Pancreatic carcinoma dr mnr

1. Pancreatic carcinoma 27-1 -17 DR MUHAMMED MUNEER M MS GENERAL SURGERY SGMC & RF TRIVANDRUM KERALA

2. Pancreatic cancer

3. TUMOURS OF THE PANCREAS The tumors of the pancreas can be - A. Non-Endocrine neoplasms B. Endocrine neoplasms

4. NON-ENDOCRINE NEOPLASMS:  Benign non-endocrine neoplasms of pancreas. Includes:- (adenoma, cystadenoma, lipomas, fibromas, haemingoma, lymphangioma and neuromas). • They are extremely rare and no clinical significance unless they become palpable or give pressure to adjacent structures and cause symptoms. • Can be solid or cystic or both. • The diagnosis should be made after exclusion of more frequent malignant tumours.

5.  Malignant non-endocrine neoplasms. The most common are:- 1.Ductal adenocarcinoma 2.Cystadenocarcinoma (Exocrine cell of pancreas )

6. ENDOCRINE NEOPLASMS: These are less common than non-endocrine tumours and generally benign and sometimes multiple. They includes:  Insulinoma  Glucogonomas  Others: - Gastrinomas - Somatostatatinomas - Vipomas (Vasoactive Intestinal Polypeptide)

7. Malignant non-endocrine neoplasms

8. Introduction • Pancreatic carcinoma is a relatively common tumor with an incidence of 7.6 per 100.000 per year in Western-Europe. • 9th MC cancer diagnosis • 4th in cancer deaths each year. • The majority of pancreatic cancers (85%) are adenocarcinoma of ductal origin (PDAC). • And the term "pancreatic cancer" is sometimes used to refer only to that type. • It is more common in men (men:woman 1.3:1) • It comprises about 2.5 % of all newly diagnosed tumors and 5% of all cancer. • 5 year survival is <5% • In spite of the limited tumor size the majority of pancreatic head cancers (80%) are not eligible for resection at the time of diagnosis.

9. Risk factors for pancreatic carcinoma • Tobacoo • Inherited susceptabilityEstablished • c/c pancreatitis • DM type 2 • Obesity ( 3 times , BMI >35) Associated • Physical inactivity • Certain pesticides • High CHO/sugar intake. Possible

10. Risk factors • Older age -cases before age 40 are uncommon • Mean 72 • Common in African Americans, though incidence in Africa is low • low socioeconomic status • Ashkenazic jewish heritage are assoc increased risk of PC • There is Association b/w risk of pancreatic cancer , H.pylori colonization and ABO blood groups. • Cirrhosis & c/c pancreatitis • A high fat or cholesterol diet, & prior cholecystectomy.

11. Risk • Diet – processed meat, red meat, and meat cooked at very high temperatures – (e.g. by frying, broiling or barbecuing) • If > one 1st -degree relative had the disease, and more modestly if they developed it before the age of 50 Meat hanging inside a smokehouse in Switzerland.

12. • The genetic events found in ductal adenocarcinoma have been well characterized, and complete exome sequencing has been done for the common types of tumor • 4 genes have each been found to be mutated in the majority of adenocarcinomas • KRAS (in 95% of cases), CDKN2A (also in 95%), TP53 (75%), and SMAD4 (55%). • The last of these are especially associated with a poor prognosis.

13. Genetic mutation in PC (gene & PC%) K ras 95-100% MC P16 82% P53 75% DPC4 55% BRCA2 7%

14. Familial pancreatic cancer( H3-AFP) • Cystic fibrosis –30 fold increase in risk of PDAC (CFTR Gene mutation) • Familial adenomatous polyposis - 4 fold increase. (APC Gene mutation ) • Predisposing conditions – Hereditary pancreatitis (40% life time risk) • PRSS1 gene mutation – HNPCC (lynch syndrome)- 8 fold increase. – Hereditary breast cancer assoc with BRCA2 mutation- 10 fold increase • BRCA2 mutation is the MC germline mutation) – Ataxia telengiectasia – FAMMM( Familial atypical multiple mole & multiple melanoma) syndrome- > 40% fold increase • CDKN2A gene mutation. – Peutz- Jeghers syndrome ( > 100 fold increase in risk of PDAC) • Carries highest relative risk of PC. • STK11 tumor suppressor gene

15. • Dysplastic nevus syndrome Or • Atypical Mole Syndrome (AMS) Or • Familial atypical multiple mole– melanoma (FAMMM) syndrome • It is a cutaneous condition described in certain families, and characterized by unusual nevi and multiple inherited melanomas

16. Ocular telangiectasia in a person Familial adenomatous polyposis • CCP

17. • Patients with pancreatic cancer with DNA mismatch repair mutation have a better prognosis. • Kras mutation and HER2 /neu over expression are the earliest changes to occur.

18. Pathogenesis of sporadic pancreatic cancer • Most cases are sporadic • 5–10% of pancreatic cancer cases have an inherited component • These cancers are thought to arise from several types of precancerous lesions within the pancreas. • But these lesions do not always progress to cancer • Apart from pancreatic serous cystadenomas (SCNs), which are almost always benign, three types of precancerous lesion are recognized. 1. pancreatic intraepithelial neoplasia (PanIN) 2. intraductal papillary mucinous neoplasms (IPMNs) 3. pancreatic mucinous cystic neoplasms (MCNs)

19. 1.pancreatic intraepithelial neoplasia (PanIN) • These are microscopic abnormalities in the pancreas, which are often found in autopsies of people with no diagnosed cancer • These may progress from low to high grade and then to a tumor. • Sequential pathway observed in the development of PDAC from PanIN to invasive cancer. • Number of tumor supressor & oncogenes are identified • PDX1, KRAS2, CDKN2A/p16, P53 & DPC4 (SMAD4)

22. Classification cystic lesions in the pancreas • Pancreatic cysts can be categorized into the following groups: • Pseudocysts • Common cystic neoplasms: – SCN - Serous cystic neoplasm (Benign ) – IPMN - intraductal papillary mucinous neoplasm – MCN - Mucinous cystic neoplasm • Uncommon cystic neoplasms: – SPEN (solid pseudopapillary epithelial neoplasm) – Tumors with cystic degeneration: adenocarcinoma neuroendocrine tumor

25. Charecteristic SCN MCN IPMN Gender F>>M 4:1 F>>>M 10:1 F=M Age 60-70 (grandma) 50-60 (mother) 60-70 Location HEAD BODY TAIL HEAD Appearance Multiple small cyst (micro cyst) seperated by internal septations with central sunburst appearance Thick walled , septated macrocyst with smooth contour, +/- solid component, egg shell ca2+ Poorly demarcated, lobulated, polycystic mass, with dilaion of main or branch ducts Communication with duct No No Yes Cytology Glycogen rich cells with +ve PAS stain Sheets & clusters of collumnar mucin containing cells Tall collumnar mucin containing cells Mucin stain -VE +VE +VE Amylase LOW LOW HIGH CEA LOW HIGH HIGH

26. Intraductal papillary mucinous neoplasms (IPMNs) • Macroscopic lesions, which occur in about 2% of all adults • 25% risk of developing into invasive cancer. • Also known as mucin secreting carcinoma • MC in head and Uncinate process of the pancreas • Types – – Side branch- dilatation of PD side branch – Main duct – abnl cystic dilatation of the main PD – Mixed type – side branch IPMN which extent to main PD • Even if removed surgically, there remains a considerably increased risk of pancreatic cancer developing subsequently

27. Age and gender

28. Clinical features • Lesion in the periampullary region, HOP, & uncinate process- obstuctive jaundice (painless) • Tumors from the body and tail of the pancreas- pain & LOW (>50%) • Pain typically arising in the epigastrium and radiating to the back, when tumor spread beyond the pancreas peripancreatic nerve plexuses are involved . Pain suggests unresectability in carcinoma pancrease. • Ascitis- when peritoneal carcinomatosis or portal vein occlusion disease.

29. • In case of pertoneal dissemination , perirectal tumor, involvement may be palpable via DRE , referred to as Blumer`s shelf. • Metastasis to liver and peritoneum most common • A palpable distended GB in 1/3rd of patients with periampullary PDAC ( courvoiser Law). • With wide spread disease , a left supra-clavicular node (Virchow`s node ) may be palpable. • Perumbilical lymphadenopathy may be palapable (sister Mary Joseph`s node) • Steatorrhoea • 2/3rd (65%) pts present with diabetes in carcinoma pancreas

30. • Symptoms include unexplained episodes of pancreatitis, nausea, vomiting. • Elderly patients with A/c pancreatitis but with out H/o ETOH or gallstones should be screened for a neoplasm • Gastric Outlet Obstruction • Clinical depression has been reported in association with pancreatic cancer in some 10–20% of cases,

31. Presenting symptoms Frequency % jaundice 75 LOW 51 Abdominalpain 39 Nausea vomiting 13 Pruritis 11 Fever 3 GI bleeding 1

32. Other findings • Trousseau`s syndrome : migratory thrombophlebitis – ( blood clots form spontaneously in the portal blood vessels, the deep veins of the extremities, or the superficial veins anywhere on the body, may be associated with pancreatic cancer, and is found in about 10% of cases) – CA lung, GI malignancies, Prostate cancer, Ovarian cancer, Lymphoma • Hypercoagulability – Mucins directly activate platelets via p selectin – May explain why heparins more effective than warfarin in adenocarcinoma related thrombosis • Trousseau’s sign : carpopedal spasm in hypocalcemia • Troisier’s sign : palpable left supraclavicular LN ( virchow’s node)

33. Periampullary carcinoma • Periampullary carcinoma is term used for juxta-pancreatic carcinomas. • They are three forms:-  Carcinoma of the ampulla  Carcinoma of the lower CBD  Duodenal carcinoma • Adenocarcinoma HOP 40-60% • Adenocarcinoma of ampulla of Vater 10-20% • Distal bile duct adenocarcinoma 10% • Duodenal adenocarcinoma 5-10% • Best prognosis: – Duodenal adenocarcinoma > Adenocarcinoma of ampulla of Vater > Distal bile duct adenocarcinoma > Adenocarcinoma Head>body >tail of pancreas

34. • Most pancreatic cancers occur in the head of the pancreas (75%), body (15%) and tail (10%). • At the time of diagnosis a pancreatic head carcinoma is usually a little larger than 3 cm. • When tumors of the pancreatic body and tail are diagnosed, they are usually much larger, because they present late with nonspecific symptoms. • These tumors are usually irresectable.

35. Diagnosis

36. Carbohydrate antigen , CA19-9 • CA 19-9 (most sensitive) • It has a sensitivity of 80% and specificity of 73% in detecting pancreatic adenocarcinoma, and is used for following known cases rather than diagnosis. • Individuals with blood Lewis antigen- negative status (10- 15%) do not develop elevation of the CA 19-9 • The degree of elevation post op is predictive of long term survival • CA19-9 is elevated by biliary obstruction per se and is elevated in other cancers (e.g., gastric, bladder…) • CEA

38. Ultrasound abdomen • US is the first line imaging test for the evaluation of these patients. • sensitivity of 75% and a specificity of 75%. • US can determine the level of obstruction in most cases (sensitivity >90%). • The overall sensitivity and specificity for determining resectability of all pancreatic carcinomas however is only 63% and 83% respectively. • In patients with a pancreatic head tumor, typically dilatation of the CBD & PD (double duct sign) is seen, which is s/o a mass in the pancreatic head, even in the absence of a visible mass. • Usg is less sensitive and will miss small tumors, but can identify cancers that have spread to the liver and ascites

39. MDCT • MDCT is the ioc for evaluation, diagnosis, staging , & follow up in CA pancreas. • For suspected periampullary pathology, a 3 phase (noncontrast, arterial, and portal venous ) CT scan with 3mm slices and coronal & 3D reconstruction should be routine. • If the cause of a distal bile duct obstruction is not revealed by US , next diagnostic test is CT. • As pancreatic carcinoma is a hypovascular tumor, it presents as a hypodens mass on a CECT.

40. • The mass is usually ill-defined. • In 10 - 15% the tumor is isodense and therefore may be difficult to detect. • Tumors smaller than 2 cm. may also be difficult to detect on CECT. • In these cases indirect signs may be helpful such as the presence of the double duct sign, atrophy of the pancreatic tail, or fullness of the pancreatic head (loss of the lobular appearance of the pancreatic parenchyma). • CxR is sufficient to R/0 pulmonary mets if suspicious lesions noted, needs CT

41. ERCP • ERCP (or MRCP) is only the next step when there is a high suspicion of bile duct stones. • ERCP reserve for cases requiring therapeutic or palliative intervention • Double duct sign on ERCP is highly s/o pancreatic head cancer. • Tissue diagnosis is not necessary prior to routine resection. • A suspicious lesion by imaging should be treated with resection. • Although ERCP has a high sensitivity for detecting pancreatic head tumors, it is nowadays no longer indicated because the diagnosis can usually be made with non-invasive tests. • No role in tumor staging information

42. EUS • For identifying lesions < 2cm that do not appear on CT scans • These pancreatic head tumors can be missed even on a technically excellent CT and therefore a 'negative' CT-scan in a patient with a strong suspicion for pancreatic head cancer requires additional imaging with endoscopic ultrasound. • Endoscopic ultrasound has also been used for local tumor staging

43. Endoscopic ultrasound Endoscopic US of small pancreatic head tumor obstructing the common bile duct

44. MRI magnetic resonance cholangiopancreatography Double duct sign indicating pancreatic head carcinoma

45. • CT and MRI both have a higher sensitivity than ultrasound for the detection of small lesion. • CT scan & EUS are used both to confirm the diagnosis and to help decide whether the tumor can be surgically removed (its "resectability") • MRCP is also very sensitive for detecting a periampullary mass, but offers no significant additional staging information FDG PETCT • To differentiate autoimmune focal pancreatitis versus adenocarcimnoma & also to identify unusual pathology (10%) • PET has currently not proven its use in the differentiation as tumor and inflammation may both show increased uptake

46. • A biopsy by fine needle aspiration, often guided by EUS may be used • Histologic diagnosis is not usually required for removal of the tumor by surgery to go ahead. • Liver function tests can show a combination of results indicative of bile duct obstruction (raised conjugated bilirubin, γ-glutamyl transpeptidase and ALP ) Differential diagnosis • Focal pancreatitis, lymphoma and metastatic disease • Most large surgical series show that, in about 5% of the patients, who undergo resection for suspicion of pancreatic head cancer only pancreatitis is eventually found in the resected specimen.

47. Pathology • The MC form of pancreatic cancer (adenocarcinoma) is typically characterized by moderately to poorly differentiated glandular structures on microscopic examination. • There is typically considerable desmoplasia or formation of a dense fibrous stroma or structural tissue consisting of a range of cell types (including myofibroblasts, macrophages, lymphocytes and mast cells) and deposited material (such as type I collagen and hyaluronic acid). • This creates a tumor microenvironment that is short of blood vessels (hypovascular) • It is thought that this prevents many chemotherapy drugs from reaching the tumor, as one factor making the cancer especially hard to treat

48. Pathological, Radiologic, and Histologic Features of Pancreatic Cancer. Hidalgo M. N Engl J Med 2010;362:1605-1617.

49. C shows ERCP imaging of a plastic stent through the ampulla of Vater in a patient with a tumor in the head of the pancreas. D (hematoxylin and eosin) shows microscopical adenocarcinoma of the pancreas with abundant tumor stroma (black arrows). E shows a peripancreatic lymph node involved with metastatic adenocarcinoma (hematoxylin and eosin, high magnification).

50. Staging • Pancreatic cancer is usually staged following a CT scan • The most widely used cancer staging system is American Joint Committee on Cancer (AJCC) together with the Union for International Cancer Control(UICC). • AJCC-UICC staging system

51. Stage T1 pancreatic cancer Stage T2 pancreatic cancer

52. Stage T3 pancreatic cancer Stage T4 pancreatic cancer

53. Pancreatic cancer in nearby lymph nodes – Stage N1 Pancreatic cancer metastasized – stage M1

55. • To help decide treatment, the tumors are divided into 3 categories – Resectable – Borderline resectable – Unresectable • Early stage ( stages I and II) - Surgical resection of the tumor can normally be performed, if the patient is willing & to be sufficiently fit. • Stage III tumors - that are judged to be "borderline resectable" (where surgery is technically feasible because the celiac axis and SMA are still free) • Stage 3 (T4) disease involving celiac artery or SMA or stage 4 (metastatic disease) are not candiadates for immediate surgery.

56. Resectable or Irresectable that's the question • It is important to stage a pancreatic tumor correctly. • Overstaging will lead to under treatment, if a laparotomy is not performed in a patient with a potentially resectable tumor. • Understaging will lead to an unnecessary laparotomy with all the associated risks.

57. The pancreatic head is surrounded by the portal vein, SMA, mesenteric root, duodenum, IVC and aorta

58. Not resectable- Liver metastases and distant lymph node metastases should allways be proven by means of cytologic or histologic biopsy before refraining from exploratory laparotomy.

60. Peritoneal metastases (arrowheads) in a patient with a pancreatic tumor

62. Locally advanced adenocarcinomas • Locally advanced adenocarcinomas have spread into neighboring organs, which may be any of the following – Duodenum >stomach> transverse colon> spleen> adrenal gland> or kidney. • Back pain or highly elevated CA19-9 • Positive peritoneal washings has same prognosis as metastatic disease so these patients considered metastatic and not locally advanced • 40% of newly diagnosed patients are locally advanced • Locally advanced -prognosis (e.g. 1 year) ,metastatic disease (6-8 months) • Typical sites for metastatic spread (stage IV disease) are the liver, peritoneal cavity and lungs, all of which occur in 50% cases

63. Non-resectable pancreatic head tumor obstructing the common bile duct and pancreatic duct. Tumor surrounds the superior mesenteric vein at the junction with the splenic vein. Paraaortic and celiac lymphnodes and a small liver metastasis.

64. Laparoscopy • Staging laparoscopy reduces the frequency of non-therapeutic laparotomy for pts with unsuspected metastatic or locally advanced unrescectable disease identified at the time of surgery. • Laparoscopy is much more sensitive than any other technique for the detection of peritoneal implants and superficial liver metastases. • For pts who appears resectable on imaging studies alone turned out to be un-resectable in 30% of cases. • Indicated in high risk occult disease – large tumors>3cm – CA 19-9 levels > 100 U/ml – Equivocal findings of metastasis on CT – Body or tail tumors – Clinical indicators of wide spread d/s- sig LOW, malnutrition, pain

65. Diagnostic laparoscopy LEFT: laparoscopic biopsy of superficial liver metastasis .RIGHT: peritoneal metastases

66. History/ surgery • The earliest recognition of pancreatic cancer has been attributed to the 18th-century Italian scientist Giovanni Battista Morgagni. • A genuine histopathologic diagnosis was eventually recorded by the American clinician Jacob Mendes Da Costa • By the start of the 20th century, cancer of the HOP had become a well-established diagnosis

67. • The first reported partial pancreaticoduodenectomy - Italian surgeon Alessandro Codivilla ( 1898) • 1912 the German surgeon Walther Kausch was the first to remove large parts of the duodenum and pancreas together (en bloc) • American surgeon Allen Oldfather Whipple (1935) published the results of a series of 3 operations at Columbia Presbyterian Hospital in New York • Two stage procedure- biliary decompression followed by pancreaticoduodenectomy.

68. • The discovery in the late 1930s that vitamin K prevented bleeding with jaundice, and the development of blood transfusion as an everyday process, both improved post- operative survival • 1970- median operating time 8.8hrs, mortality -25% • 2000s- median operating time 5.5 hrs, mortality -1 % • 1000 pancreaticoduodenectomies performed by a single surgeon from Johns Hopkins Hospital Baltimore between 1969 -2003 (Trimble & colleagues) • 2,050 operations at the Massachusetts General Hospital 1941 - 2011

70. Treatment • The only curative treatment option is surgical resection. Tumor of HOP Pylorus preserving Pancreaticoduodenectomy or Longmire-Traverso procedure is preferred. Tumor of body and tail Distal pancreatectomy & en-bloc splenectomy

72. Pancreaticoduodenectomy ( Whipple’s procedure) • It consist of complete removal of the pancreas and hepatoduodenal ligament lymph nodes, the duodenum with a short segment of the proximal jejunum and the distal half of 2/3rd of the stomach with the right half of the greater omentum • Whipple’s procedure involves the resection of – Distal stomach – GB – CBD – Head of pancrease – Duodenum – Proximal jejunum – Regional LN

73. Restoration of GI continuity requires Pancreticojejunostomy Hepaticojejunostomy Gastrojejunostomy.

75. • Whipple is now reserved for situation in which – the entire duodenum has removed (eg in FAP) or – when the tumor encroaches on the first part of D or – distal stomach & a PPPD would not achieve a clear resection margin Middle or central or segmental pancreatectomy Middle pancreatectomy is a safe, effective procedure for treatment of benign & low grade malignant neoplasms of mid pancreas. •Indications •benign & low grade malignant neoplasms ( NET, serous cystadenoma, branch duct IPMNs) •Location in neck or its contiguous position •A distal pancreatic stump of at least 5 Cm in length

76. Middle or central or segmental pancreatectomy • In experienced hands it is assoc with no mortality, even if rate of clinical “ pancreatic fistula is about 20%. • Middle pancreatectomy is avoided in pts affected by main duct IPMN • Advantage – Preserve pancreatic parenchyma – Reduce the risk of exocine and endocrine insufficiency – Consists of limited resection of the mid portion of the pancrease.

77. Morbidity following pancreaticoduodenectomy COMPLICATIONS FREQUENCY % DELAYED GASTRIC EMPTYING Most common 18 PANCREAS FISTULA 12 WOUND INFECTION 7 INTRAABDOMINALABSCESS 6 CARDIAVC EVENTS 3 BILE LEAK 2 OVERALL REOPERATION 3 • MC cause of death following pacreaticoduodenectomy is cardiopulmonary complications. • Most important predictor of post-operative survival is R0 resection • Most important margin in pacreaticoduodenectomy is retropertoneal or uncinate margin.

78. Resectional surgery for pancreatic body and tail tumors • Most of body and tail tumors have already metastasized to distant sites or extended locally to involve nodes, nerves, or major vessels by the time of diagnosis • Splenic vein involvement or occlusion is not a sign of nonresectability • Involvement of splenic and SMV confluence generally precludes resection • Resection involves a distal pancreatectomy either with or without concomitant splenectomy

79. Palliative therapy for PC Biliary obstruction 1)ERCP with metal stent placement (best) 2)Roux-en – Y hepaticojejunostomy GOO 1)Endoscopic stenting (prefered) 2)Double bypass (Roux-en-Y hepaticojejunostomy + gastrojejunostomy) Pain 1)NSAIDs or Opiates 2) Celiac nerve block

80. Chemotherapy • Gemcitabine is current standard of care with metastatic PC. • Folfirinox regimen- Nearly 3.6 month survival benefit compared to Gemcitabine alone (FOL – folinic acid (leucovorin), F – fluorouracil (5-FU), IRIN – irinotecan (Camptosar), OX – oxaliplatin (Eloxatin)) • Folfox regimen : (FOL– Folinic acid (leucovorin) F – Fluorouracil (5-FU) OX – Oxaliplatin (Eloxatin) • Prognosis – 5 yr survical after curative resection (pacreaticoduodenectomy) approaches 15-20% – Overall , 5 yr survival rate with PC is 5 %.

82. Meta-analysis in JCO, 2007 • Chemo is better than supportive care in terms of survival • Gemcitabine better than 5FU • Combinations of other drugs with gemcitabine slightly superior to gem alone • Tissue diagnosis- But in specific patients a tissue diagnosis may be needed such as in patient entering a clinical trial, prior to neoadjuvant chemoRx, and prior to chemoRx in advanced tumors. Sultana, A. et al. J Clin Oncol; 25:2607-2615 2007

84. Controversy Chemo-radiation vs chemotherapy alone in locally advanced disease Small old trial showed adding 5FU to radiation improves survival compared to radiation alone but another trial showed 5FU alone was as good as 5FU+radiation Recent trial did not show benefit to adding radiation in locally advanced disease New chemotherapy regimens are more effective and have higher response rates further putting into question role of radiation

85. Metastatic tumor to pancreas • MC site of primary : RCC> malignannt melanoma • On autopsy MC site of primary : CA Lung

86. Outcomes • For locally advanced and metastatic pancreatic adenocarcinomas, which together represent over 80% of cases • Numerous recent trials comparing chemotherapy regimes have shown increased survival times, but not to > one year • Overall 5 year survival for pancreatic cancer in the US has improved from- – 2% in cases diagnosed in 1975–77 – 4% in 1987–89 diagnoses – 6% in 2003–09. – localized and small cancerous growth (<2 cm) -20% Resectable disease (stage I &II) 15-20 months Locally advance d/s (stageIII) 6-10 months Metastatic disease (stage IV) 3- 6 months

88. Research directions • Targeted therapies against the cancer cells (ruloxitinib with capecitabine. (Jak activation is present in pancreatic cancer) • Still others aim to affect the non-neoplastic stroma and microenvironment of the tumor, which is known to influence cell proliferation and metastasis • A further approach involves the use of immunotherapy, such as Oncolytic viruses • Irreversible electroporation

89. Irreversible electroporation IRE or NTIRE • A novel ablation technique • IRE or NTIRE for non-thermal irreversible electroporation is a soft tissue ablation technique using ultra short but strong electrical fields to create permanent and hence lethal nanopores in the cell membrane, to disrupt the cellular homeostasis. • It is especially suitable for treatment of tumors that are in proximity to peri-pancreatic vessels without risk of vascular trauma

90. Thank u

Pancreatic carcinoma dr mnr

Pancreatic carcinoma dr mnr

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