptomatic prostate cancer, and subsequently an increase in incidence and survival rates.^1,2

  There are only three well established risk factors for prostate cancer; age, family history and ethnicity.³ In contrast to many other types of tumour, smoking, alcohol and a sedentary lifestyle are not currently thought to be involved in the development of prostate cancer.⁴

  Classification of prostate cancer can take two forms; histological classification is used to generate a Gleason score,⁵ while the spread of the disease is classified using the tumour-node-metastasis (TNM)system.³

  The majority of prostate cancer diagnoses are made following screening as most patients are asymptomatic.^3,6 However further investigations should be conducted if a patient presents with symptoms. Numerous management options are available dependent on the stage at which a patient presents with prostate cancer, however as most men do not die from prostate cancer it is important to determine which patients will benefit from therapy.^5,7

  Enter the Knowledge Centre

  What’s in the Prostate Cancer Knowledge Centre

  • Home
  • Epidemiology and Classification
  Incidence and Mortality
  Risk Factors
  Classification
  • Detection of Prostate Cancer
  Symptons
  Screening
  Diagnosis
  Staging
  Risk Stratification
  • Management Options
  Overview
  Deferred Treatment
  Local Treatments
  Systemic Treatments
  Clinical Updates
  • Resources
  Physicians
  Patients

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  References

  1. Ferlay J, Autier P, Boniol M, Heanue M, Colombet M, Boyle P. Estimates of the Cancer Incidence and Mortality in Europe in 2006. Ann Oncol. 18:581-92; 2007
  2. World Health Organization. The Global Burden of Disease: 2004 Update. Geneva: WHO; 2004
  3. European Association of Urology. Guidelines on Prostate Cancer, 2010.
  4. Grönberg H. Prostate Cancer Epidemiology. Lancet. 361:859-64; 2003
  5. Kirby RS, Patel MI. Fast facts: prostate cancer (5th ed). Health Press Ltd: Oxford; 2008.
  6. American Urological Association. Prostate-specific antigen best practice statement: 2009 update; 2009
  7. Coleman MP, Quaresma M, Berrino F; CONCORD Working Group. Cancer survival in five continents: a worldwide population-based study (CONCORD). Lancet Oncol. 9:730-56; 2008

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• Renal Cell Carcinoma

  

  Kidney cancer is the 14th most common cancer and there were approximately 200,000 new kidney cancer cases worldwide in 2002. RCC is a global problem, but its incidence varies considerably by geographical location. Rates of RCC are high in North America, Europe and Australia, whereas rates are low in Africa, India and China.

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  Kidney cancer is the 14th most common cancer and there were approximately 200,000 new kidney cancer cases worldwide in 2002. RCC is a global problem, but its incidence varies considerably by geographical location. Rates of RCC are high in North America, Europe and Australia, whereas rates are low in Africa, India and China. Until recently, the worldwide incidence of RCC has increased by approximately 2% every year.

  It is estimated that there will be 54,390 new cases of kidney cancer and 13,010 kidney cancer-related deaths in the US in 2008 alone. Global incidence data on mRCC are lacking, but can be estimated from figures for overall RCC rates.

  In 2006, there were estimated to be 63,300 new cases of kidney cancer (tenth most common cancer in the European Union [EU]¹) and 26,400 kidney cancer-related deaths in the EU. The Czech Republic, Estonia and Iceland have the highest RCC rates in Europe. Although the worldwide incidence of RCC is thought to be increasing,² data from a recent European study, which analysed kidney cancer incidence in 1980– 2004, indicate a shift towards stabilization or a decrease in incidence in recent years in both sexes. Recently, kidney cancer incidence rates also have decreased or stabilized in some countries in Northern Europe, except for England, Scotland and Ireland, whereas incidence in Eastern Europe has generally increased (except for women in the early 2000s). The highest sustained decreases in incidence rates were seen in Sweden; declines were observed in both sexes throughout the 25-year study period.

  Enter the Renal Cell Carcinoma Knowledge Centre

  What’s in the Renal Cell Carcinoma Knowledge Centre?

  • Overview
  • Incidence
  • Prevalence
  • Aeitology
  • Classification
  • Diagnosis and Staging
  • Radiological Investigations
  • Renal Biopsy
  • Histological Diagnosis
  • Disease Staging
  • Management and Treatment
  • Treatment Options
  • Adjuvant Therapy
  • Prognostic Factors
  • Treatment Guidelines
  • Resources

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  References

  1.Ferlay J, Autier P, Boniol M et al. Estimates of the cancer incidence and mortality in Europe in 2006. Ann Oncol 2007; 18:581-592.
  2. Matthew A, Devesa SS, Fraumeni JF, Jr.., Chow WH. Global Increases in kidney cancer incidence, 1973-1992. Eur J Cancer Prev. 2002;11:171-178.

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• Soft Tissue Sarcoma

  

  Soft Tissue Sarcomas (STS) are malignant (cancerous) tumors that develop in tissues which connect, support, or surround other structures and organs of the body. Muscles, tendons (bands of fiber that connect muscles to bones), fibrous tissues, fat, blood vessels, nerves, and synovial tissues are types of soft tissue.

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  Soft Tissue Sarcomas (STS) are malignant (cancerous) tumors that develop in tissues which connect, support, or surround other structures and organs of the body. Muscles, tendons (bands of fiber that connect muscles to bones), fibrous tissues, fat, blood vessels, nerves, and synovial tissues are types of soft tissue.

  Soft tissue sarcomas are grouped together because they share certain microscopic characteristics, have similar symptoms, and are generally treated in similar ways¹. They are usually named for the type of tissue in which they begin.

  Every year approximately 13,000 new cases of soft tissue sarcomas are diagnosed in adults and children in Europe. The 5-year survival rate for patients with soft tissue sarcoma is around 90% if the cancer is detected in early phases and before it has spread. However, the 5-year survival rate is 10% to 15% for sarcomas with metastasis.

  Management of STS depends on the stage of disease and histological subtype². Surgery is the mainstay of treatment for patients with localised disease and is often curative. However, as recurrence is likely to occur when tumour cells remain after surgery, adjuvant radiotherapy is often also considered, especially for patients with intermediate or high-grade tumours. Radiotherapy is also often administered for patients in whom surgery is inappropriate or who decline surgery.²

  There are a number of Associations and Organisations across Europe who strive to inform others of this disease as well as offer help and support to those affected or to those who know and want to help those suffering.

  Enter the Soft Tissue Sarcoma Knowledge Centre

  What’s in the Soft Tissue Sarcoma Knowledge Centre?

  • Home
  • Soft Tissue Sarcoma
  • Introduction
  • Staging and Risk Assessment
  • Chemotherapy
  • Disease Progression
  • Management - Overview
  • Novel Therapy - Trabectedin - Clinical Studies
  • Novel Therapy - Trabectedin - Clinical Updates
  • Novel Therapy - Trabectedin - Efficacy
  • Novel Therapy - Trabectedin - Mode of action
  • Novel Therapy - Trabectedin - Research and Advances
  • Novel Therapy - Trabectedin - Safety and Tolerability
  • Novel Therapy - Trabectedin
  • Radiotherapy
  • Surgery
  • Associations and Organisations
  • Congresses
  • Glossary
  • Guidelines
  • Research Groups
  • Classification
  • Clinical Presentation
  • Epidemiology
  • Types By Site

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  References

  1. Cormier JN, Pollock RE. Soft tissue sarcomas. CA: A Cancer Journal for Clinicians 2004; 54(2):94–109.
  2. Clark MA, Fisher C et al. (2005) “Soft-tissue sarcomas in adults.” N Engl JMed 353(7): 701–11.

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