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Biomedical subjects

Muhammad Wasif Saif

Publications and source records attributed to Muhammad Wasif Saif.

At least 19 recordsLinked to original sources
PubMed2007

Epidermal growth factor receptor inhibition strategies in pancreatic cancer: past, present and the future.

Pancreatic carcinoma is an unusually lethal disease and to date treatment with standard chemotherapy has yielded disappointing results. The epidermal growth factor receptor (EGFR) is known to be over-expressed in pancreatic cancer and there is data to suggest that this molecular characteristic may be a poor prognostic factor as it may denote a more aggressive form of the disease. Current therapeutic modalities to target the EGFR include monoclonal antibodies directed against the extracellular domain of the receptor as well as tyrosine kinase inhibitors that disable the activating portion of the receptor. Preclinical studies in pancreatic cancer models have demonstrated the efficacy of both of these treatment options and at present they are in various stages of clinical testing in combination with other cytotoxic drugs, with other biologic therapies and in conjunction with radiotherapy. The combination of gemcitabine and one of the tyrosine kinase inhibitors, erlotinib, is the first combination therapy to demonstrate survival benefits in pancreatic cancer in a phase III study albeit a modest one. Increased understanding of the EGFR pathway may permit the use of other targeted agents to either augment therapeutic efficacy or circumvent resistance. Additional EGFR targeted strategies for pancreatic cancer are being developed that may further circumvent mechanisms resistance to EGFR inhibition.

Antibodies, Monoclonal↗
PubMed2007

Pancreatoblastoma.

Pancreatoblastoma (PB), or infantile pancreatic carcinoma, is an extremely rare pancreatic tumor in childhood, comprising 0.5% of pancreatic non-endocrine tumors. Although PB mainly presents during childhood but can also occur in adults. PB tend to be less aggressive in infants and children compared to adults. Children with PB usually present late with upper abdominal pain and many have a palpable mass in the epigastrium. Mechanical obstruction of the upper duodenum and gastric outlet by tumor in the head of the pancreas may be associated with vomiting, jaundice and gastrointestinal bleeding. Histologically, PB is characterized with distinct acinar and squamoid cell differentiation. PB has been associated with alterations in the Wnt signaling pathway and chromosome 11p loss of heterozygosity (LOH), Beckwith-Wiedemann syndrome and familial adenomatous polyposis. The majority of these tumors arise in the head of the pancreas. Alpha-fetoprotein may be elevated in up to 68% of patients with PB. Ultrasound and CT scan may be useful but preoperative diagnosis is often quite difficult. The treatment of choice is complete resection, that may often be curative. The role of adjuvant chemotherapy or radiotherapy is still under discussion due to small number of patients treated as yet. Chemotherapy regimens consisting of cyclophosphamide, etoposide, doxorubicin, and cisplatin have been used in neoadjuvant setting with anecdotal benefit. Prognosis of this rare tumor is good, when resected completely. Prognosis is poorer, when there is metastasis or when it is inoperable. On the whole, PB is regarded to be a curable tumor; hence the clinical diagnosis should be made early. Awareness of this rare tumor of pancreas is essential for early detection and proper management. The author review the clinical presentation, etiology, diagnosis, treatment and prognosis of PB in this presentation.

Adolescent↗
PubMed2007

Panitumumab the first fully human monoclonal antibody: from the bench to the clinic.

Panitumumab (formerly known as ABX-EGF) is the first fully human monoclonal antibody to epidermal growth factor receptor to enter clinical trials for the treatment of solid tumors. Like cetuximab (Erbitux; BMS), it is directed against the extracellular ligand-binding domain of the receptor and results in blockade of the essential downstream signaling pathways that are known to govern apoptosis, proliferation and differentiation of both normal and neoplastic cell types in a wide array of tissues. It has a very high affinity for epidermal growth factor receptor and has been generally well tolerated and associated with very few infusion reactions. As a fully human agent, panitumumab has not been associated with the formation of any antibodies directed against it that has been evidenced by a very reliable pharmacokinetic profile with possible dosing schedules ranging from 1 to 3 weeks. Similar to other agents targeting the epidermal growth factor receptor pathway, a rash has been the primary toxicity and is dose dependent up to 2.5 mg/kg at which dose 100% of all patients have been affected. The anti-tumor activity of panitumumab has been tested in vitro and in vivo, and inhibition of tumor growth has been observed in numerous cancer models, particularly lung, kidney and colorectal. It has been efficacious and well tolerated both as monotherapy and in combination with other chemotherapeutic agents. Several phase I trials, two phase II trials and most recently a phase III trial in pretreated colorectal cancer have been carried out to date. Currently, there is also a randomized phase III trial (Panitumumab Advanced Colorectal Cancer Evaluation Study) investigating the role of panitumumab in the first-line treatment of colorectal cancer. No unfavorable drug-drug interactions have been observed nor has there been any effect on the pharmacokinetics of drugs with which it is being used. Recent progress in preclinical and clinical studies of panitumumab is reviewed.

Animals↗
PubMed2006

Increased prevalence of dihydropyrimidine dehydrogenase deficiency in African-Americans compared with Caucasians.

PURPOSE: African-American patients with colorectal cancer were observed to have increased 5-fluorouracil (5-FU)-associated toxicity (leukopenia and anemia) and decreased overall survival compared with Caucasian patients. One potential source for this disparity may be differences in 5-FU metabolism. Dihydropyrimidine dehydrogenase (DPD), the initial and rate-limiting enzyme of 5-FU catabolism, has previously been shown to have significant interpatient variability in activity. Several studies have linked reduced DPD activity to the development of 5-FU toxicity. Although the distribution of DPD enzyme activity and the frequency of DPD deficiency have been well characterized in the Caucasian population, the distribution of DPD enzyme activity and the frequency of DPD deficiency in the African-American population are unknown. EXPERIMENTAL DESIGN: Healthy African-American (n=149) and Caucasian (n=109) volunteers were evaluated for DPD deficiency using both the [2-(13)C]uracil breath test and peripheral blood mononuclear cell DPD radioassay. RESULTS: African-Americans showed significantly reduced peripheral blood mononuclear cell DPD enzyme activity compared with Caucasians (0.26+/-0.07 and 0.29+/-0.07 nmol/min/mg, respectively; P=0.002). The prevalence of DPD deficiency was 3-fold higher in African-Americans compared with Caucasians (8.0% and 2.8%, respectively; P=0.07). African-American women showed the highest prevalence of DPD deficiency compared with African-American men, Caucasian women, and Caucasian men (12.3%, 4.0%, 3.5%, and 1.9%, respectively). CONCLUSION: These results indicate that African-Americans, particularly African-American women, have significantly reduced DPD enzyme activity compared with Caucasians, which may predispose this population to more 5-FU toxicity.

Adult↗
PubMed2006

Pancreatic cancer: highlights from the 42nd annual meeting of the American Society of Clinical Oncology, 2006.

Despite advances in our understanding of the molecular and genetic basis of pancreatic cancer, the disease remains a clinical challenge. Gemcitabine, the standard chemotherapy for pancreatic cancer, offers modest improvement of tumor-related symptoms and marginal advantage of survival. New approaches, alone and in combination with gemcitabine, are being developed to combat this cancer. Combination chemotherapy trials incorporating gemcitabine, cisplatin, 5-fluorouracil, oxaliplatin, or irinotecan generally show improved outcomes in objective response rates but with little or no improvement in survival in phase III trials. In this article, the author describes the key studies presented at the Annual Meeting of ASCO, held in Atlanta, GA from June 2nd to 6th. The studies discussed here include the following: RTOG 9704 (#4007), FFCD-SFRO study (#4008), meta-analysis of gemcitabine plus cisplatin and gemcitabine plus oxaliplatin vs. gemcitabine alone (GERCOR #4003), and ECOG 6201 (Late Breaking Abstract #4004). Based on the results presented at the annual meeting, it comes to us that patients with locally advanced vs. metastatic pancreatic cancer should be studied separately, better understanding of the biology of pancreatic cancer is mandatory and evaluation of novel agents is crucial. We as oncologist have to change our attitudes towards clinical trials and need to think beyond a trial design such as gemcitabine vs. drug of our choice. Environment within which research is being conducted also has to be changed and last but not the least, access to trials for patients with pancreatic cancer is the key step in the fight against pancreatic cancer.

Adenocarcinoma↗
PubMed2006

Primary pancreatic lymphomas.

Primary pancreatic lymphomas are extremely rare. Clinically, primary pancreatic lymphomas usually present with symptoms of carcinoma of the pancreatic head. Patients with primary pancreatic lymphomas are between 35 and 75 years of age and with a strong male predominance. Common clinical manifestations include abdominal pain, jaundice, acute pancreatitis, small bowel obstruction, and diarrhea. An accurate cytopathologic diagnosis by fine-needle aspiration (FNA) is imperative because the primary treatment is non-surgical. Cytomorphologic features include hypercellularity with discohesive cells with round nuclei, often prominent nucleoli, mitoses, and karyorrhexis. Flow cytometry analysis demonstrates a monoclonal pattern of immunoglobulin light chain expression. FNA coupled with flow cytometry analysis appears to be highly accurate in the diagnosis of primary pancreatic lymphomas. Fluorescence in-situ hybridisation technique has been established its role in the diagnosis of lymphoid malignancies, including primary pancreatic lymphomas. LDH and beta-2 microglobulin are important diagnostic and prognostic tumor markers. The differential diagnoses of primary pancreatic lymphomas include secondary lymphoma, pancreatic endocrine neoplasm, and florid chronic pancreatitis. The role of surgery is limited to the rare occasions when initial FNA and flow cytometry analysis are non-diagnostic. Treatment usually consists of a combination of chemotherapy and radiation therapy, or stem cell transplantation. Primary pancreatic lymphomas has a much better prognosis than adenocarcinoma of the pancreas.

Humans↗
PubMed2006

Pulmonary thromboembolism in AIDS patient with chronic venous insufficiency, pulmonary tuberculosis and breast cancer: a case report and pathophysiology review.

Recent literature reports thrombotic episodes occurring in patients with HIV infection associated with other abnormalities including neoplasms and infections predisposing to a hypercoagulable state. We report a 47-year-old woman who developed pulmonary thromboembolism in association with HIV infection, pulmonary tuberculosis and breast cancer. She was treated with rifampin, isoniazid, pyrazinamide; heparin, phenprocoumon, zidovudine, lamivudine and efavirenz. Acid fast bacilli were visualized in a sputum smear and three months after, Mycobacterium tuberculosis was isolated from lymph node biopsy during a episode of immune reconstitution. The isolated mycobacteria showed sensitivity to all first-line drugs. HIV infection, breast cancer and pulmonary tuberculosis have several mechanisms that induce hypercoagulable state and can lead to thromboembolic complications. Pulmonary thromboembolism in this patient was a diagnostic challenge because of all the other severe diseases that she experienced at the same time.

Acquired Immunodeficiency Syndrome↗
PubMed2006

Radiation recall phenomenon secondary to capecitabine: possible role of thymidine phosphorylase.

BACKGROUND: The first reported case of radiation (XRT) recall related to capecitabine described dermatitis in a previously radiated field in a breast cancer patient (Ortman; JCO). We previously reported the first case of recall syndrome manifesting as diffuse gastritis and duodenitis related to capecitabine with prior XRT with 5-FU in a pancreatic cancer patient (Saif; JARCET). We report here another pancreatic cancer patient with a radiation recall receiving capecitabine following capecitabine-XRT. PATIENTS AND METHODS: From April 2004 to June 2005, 20 patients with locally advanced pancreatic adenocarcinoma were treated with capecitabine 1,600 mg/m2 daily with concomitant radiation (5040cGy) Monday-Friday (weekends off) for a total of 6 weeks, followed by capecitabine 2,000 mg/m2 daily for 14 days every 3 weeks. One male patient with tumor in the neck and body of pancreas and not infiltrating the duodenum dropped hemoglobin to 7.3 g/dl at the end of the ninth week, and melena on rectal examination. Specimen of primary pancreatic ductal adenocarcinoma was obtained via EUS-guided biopsy before starting XRT on day 1 and utilized for RNA extraction. TP mRNA level was determined by real-time quantitative PCR (RT-Q-PCR). RESULTS: Upper endoscopy revealed gastritis consistent with radiation toxicity. Colonoscopy was negative. Transfusion of three units of packed red blood cells (PRBCs) was given. The dose of capecitabine was reduced by 25%. His anemia continued to progress, a CT scan revealed 39% decrease in the tumor size (PR). Analysis of tumor specimen prior to the start of capecitabine-XRT showed TP expression of 183.16 (high). In addition to TP, DPD was 7.40, and TNF-alpha 4,114.56. CONCLUSION: We believe this case to be the second case of radiation recall presenting as diffuse gastritis in a patient receiving capecitabine after previous treatment with XRT. Further studies, including the role of TP are warranted into the pathogenesis of this unique phenomenon.

Aged↗
PubMed2006

Anti-angiogenesis therapy in pancreatic carcinoma.

Pancreatic adenocarcinoma is a leading cause of cancer death in the United States and represents a challenging chemotherapeutic problem. The treatment of advanced pancreatic cancer with gemcitabine has only modest activity with a small survival benefit, and toxicity continues to be a major obstacle. New therapeutic strategies that notably lack cross resistance with established treatment regimens are much needed in pancreatic cancer. One such approach is the pharmacological control of angiogenesis that represents a novel approach to the management of pancreas cancer, since the pathological development of vascular supply is a critical step for tumor growth and may affect its prognosis. Since pancreatic carcinoma show strong tumor neoangiogenesis, overexpression of vascular endothelial growth factor (VEGF), a key mediator of angiogenesis, in pancreatic cancer and consequently are highly vascularized, the role of anti-angiogenic therapies is under exploration at present. Hence, this review covers the summary of the development of anti-angiogenesis as anti-antitumor therapy in pancreatic carcinoma, including matrix-metalloproteinase inhibitors (MMPIs), such as marimastat and BAY 12-9566, anti-VEGF agent, bevacizumab (Avastin, Genentech, South San Francisco, CA, USA), celecoxib (a cyclooxygenase-2 inhibitor), thalidomide and others. Role of markers of angiogenesis in predicting response to therapy is also discussed.

Adenocarcinoma↗
PubMed2006

Dihydropyrimidine dehydrogenase deficiency in an Indian population.

BACKGROUND: Dihydropyrimidine dehydrogenase (DPD) deficiency is prevalent in 3-5% of the Caucasian population; however, the frequency of this pharmacogenetic syndrome in the Indian population and other racial and ethnic groups remains to be elucidated. PATIENTS AND METHODS: We describe an Indian patient who presented to clinic for the treatment of gastric adenocarcinoma with 5-flurouracil (5-FU) therapy who subsequently was diagnosed with DPD deficiency by using the peripheral blood mononuclear cell (PBMC) DPD radioassay. This observation prompted us to examine the data generated from healthy (cancer-free) Indian subjects who were enrolled in a large population study to determine the sensitivity and specificity of the uracil breath test (UraBT) in the detection of DPD deficiency. Thirteen Indian subjects performed the UraBT. UraBT results were confirmed by PBMC DPD radioassay. RESULTS: The Indian cancer patient demonstrated reduced DPD activity (0.11 nmol/min/mg protein) and severe 5-FU toxicities commonly associated with DPD deficiency. Of the 13 Indian subjects [ten men and three women; mean age, 26 years (range: 21-31 years)] enrolled in the UraBT, 12 Indian subjects demonstrated UraBT breath profiles and PBMC DPD activity within the normal range; one Indian subject demonstrated a reduced breath profile and partial DPD deficiency. CONCLUSIONS: DPD deficiency is a pharmacogenetic syndrome which is also present in the Indian population. If undiagnosed, the DPD deficiency can lead to death. Future epidemiological studies would be helpful to determine the prevalence of DPD deficiency among racial and ethnic groups, allowing for the optimization of 5-FU chemotherapy.

Adult↗
PubMed2006

Peripheral neuropathy exacerbation associated with topical 5-fluorouracil.

Peripheral neuropathy secondary to 5-flourouracil and capecitabine (Xeloda) has been reported. We report the first case of exacerbation of peripheral neuropathy related to topical 5-flourouracil (Efudex). A 70-year-old Caucasian male with a history of actinic keratosis for 15 years was treated intermittently with topical application of 5-flourouracil. He also developed sensory peripheral neuropathy around the same time, but extensive work-up disclosed no clear etiology. In early 2005, he developed an exacerbation of his peripheral neuropathy following a 21-day course of topical 5-flourouracil for actinic keratosis, especially pain and parasthesias. Dihydropyrimidine dehydrogenase activity was evaluated in the peripheral mononuclear cells both by radioassay and by [2-C] uracil breath test. Dihydropyrimidine dehydrogenase activity was within the normal range by both methods. Stopping topical 5-flourouracil resolved the symptoms to baseline. Instead of topical 5-flourouracil, topical imiquimod was used which did not exacerbate his neuropathy. He was not re-challenged with topical 5-flourouracil. Topical 5-flourouracil has been known to cause mainly dermatological adverse effects, but systemic effects because of absorption are possible, especially in dihydropyrimidine dehydrogenase-deficient patients. As our patient had no other cause responsible for his neuropathy, the onset of symptoms coincided historically with topical application of 5-flourouracil and the 5-flourouracil usage preceded an exacerbation of sensory symptoms, we conclude that this drug was responsible for his polyneuropathy.

Aged↗
PubMed2006

Skin rash secondary to bevacizumab in a patient with advanced colorectal cancer and relation to response.

Bevacizumab (Avastin) in combination with intravenous 5-fluorouracil-based chemotherapy as first-line as well as second-line treatment of metastatic colorectal cancer improves survival. Although skin rash (type unspecified) has been described in some patients following infusion of bevacizumab, it is not a common toxicity of bevacizumab, while acneiform rash occurs in more than 90% of patients who receive cetuximab (Erbitux), the severity of which appears to be predictive of response. We report a patient with colorectal cancer who developed a rash secondary to bevacizumab that correlated with response. A 40-year-old patient with stage IV colorectal cancer received FOLFOX-4 and bevacizumab, which he tolerated very well except for a skin rash related to bevacizumab. The rash cleared every time bevacizumab was eliminated from the chemotherapy regimen. When use of bevacizumab was resumed, similar rash reappeared. Therefore, we believe that this observation of the rash emergence was linked to bevacizumab administration. The most common toxicities associated with bevacizumab include hypertension, hemorrhage, gastrointestinal perforation, arterial thromboembolism, wound healing and proteinuria. Exfoliative dermatitis and a nonspecific rash have been reported with bevacizumab. This case report, we believe, is the first report of a possible correlation between a rash and a positive drug response associated with bevacizumab, and may initiate further investigation of similar observation.

Adenocarcinoma↗
PubMed2006

Hand-foot syndrome variant in a dihydropyrimidine dehydrogenase-deficient patient treated with capecitabine.

We present a case with dihydropyrimidine dehydrogenase (DPD) deficiency that manifested a variant of hand-foot syndrome (HFS). A 52-year-old man received capecitabine for adjuvant treatment of rectal cancer. On the ninth day of the first cycle, he presented to the clinic with a rash on the dorsum of both hands accompanied by symptoms of pain, erythema, swelling, and desquamation consistent with grade 3 HFS. The palms of his hands and soles of his feet were only tender with no apparent rash or discoloration. Dihydropyrimidine dehydrogenase activity was evaluated by radio assay using peripheral blood mononuclear cells. Dihydropyrimidine dehydrogenase activity was below normal: 0.12 nmol/minute/mg protein. Capecitabine was not resumed, and the rash resolved in 3 weeks with the use of pyridoxine and Udderly Smooth balm. Interestingly, HFS is rarely seen with 5-fluorouracil regimens containing selective DPD-inhibitors. This patient with DPD deficiency manifested a variant of HFS. The pharmacologic basis for the development of HFS in DPD-deficient patients warrants further investigation. Dihydropyrimidine dehydrogenase deficiency, if undiagnosed, can lead to death. In addition to severe to life-threatening toxicities akin to 5-fluorouracil, capecitabine can lead to unusual variants of common toxicities, including HFS, in DPD-deficient patients.

Antimetabolites, Antineoplastic↗
PubMed2005

5-Fluorouracil dose escalation enabled with PN401 (triacetyluridine): toxicity reduction and increased antitumor activity in mice.

PURPOSE: PN401, an oral prodrug of uridine yields more bioavailable uridine than oral administration of uridine itself. PN401 may therefore be useful for permitting dose escalation of 5-fluorouracil (5-FU) with consequent improvements in antitumor efficacy. EXPERIMENTAL DESIGN: Female BALB/c mice (Colon 26 adenocarcinoma) were treated with 5-FU with PN401 to define the MTD, and pharmacokinetic analyses were done. A comparison of 5-FU/PN401 was made to 5-FU/eniluracil (EU) and 5-FU/LV. The best timing of the first dose of PN401 relative to 5-FU was evaluated by administering groups of mice PN401 beginning 2, 24, or 48 h after 5-FU dose. RESULTS: The MTD of 5-FU was 100 mg/kg/week whereas the MTD of 5-FU + PN401 was 200 mg/kg/week. A complete response (CR) of 80% and partial response (PR) of 20% was observed with 5-FU (200 mg/kg) + PN401, CR of 40% and PR of 60% with 5-FU (175 mg/kg) + PN401, PR of 10% with 5-FU (150 mg/kg) + PN401 while no response with 5-FU (100 mg/kg) + PN401. Analysis of 5-FU pharmacokinetics displayed nonlinearity as a function of administered dose in mice. In the comparison study, the best response was achieved with PN401 when compared to EU and LV. Mice that did not receive PN401 died by day 12, while other groups were alive at day 31. The proportion of mice surviving was highest in the group which received PN401 at 2 h followed by 24 and 48 h. CONCLUSIONS: There is a threshold 5-FU dose after which the efficacy is dramatically improved-in mice bearing Colon 26 adenocarcinoma, that threshold is a dose of >150 mg/kg/week, and the increased efficacy correlates with about a fourfold increase in the AUC of 5-FU. PN401 used to rescue mice from the lethal toxicity of 5-FU entails that PN401 can be used as an antidote even when used up to 48 h after a 5-FU overdose.

Acetates↗
PubMed2005

Gastrointestinal bleeding associated with concurrent capecitabine and radiotherapy in patients with pancreatic cancer.

CONTEXT: Capecitabine is currently being evaluated for the treatment of a variety of gastrointestinal malignancies. OBJECTIVE: The aim of this study is to report on the incidence of late gastrointestinal bleeding in patients with pancreatic cancer who received concurrent capecitabine and abdominal irradiation followed by prolonged capecitabine therapy. PATIENTS: We reviewed the medical records of 24 patients (13 female, 11 males; median age of 64.5 years): 22 cases of adenocarcinoma and 2 cases of neuroendocrine carcinoma. Initially, 4 patients underwent surgical resection. Median follow-up was 10.3 months. INTERVENTIONS: Patients received capecitabine (600-800 mg/m2 orally twice daily) with concurrent radiation (50.4-54.0 Gy). Patients who were resected received an additional 2-4 cycles of capecitabine; otherwise, capecitabine was given indefinitely until disease progression occurred. MAIN OUTCOME MEASURE: Incidence of late gastrointestinal bleeding. RESULTS: Three patients developed gastro-intestinal bleeding after concurrent capecitabine and irradiation and 2 of these patients died as a result of this toxicity. CONCLUSIONS: Our study indicates that serious gastrointestinal bleeding is a possible late complication associated with concurrent capecitabine and irradiation therapy for pancreatic cancer followed by additional capecitabine therapy. Caution and close monitoring should therefore be used when continuing capecitabine therapy in this setting.

Adenocarcinoma↗
PubMed2005

Hemolytic-uremic syndrome associated with gemcitabine: a case report and review of literature.

CONTEXT: Hemolytic uremic syndrome is a rare condition compromising the clinical triad of acute renal failure, microangiopathic hemolytic anemia, and thrombocytopenia. Hemolytic uremic syndrome may be associated with a variety of etiologies, and chemotherapeutic agents have also been reported to be associated with hemolytic uremic syndrome, including mitomycin, cisplatin, bleomycin, and most recently gemcitabine. CASE REPORT: A 72-year-old Caucasian male treated with four cycles of gemcitabine at 1,000 mg/m2 developed clinical and laboratory findings compatible with hemolytic uremic syndrome. He developed microangiopathic hemolysis, rapidly declining renal function with proteinuria and hematuria, and renal biopsy revealed thrombotic microangiopathy. Hemodialysis, plasmapheresis, and corticosteroid therapy were utilized but the process ultimately was irreversible. CONCLUSION: With multiple reports of hemolytic uremic syndrome complicating gemcitabine therapy, it is imperative that clinicians heighten their awareness of this potentially lethal complication.

Aged↗
PubMed2005

Impact of ethnicity on outcome in pancreatic carcinoma.

CONTEXT: Ethnicity is an important factor known to impact the biology and outcome of many cancers. In pancreatic cancer, African Americans are thought to have a higher incidence and poorer prognosis than Whites. PATIENTS: A total 645 pancreatic cancer patients were identified in the database, of which, 530 patients were eligible for this study and retained for the statistical analysis. Of the 530 patients, 137 (25.8%) were Blacks, 393 (74.2%) were Whites, 275 (51.9%) were males and 255 (48.1) were females. Ages ranged from 21 to 93 years with values of 62.3+/-13.3 years, 64.2+/-11.6 years, 63.1+/-10.9 and 64.3+/-13.3 (mean+/-SD) for Blacks, Whites, males, and females, respectively. Overall, 132 patients out of 415 (31.8%) were seen in stage I, 61 (14.7%) in stage II, 105 (25.3%) in stage III, 117 (28.2%) in stage IV, while 115 patients (21.7%) had missing stage. RESULTS: There were no significant differences between Blacks and Whites with respect to distributions across stages (P=0.422). Adenocarcinoma was the most common histology in both ethnicities with poor differentiation in 47.4% of Blacks and 57.0% of Whites. Overall, 125 (23.6%) received surgery alone, 54 (10.2%) surgery with chemotherapy, 5 (0.9%) surgery with external radiation therapy, 10 (1.9%) external radiation therapy alone, 68 (12.8%) chemotherapy alone, 58 (10.9%) chemo-external radiation therapy, and 210 (39.6%) no therapy. Overall, only 22 patients survived at 5-yr (4.2%). Median survival was 8.0 months for Blacks (95% CI: 6.4-10.2) and 8.1 months for Whites (95% CI: 7.1-9.7) and there was no significant difference in survival between Blacks and Whites (P=0.971). There were more survivors in females (43/255, 16.9%) than in males (25/275, 9.1%; P=0.009), and females had significantly greater survival times as compared to males (P=0.022). CONCLUSIONS: Pancreatic cancer is a disease of both ethnicities with a slight male predominance among Whites and female predominance among Blacks. We did not find any significant difference in the treatment specific outcome and survival between Blacks and Whites.

Adenocarcinoma↗