This document summarizes the management of urinary bladder cancer. It discusses staging, histopathologic types, and treatment options for non-muscle invasive and muscle invasive bladder cancer as well as metastatic disease. Standard first-line chemotherapy for metastatic bladder cancer includes gemcitabine and cisplatin or MVAC. Newer chemotherapy regimens and agents are also discussed.
Target audience : Oncology fellows and Oncologists.
Four challenging cases of Bladder cancer and managing decisions including latest management principles are discussed here.
Bladder Cancer Diagnostic-Initial Team ProjectSagar Desai
A mini-project to find biomarkers for bladder cancer diagnosis. We narrowed down our list of viable candidates down to three that could be used in combination to provide sensitivity and specificity values greater than 94%. Furthermore, we calculated long-term monitoring and payor costs as well as potential profit.
Target audience : Oncology fellows and Oncologists.
Four challenging cases of Bladder cancer and managing decisions including latest management principles are discussed here.
Bladder Cancer Diagnostic-Initial Team ProjectSagar Desai
A mini-project to find biomarkers for bladder cancer diagnosis. We narrowed down our list of viable candidates down to three that could be used in combination to provide sensitivity and specificity values greater than 94%. Furthermore, we calculated long-term monitoring and payor costs as well as potential profit.
intravesical Gemcitabine in High risk non muscle invasive bladder cancerDr Mayank Mohan Agarwal
Gemcitabine, in conjunction with cisplatin, is well established chemotherapeutic agent for systemic treatment of advanced bladder cancer (urothelial carcinoma). however, its role in high risk NMIBC is controversial.
This presentation describes the chemical properties of gemcitabine (which make it the ideal molecule for intravesical therapy), discusses the role in primary NMIBC, recurrent NMIBC (high risk) and compares its safety and efficacy with intravesical BCG.
Bladder cancer is a disease of urinary bladder in which cells grow abnormally and have the potential to spread to other parts of the body. This is one of four parts of presentations on Bladder cancer. Please do go through the rest of the presentations too.
Bladder cancer is a disease of urinary bladder in which cells grow abnormally and have the potential to spread to other parts of the body. This is one of four parts of presentations on Bladder cancer. Please do go through the rest of the presentations too.
urinary bladder malignancy
incidence
risk factors and pathogenesis
staging of the disease
histopathology
transitional and non transitional cell carcinomas
clinical features
laboratory findings
imaging
molecular markers
treatment options
chemotherapy
radiotherapy
surgery
intravesical Gemcitabine in High risk non muscle invasive bladder cancerDr Mayank Mohan Agarwal
Gemcitabine, in conjunction with cisplatin, is well established chemotherapeutic agent for systemic treatment of advanced bladder cancer (urothelial carcinoma). however, its role in high risk NMIBC is controversial.
This presentation describes the chemical properties of gemcitabine (which make it the ideal molecule for intravesical therapy), discusses the role in primary NMIBC, recurrent NMIBC (high risk) and compares its safety and efficacy with intravesical BCG.
Bladder cancer is a disease of urinary bladder in which cells grow abnormally and have the potential to spread to other parts of the body. This is one of four parts of presentations on Bladder cancer. Please do go through the rest of the presentations too.
Bladder cancer is a disease of urinary bladder in which cells grow abnormally and have the potential to spread to other parts of the body. This is one of four parts of presentations on Bladder cancer. Please do go through the rest of the presentations too.
urinary bladder malignancy
incidence
risk factors and pathogenesis
staging of the disease
histopathology
transitional and non transitional cell carcinomas
clinical features
laboratory findings
imaging
molecular markers
treatment options
chemotherapy
radiotherapy
surgery
This is a powerpoint on Bladder Cancer. Sources are on the last slide of the powepoint! No copy right intended! Enjoy! I hope you learn a lot and I hope you live your life Bladder Cancer free! Also the red words are what I would say during the presentation, basically extra details! So keep that in mind!
-Shelby
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?
H. Khaled - Bladder cancer - State of the art
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2. Management of Urinary Bladder Cancer : State of the Art Hussein M. Khaled Prof. Medical Oncology Vice President for Post graduate Studies and Research Cairo University By:
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4. Ranking of ASIR of Bladder Cancer worldwide rates (Males) 0 10 20 30 40 50 60 70 80 90 100 The Gambia 1.3 Belgium 42.5 Louisiana 16.6 Egypt 26.3 Western Europe Percentiles
15. Non-muscle invasive TCCU Prognostic Factors * PUNLMP: Papillary Urothelial Neoplasm of Low Malignant Potential Low risk tumours Single Ta Low grade or PUNLMP* diameter < 3cm, non-recurrent Intermediate risk tumours Low-grade Ta, or PUNLMP multifocal and/or recurrent low-grade T1 High risk tumours High grade Ta (Gr3), T1 Gr3 , recurrent T1, Cis
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18. Non-muscle invasive TCCU Summary of Therapeutic Sequence & Monitoring Close follow-up is required Non-muscle invasive urothelial tumour Stage Treatment Monitoring Low-risk tumour Complete TUR Cystoscopy 3m, 9m, then annually for 15y (if normal) Intermediate-risk tumour CompleteTUR + local CT or BCG Cystoscopy and cytology 3m, 6m, 12m, then annually for at least 15y High-risk tumour Complete TUR + BCG with maintenance treatment Cystoscopy and cytology Every 3 months (2y) Every 4-6 months (3y), Then annually for 15 years
22. Supervised analysis 55 genes differentially expressed with expression values significantly correlated to survival Columns: Patients Listed according to survival Rows: Genes Listed according to protein function
29. Chemotherapy in metastatic bladder cancer Mead GM et al. Br J Cancer. 1998 C MV vs. MV N 214 patients Median survival 7 months vs. 4.5 months 1-year survival 29% vs. 16% Hazard ratio 0.68
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35. From MVAC to other cisplatin-containing regimens
36. Paclitaxel + Cisplatin in metastatic bladder cancer Dreicer R et al. J Clin Oncol. 2000 Burch PA et al. J Urol. 2000 Murphy BA et al. J Clin Oncol. 1996 Studies (n) Patients (n) OR rate ( % ) CR rate (%) Median survival (m onths ) 3 104 60% 19% 10.6 - 13.0
37. Docetaxel + Cisplatin in metastatic bladder cancer Dimopoulos MA et al. Ann Oncol. 1999 Garcia del Muro X et al. Br J Cancer. 2002 Sengelov L et al. J Clin Oncol. 1998 Studies (n) Patients (n) OR rate ( % ) CR rate (%) Median survival (m onths ) 3 129 55% 17% 8.0 - 13.6
38. Docetaxel + Cisplatin vs. MVAC in metastatic bladder cancer N=220 Bamias A et al. J Clin Oncol. 2004 Drug regimen Overall response Median survival D + C MVAC 37% 54% 9.3 months 14.2 months
39. Paclitaxel + Carboplatin in metastatic bladder cancer Studies (n) Patients (n) OR rate ( % ) CR rate (%) Median survival (m onths ) 6 165 43% 13% 8.5 - 9.5
40. Paclitaxel + Carboplatin vs. MVAC in metastatic bladder cancer N=85 Dreicer R et al. Cancer. 2004 Drug regimen Overall response Median survival PAC + Carbo MVAC 28% 36% 13.8 months 15.4 months
41. Gemcitabine + Cisplatin in metastatic bladder cancer Study Prior CT Patients (n) CR/PR (n) OR% (CR%) Survival (months) von der Maase 1999 N 38 7/9 42% (18%) 12.5 Kaufman 2000 N 46 10/9 41% (22%) 14.3 Moore 1999 N 28 6/10 57% (21%) 13.2 Lorusso 2000 N 54 8/18 48% (15%) 12.5 Wilson 2002 N 20 2/8 50% (10%) NR
42. Randomized phase III study in metastatic bladder cancer T4B N2, N3 M1 GC (203 patients) MVAC (202 patients) Study initiated Nov. 1996 - recruitment completed Sept. 1998
50. Progression-Free Survival Gem/Cis median 7.7 mo 1 Pac/Cis/Gem median 8.8 mo 0.87 (0.74-1.03) Bellmunt J et al. ASCO 2007 Progression-free survival
51. Overall Survival Gem / Cis median 12.8 mo 1 Pac / Cis / Gem median 15.7 mo 0.86 (0.72-1.03) Bellmunt J et al. ASCO 2007 Overall duration of survival
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55. Trials on 2 nd line treatment of TCCU Vinflunine monotherapy in TCCU after failure of a prior platinum-containing regimen Two phase II trials Culine S et al. Br J Cancer. 2006 Vaughn DJ et al. Cancer. 2009 * PS 0 = 320 mg/m²/q3w ** PS 0 with pelvic irradiation and PS 1 = 280 mg/m²/q3w
56. Efficacy results * PS 0 = 320 mg/m²/q3w ** PS 0 with pelvic irradiation and PS 1 = 280 mg/m²/q3w Culine S et al. Br J Cancer. 2006 Vaughn DJ et al. Cancer. 2009 Culine et al. Vaughn et al. Number of treated patients n (%) 51 151 Initial dose (mg/m², q3w) 320 320*/280** Objective Response Rate n (%) 95% CI 9 (17.6) [8.4 - 30.9] 22 (14.6) [9.4 – 21.2] Disease control rate n (%) IRP 95% CI 34 (66.7) [52.1 - 79. 3 ] 86 (56.9) [48,7 - 65] Median Duration of response months IRP 95% CI 9.1 [4.2 - 15.0] 6.0 [5.4 – 9.5] Median PFS months 95% CI 3.0 [2.4-3.8] 2.8 [2.6 - 3.8] Median OS months 95% CI 6.6 [4.8 - 7.6] 8.2 [6.8 – 9.6]
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58. > 3.5 -year follow-up Eur Urol Suppl. 2010;9(2):38 Updated survival analysis - ITT population VFL + BSC arm BSC arm 2.3 months Overall Survival [months]
59. Bladder Guidelines Recommend Vinflunine Use as Second Line Therapy † Based on one good quality RCT ‡ Based on clinical studies of good quality and consistency addressing the specific recommendations and including at least one randomized trial Post failure of a platinum based combination Level 1b recommendation † Recommended as second line therapy after platinum failure
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61. Era of "molecularly targeted therapy" Sorafenib 2006 Sunitinib 2006 Bevacizumab + IFN 2007 Temsirolimus 2007 Everolimus 2008 Sunitinib 2006 Imatinib 2002 Sorafenib 2008 Cetuximab + radiotherapy 2006 Bevacizumab + chemotherapy 2006 Cetuximab + chemotherapy 2008 Erlotinib 2005 Trastuzumab + chemotherapy 2001 Lapatinib + capecitabine 2006 Cetuximab 2007 Panitumumab 2007 Bevacizumab + chemotherapy 2004 Bevacizumab + paclitaxel 2007 HCC GIST RCC NSCLC CRC Breast cancer MM = malignant melanoma - HCC = hepatocellular carcinoma - GIST = gastrointestinal stromal tumour - RCC = renal cell carcinoma - NSCLC = non-small cell lung cancer - CRC = colorectal cancer - IFN = interferon Cetuximab + chemotherapy 2008 Ipilimumab 2010 MM Pazopanib 2009 Head and neck cancer … ERA OF MOLECULAR TARGETED THERAPY
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66. VEGF Trap Treatment Plan Patients receive a dose of VEGF Trap 4 mg/kg IV administered over 1 hour on D1 of each 14 day cycle
93. What happened to bilharziasis and to Bladder Cancer in Egypt in the past three decades?
94. Oral Antibilh. AbdelWahab, 7% El-Khoby, 0.5% Miller, 30% MPH, 45% Scott, 60% THE DECLINE OF PREVALENCE OF S. HEMATOBIUM IN THE NILE DELTA IN 70 YEARS (POPULATION SURVEYS BY URINE ANALYSIS) High dam Anti-Bilh.
95. TIME TREND ANALYSIS OF BLADDER CANCER IN 37 YEARS (NCI, 9843 Pts.) 1970- 1974 1985- 1989 2003- 2007 A B C 3212 3988 2643 Gouda, Mokhtar, Belal & El-Bolkainy, J. Egypt. NCI, 2007 .
96. Bladder cancer Eggs positive 82% 55% 28% 12% THE DECLINE OF BLADDER CANCER & BILHARZIAL ASSOCIATION IN 37 YEARS (NCI – 9843 PATIENTS)
97. Squamous Transitiona l Others 76% 28% 16% 66% 8% 6% THE CHANGE OF HISTOLOGIC PROFILE OF BLADDER CARCINOMA IN 37 YEARS (NCI – 9843 PATIENTS)
98. THE CHANGE OF DEMOGRAPHIC FEATURES OF BLADDER CANCER IN 37 YEARS No. of cases 3212 2643 NCI, Pathology Registry Years 1970-1974 2003-2007 Mean Age 47.4 60.5 M/F ratio 5.4 3.3
109. GEMZAR + Cisplatin in Bilharzial Bladder Cancer NCI - Cairo Treatment Schedule Gemcitabine 1000 mg/m 2 I.V. days 1,8 & 15 Cisplatin 70 mg/m 2 I.V. day 2 Every 28 days
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111. Gemcitabine plus Cisplatin is an active combination for Bilharzial related bladder cancer ( Response rate 54 %), with a moderate toxicity profile European J. Cancer (2000) , 36: s34-s37
120. Egyptian Bladder Cancer Cooperative gp T2b,3,4a N0-2 Bladder Cancer Cystectomy 3 Courses Gem+Cis SD PR CR 3 courses Gem+Cis Cystectomy 3 courses Gem+Cis Cystectomy Radical Radiotherapy
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123. Adjuvant Chemoradiotherapy High Risk Patients (P3b,4a,G3+/-LN+) Radical Cystectomy PORT 4500cGy/3wks/30 F 2 Courses (Gem Cis ) 1000 mg/m2 D1&D8 70 mg /m2 D1 PORT 4500cGy/3wks/30F 2 Courses (Gem Cis ) Same regimen
124. Bilharzial Bladder Cancer Drug Therapy Invasive Tumors Superficial Tumors Advanced, metastatic, and recurrent Invasive operable Single agent phase II trials 1975 now Neoadjuvant Pilot study Phase III trial Combination Chemotherapy phase II trials Epi VCR - Ifo VP16 Gemz – DDP (2) Phase III trial (combination vs single agent) Adjuvant Classic surgery Modified surgery Little experience CT-RT
As introduction , lets begin by an overview of management trends in urothelial carcinomas, which is mainly based on surgical procedures up to the advanced stage, possibly combined with additional treatments such as CT, RT or immune-therapy.
In 2004 the World Health Organisation developed a new grading system for early bladder cancer, which is increasingly being used. This system divides bladder cancers into the following groups Urothelial papilloma - non cancerous (benign) tumour Papillary urothelial neoplasm of low malignant potential (PUNLMP) - slow growing and unlikely to spread Low grade papillary urothelial carcinoma - slow growing and unlikely to spread High grade papillary urothelial carcinoma - more quickly growing and more likely to spread
as above, this is a 13% reduction in the risk of progression/death. This is a relative and not absolute difference and it is incorrect to say 13% improvement. A 13% reduction in the risk of progression/death corresponds to a 15% relative increase in progression/survival. The best way to state this is a 13% reduction in the risk of progression/death. 13% reduction in the relative risk of progression/death Or 15% relative increase in Progression/survival
this is a 14% reduction in the risk of death. This is a relative and not absolute difference and it is incorrect to say 14% improvement. A 14% reduction in the risk of death corresponds to a 16% relative increase in survival. The best way to state this is a 14% reduction in the risk of death. In the design of the study, we were looking for a 22% reduction in the risk of death. 14% Relative reduction in the risk of death. Or 16% relative increase in survival In the study we were looking a 22% reduction in the risk of death
With the introduction of molecular-targeted therapies, cancer outcomes continue to improve. References Bonner JA, et al. N Engl J Med 2006;354:567–78 (Head and neck cancer, cetuximab + radiotherapy) Llovet JM, et al. New Engl J Med 2008;359:378–90 (HCC, sorafenib) Demetri G, et al. N Engl J Med 2002;347:472–80 (GIST, imatinib) Demetri GD, et al. Lancet 2006;368:1329–38 (GIST, sunitinib) Motzer RJ, et al. New Engl J Med 2007;356:115–24 (RCC, sunitinib) Escudier B, et al. Lancet 2007;370:2103–11 (RCC, bevacizumab + IFN) Hudes G, et al. New Engl J Med 2007;356:2271–81 (RCC, temsirolimus) Escudier B, et al. New Engl J Med 2007;356:125–34 (RCC, sorafenib) Motzer RJ, et al. Lancet 2008;372:449–56 (RCC, everolimus) Shepherd FA, et al. N Engl J Med 2005;353:123–32 (NSCLC, erlotinib) Sandler A, et al. N Engl J Med 2006;355:2542– 50 (NSCLC, bevacizumab + chemotherapy) Pirker R, et al. J Clin Oncol 2008;26: suppl; abstr 3 (NSCLC, cetuximab + chemotherapy) Hurwitz H, et al. N Engl J Med 2004;350:2335–42 (CRC, bevacizumab + 5-FU-based chemotherapy Jonker DJ, et al. New Engl J Med 2007;357:2040–8 (CRC, cetuximab) Van Cutsem E, et al. J Clin Oncol 2007;25:1658–64 (CRC, panitumumab) Slamon DJ, et al. N Engl J Med 2001;344:783–92 (Breast cancer, trastuzumab + chemotherapy) Geyer CE, et al. New Engl J Med 2006;355:2733–43 (Breast cancer, lapatinib + capecitabine) Miller K, et al. New Engl J Med 2007;357:2666–76 (Breast cancer, bevacizumab + paclitaxel)