Your SlideShare is downloading. ×
Interpretation and Management of Pancreatic cancer
Upcoming SlideShare
Loading in...5

Thanks for flagging this SlideShare!

Oops! An error has occurred.

Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

Interpretation and Management of Pancreatic cancer


Published on

A descriptive approach for interpretation and managent of pancreatic cancer.

A descriptive approach for interpretation and managent of pancreatic cancer.

  • Be the first to comment

No Downloads
Total Views
On Slideshare
From Embeds
Number of Embeds
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

No notes for slide


  • 1. INTERPRETATION AND MANAGEMENT OF PANCREATIC CANCER JAIPUR NATIONAL UNIVERSITY Project work submitted for partial fulfilment for award of Bachelor of Pharmacy(B.Pharmacy) degree. Supervised by: Mr. Ganesh N. Sharma Asst. Professor (Pharmacology), School of Pharmaceutical Science, Jaipur National University (Raj.) Submitted by: Bibin Mathew B.Pharm (4th year), Enrollment No: JNU-jpr2009/01508.
  • 2. S.No. TITLES & SUBTITLES 1. INTRODUCTION 1.1 Cell Cycle 2. PANCREATIC CANCER 2.1 Functions of pancreas. 2.2 Epidemiology of pancreatic cancer. 2.3 Types of pancreatic cancer. 3. INTERPRETATION OF PANCREATIC CANCER 4. CAUSES OF PANCREATIC CANCER 5. SIGNS AND SYMPTOMS 6. DIAGNOSIS 6.1 Recent advancement in diagnosis 7. MANAGEMENT OF PANCREATIC CANCER 7.1 Recent approaches in management of pancreatic cancer 8. CONCLUSION 9. REFERENCES
  • 3. 1. INTRODUCTION  Pancreatic cancer is a malignant neoplasm originating from transformed cells arising in tissues forming the pancreas. The most common type of pancreatic cancer, accounting for 95% of these tumors, is adenocarcinoma.  Tumors of Pancreas Broadly there are three basic types:  Ductal adenocarcinoma is 90% of pancreatic cancers with a 4% 5-year survival (worst of any cancer).  Neuroendocrine tumors ( islet-cell tumors).  Cystic neoplasm account for <1% of pancreatic cancer.
  • 4. 1.1 Cell Cycle Phases Events Gap 0 (G0) Resting phase Gap 1 (G1) Cells increase in size, control mechanism to ensure that everything is ready for DNA synthesis. DNA replication occurs during this phase. Synthesis (S) Checkpoint control mechanism ensures that everything is ready to enter the M (mitosis) phase and divide. Mitosis (M) Cell growth stops at this stage and cellular energy is focused on the orderly division into two daughter cells. Gap 2 (G2)
  • 5. 2. PANCREATIC CANCER  Usually, cancer is named after the body part in which it originate thus pancreatic cancer refers to the erratic growth and proliferation of cells that originate in the pancreatic tissue. Human Pancreas
  • 6. The pancreas is prismoid in shape and appears triangular with two major regions i.e. head and tail portion. The head of the pancreas lays in the duodenal C loop in front of the inferior vena cava (IVC) and the left renal vein. The body and tail of the pancreas run obliquely upward to the left in front of the aorta and left kidney. The main pancreatic duct (Duct of Wirsung) runs from the tail through the body to the head of the pancreas where it descends into the lower (inferior) part of the head. There it joins the duct of the uncinate process coming from left and then the lower part of the common bile duct to form a common channel (hepatopancreatic ampulla). This duct runs through the medial duodenal wall and opens on the dome of the major duodenal papilla.
  • 7. 2.1 Functions of pancreas Exocrine Endocrine Enzyme Substrate Product Amylase (active) Starch, glycogen Glucose, maltose. Trypsinogen, Trypsin (active) Chymotrypsin (active). Cleave peptide bonds in amino acids Free amino acids and dipeptides. Pancreatic Triglyceride Mono lipase (active) glycerides fatty acids. Beta cells (Insulin) D-Cells (Somato statin) Alpha Cells (Glucagon) Inhibition Stimulation
  • 8. 2.2 Epidemiology of pancreatic cancer Pancreatic cancer is currently the fourth leading cause of cancer death in the western countries, claiming 32,000 lives annually. The rate of incidence is increasing which means that the disease is becoming more common and it is also extremely difficult to treat. Signs and symptoms of the disease seldom appear until more advanced stages of cancer. By the time symptoms appears, cancer cells are likely to have metastasized to other parts of the body. While currently pancreatic cancer can be removed by surgery followed by chemotherapy.
  • 9. 2.3 Types of Pancreatic Cancer • Pancreatic cancer has been classified into two classes viz. exocrine and endocrine pancreatic cancer. The endocrine and exocrine pancreatic carcinomas are further classified into various subclasses. Passaro’s triangle. Typical location of a Gastrinoma
  • 10. Subclasses of endocrine pancreatic cancer Gastrinoma (Zollinger- • Gastrinomas overproduce gastrin. Most are malignant or have the ability to Ellison Syndrome) become malignant. Glucagonoma Insulinoma Nonfunctional Islet Cell Tumor (NICT) • Glucagonomas overproduce glucagon. They are usually large, often metastasize and about 70% are malignant. • Insulinomas overproduce insulin. They are the most common pancreatic neuroendocrine tumors. • Nonfunctional islet cell tumors are usually malignant. They are hard to detect.
  • 11. Somatostatinoma • Somatostatinomas overproduce somatostatin. They can occur anywhere in the pancreas and in the duodenum. • VIPomas overproduce vasoactive Vasoactive Intestinal intestinal peptide (VIP). These tumors are Peptide-ReleasingTumor usually located in the body and tail of the pancreas.
  • 12. Various subclasses of exocrine pancreatic cancer Acinar Cell Carcinoma • Rare form of pancreatic cancer that may cause excessive production of pancreatic lipase, the enzyme secreted to digest fats. Adenocarcinoma • Adenocarcinoma accounts for about 90% of all pancreatic cancers and it begins in cells lining the pancreatic duct. Adenosquamous Carcinoma • Adenosquamous carcinoma is similar to adenocarcinoma in that it forms glands but it flattens as it grows. Intraductal PapillaryMucinous Neoplasm • Grows from the main pancreatic duct or from side branches. The tumor appear as a finger-like projection into the duct.
  • 13. Mucinous Cystadenocarcinoma Pancreatoblastoma • Mucinous cystadenocarcinoma is a rare, malignant, spongy, cystic tumor. The cyst is filled with a thick fluid called mucin. • Pancreatoblastoma is a rare form of pancreatic cancer found in children under the age of 10. It is often called “pancreatic cancer of infancy.”
  • 14. 3. INTERPRETATION OF PANCREATIC CANCER  There are several stages involved in pancreatic cancer, and two models for accurately describing them are TNM and Stage models 1. TNM Model In the Tumor, Node, Metastasis (TNM) system, tumor size, lymph node health and metastasis activity are measured separately, each with its own number scale. 2. STAGE Model The second model for pancreatic cancer involves 4 numbered stages, as follows:  Stage1  Stage2  Stage3  Stage 4
  • 15. TNM MODEL TUMOR • T1 :Tumor is less than 2cm across in any direction. • T2 :Tumor is larger than 2cm across. • T3 : Tumor has started to grow into the tissues, duodenum and bile duct. • T4: Tumor has grown into spleen, large intestine and major blood vessel. NODE • N0 : There are no lymph nodes containing cancer. • N1 : Lymph nodes containing cancer and so the tumor has likely metastasized beyond the pancreas. METASTASIS • M 0 : The tumor has not spread. • M1 The tumor has spread.
  • 16. STAGE MODEL Stages TNM Equivalent Description Stage 1 1 or 2,0,0 There has been not spread and is relatively small. Tumor has not progressed outside pancreas. Stage 2 3,0,0 Tumor has grown into nearby tissues and perhaps the duodenum. Lymph nodes are not affected. Stage 3 2 or 3,1,0 Tumor may be quite large and has spread to the lymph node system. Stage 4 4A 4,2,0 Tumor has grown into nearby organs including the spleen and/or stomach, as well as blood vessels. 4B 1,2,3 or 4,1,1 Tumor has spread to other organs such as the liver or lungs.
  • 17. 4. CAUSES OF PANCREATIC CANCER 5 Major causes: Pancreatic cancer
  • 18. 5. SIGNS AND SYMPTOMS Fig. No.4 Upper abdominal pain that may extend to middle or upper back. Fig.No.5 Weight loss due to malignant cancer cells tendency to deprive healthy cells of nutrients. Fig.No.6 Jaundice leads to yellowing of skin and eyes. Fig.No.7 Nausea and vomiting can occur during later stages, if a pancreatic tumor has grown sufficiently larger Fig. No. 8 Due to Zollinger Ellison syndrome stomach ulcers can also happen.
  • 19. 6. DIAGNOSIS Following methods are used for diagnosis of pancreatic cancer: 1.Ultrasound of the abdomen. 2.Endoscopic Ultrasonography (EUS). 3.Endoscopic Retrograde Cholangiopancreatography (ERCP). 4.Computed Tomography (CT). 5.Carbon nanotubes.
  • 20. 7. MANAGEMENT OF PANCREATIC CANCER A number of approaches can be made for the management of pancreatic cancer which are as follows: 1.Surgery Whipple procedure for pancreatic cancer surgery.
  • 21. 2. Radiation Therapy  Radiation therapy ( radiotherapy, x-ray therapy, or irradiation) is the use of a beam of energy (called ionizing radiation) to kill cancer cells and shrink tumors.  Radiation therapy injures or destroys cells in the area being treated (the “target tissue”) by damaging their genetic material (DNA), making it impossible for these cells to continue to grow and divide.  Major side effect is radiation damages both cancer cells and normal cells, most normal cells can recover from the effects of radiation and function properly.  The goal of radiation therapy is to damage as many cancer cells as possible, while limiting harm to nearby healthy tissue.
  • 22. 3. Chemotherapy 1. Chemotherapy For exocrine pancreatic cancer Drugs Gemcitabine, 5Floro uracil. 2. Target therapy in exocrine Erlotinib, Erlotinib+Gem. 3. For endocrine pancreatic cancer Doxorubicin, Streptozocin 4. Target therapy for endocrine Sunitinib , Everolimus 5. Other drugs for neuroendocrine Octreotide,Paseriotide 6. For Zollinger Ellison Syndrome Proton Pump Inhibitors 7. For Insulinomas( before surgery) Diazoxide
  • 23. Gemcitabine: A boon for pancreatic cancer Gemcitabine mechanism
  • 24. 7.1 Recent approaches in management of pancreatic cancer: Gene Therapy • Introduction of functional genetic material into target cells to replace or supplement defective genes or modify target cells. Oncogenes Inactivation • Mutations in KRAS are found in more than 90% of patient . Its inactivation using suitable vectors is a novel approach. Immune enhancement • Autologous natural killer (NK) cell and activated T lymphocyte based immunotherapy termed as autologous immune enhancement therapy. Enzyme therapy • Enzymes which are generally given in this therapy are lipase, protease and amylase.
  • 25. 8. CONCLUSION  Pancreatic cancer i.e. mainly adenocarcinoma is the major cause of death associated with pancreatic cancer. Apart from familial disorders the minor risk factors also cannot be ignored as smoking causes 40% of pancreatic cancer.  Due to its poor prognosis mortality rate with pancreatic cancer is high so the newly developed cheaper and sensitive diagnostic could create a breakthrough in determining pancreatic cancer.  Gemcitabine has proved a boon to pancreatic cancer patient Apart from chemotherapy, gene therapy, oncogens inactivation and enzyme therapy can be helpful to patients.  With advances in screening, diagnosis, and treatment, the death rate for pancreatic cancer has declined. Research is ongoing to develop even more effective screening and treatment programs.
  • 26. 9. REFERENCES 1. Bertran K, Masters S and Anthony T. “Basic and Clinical Pharmacology”, Tata McGraw hill education Pvt. ltd, New Delhi, 10th edition, 2009, 72151. 2. Neoptolemos John,, “Pancreatic Cancer”, Springer science, USA, 1st edition 2010,vol-1, 4-60. 3. Heiken Jay, “Pancreatic Cancer”, Cambridge University press, USA, 1st edition, 2008, vol-1,60-150. 4. Bennet PN and Brown MJ, “Clinical Pharmacology”, Elseiver India Pvt. ltd, New Delhi, 9th edition,2005, 659-665. 5. Walker R and Whittlesea C, “Clinical Pharmacy and Therapeutics”, Churchill Livingstone Elseiver, New Delhi, 4th edition, 2008, 480-85. 6. Collinus K, Jacks T and Pvletich PN, “The Cell Cycle and Cancer”, PNAS, Springer science, USA, 1997 April 1, vol-94, 2776-2778. 7. Goyton AC and Hall JE, “Textbook of Medical Physiology”, Reed Elsevier India Pvt. ltd, New Delhi, 10th edition, 2004, 747-766. 8. Gelone S, Gennaro, Alfonso R (Editors), “Remington The science and practice of pharmacy, Lippincott Williams & Wilkins, USA, 21st edition, 2005, 1110-1115.
  • 27. 9. Satou A, Nakamura, “Pancreas Anatomy, Diseases and Health Implications, Nova Sciences Publishers, NY, 2012, vol-45, 50-110. 10. Bhattacharya SK,, “Pharmacology”, Elesevier India, New Delhi, 6th edition, 2004, 335-340. 11. Bell RH, “Atlas of pancreatic surgery: Digestive tract, Lippincott, Philadelphia, 2nd edition, 1996,963 12. DeLellis,, (Editors), “WHO classification of Tumors, Pathology and Genetics of Endocrine Organs”, IARC Press, London, 2004, 175-200. 13. Cancer – Its various types along with causes, symptoms, treatments and stages, cancer info guide,2009 ( retrieved from at 16:00hrs). 14. Tamm PE, SilverMan MP,, “Diagnosis staging and Survillence of pancreatic cancer, American Journal Of Pancreatic Cancer”, American journal of roentgenology, USA, May 2003,vol-180,5. 15. Hidalgo Manual, “Pancreatic cancer” The New England journal of medicine”, IARC Press, London, 2010, vol-362, 1605-1617. 16. Heiser PW and Hebrok M, “Development and Cancer”, Lessons learned in pancreatic cancer, Cell cycle, 2004, vol-3, 270-2. 17. Klein MW, Hruban RH,, “Direct correlation between proliferative activity and dysplasia in Pancreatic Intra Epithelial Neoplasia”, Modern Pathology, 2002, vol- 15, 441-447.
  • 28. 18. Brunton LL, Lazo SJ, Parker Keith, “Goodman & Gilman’s, The Pharmacological Basis of Therapeutics”, McGraw Hill medical publishing division, New Delhi, 11th edition, 2005, 401-20. 19. Khosronia I, “Smoking and pancreatic cancer”, Medical journal of Iranian hospital, vol-4, January 2002, 50-60. 20. Gukovsky I, Todorin J and Karin M, “Inflammation autophagy and Obesity: Common features in pathogenesis of pancreatitis and pancreatic cancer”, Gastroenterology, June2013, vol-144(6), 1999-2000. 21. Rang H.P, Dale M.M, Ritter.J.M, Flower.R.J, “Rang and Dales Pharmacology, Elsevier publication, New Delhi, 6th edition, 2007, 525-530 22. Casper ES, Green MR, Kelsen DP, et al, “ Phase II trial of gemcitabine in patients with adenocarcinoma of the pancreas”, Invest New Drugs ,1994,vol-12, 29 23. Loscalzo, Hauser,, “Harrison’s Priciples of Internal Medicine”, Mc Graw Hill medical publishers, New Delhi, Vol-1, 17th edition, 580-620. 24. Lynch HT, Smyr KT,, “Familial pancreatic cancer: A rievew, Europe Pubmed, Central, 1996, vol-23(2), 251-275. 25. Valiang WG, Anna G and Stephan JP, “Alcohol and pancreatic cancer”, Alcohol Journal, Elseiver, USA, April 2005, vol-35,205-211. 26. NCCN Clinical Practise Guidelines in Oncology: Pancreatic Adenocarcinoma, 2011, vol-2,112 27. Karlson BM, Ekbom Anders,, “Abdominal US for Diagnosis of Pancreatic Tumor: Prospective Cohort Analysis”, Radiology, Radiological Society of North America, October 1999, 213, 107-111.
  • 29. 28. Pellegta NS, Sessa, “K-ras and p-53 gene mutation in pancreatic cancer: ductal and non ductal tumor progress through different genetic lesions”, Cancer Research, AARC, Philadelphia, March 15, 1994,Vol-54,1556. 29. Beard J,, “The Enzyme treatment of pancreatic cancer and its scientific basis”, New Spring Press, NY, 1911, 21-50. 30. Venugopal D,, “Pancreatic enzyme supplementation in pancreatic cancer”, The journal of supportive oncology, Elseiver, USA, vol-6, 393400.
  • 30. THANK YOU