Dr. Brijesh Maheshwari presented on neuroblastoma. Key points:
1. Neuroblastoma originates from neural crest cells and most commonly affects children under 5, often presenting with abdominal pain or mass.
2. Staging systems include International Neuroblastoma Staging System (INSS) and International Neuroblastoma Risk Group (INRG) system. Over half of cases present with metastatic disease.
3. Prognostic factors include age at diagnosis, tumor biology like MYCN amplification, and response to initial treatment. A multidisciplinary approach is used including surgery, chemotherapy, radiation, stem cell transplant, and immunotherapy.
Hypofractionation in early breast cancer is no more a research scholars topic. Multiple studies with robust data have proven its utility. It may hold an important role in many countries with constrained resources. This is a short presentation incorporating important completed and ongoing trials. Feel free to use this.
Accelerated partial breast irradiation is an alternative to whole breast irradiation in carcinoma breast patients Post breast conserving surgery with equivalent outcome, less duration & less burden on the patient.
Overview about evolution of the term Oligometastases,the paradigm and various states of oligometastases,treat options ,clinical trials and relevance in current clinical practice
Hypofractionation in early breast cancer is no more a research scholars topic. Multiple studies with robust data have proven its utility. It may hold an important role in many countries with constrained resources. This is a short presentation incorporating important completed and ongoing trials. Feel free to use this.
Accelerated partial breast irradiation is an alternative to whole breast irradiation in carcinoma breast patients Post breast conserving surgery with equivalent outcome, less duration & less burden on the patient.
Overview about evolution of the term Oligometastases,the paradigm and various states of oligometastases,treat options ,clinical trials and relevance in current clinical practice
Neuroblastoma is the most common cancer in babies and the third-most common cancer in children after leukemia and brain cancer, proper diagnosis, treatment must be done in appropriate time. As it a fatal condition psychosocial support is most important for patient and family.
complete information (pictural) of carcinoma urinary bladder from anatomy to management(Investigations, Surgery ,Radiotherapy, Chemotherapy) including NCCN, trials
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
Follow us on: Pinterest
Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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
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
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
2. Introduction-
Neuroblast oma
Neural crest cells Tumor
When foetus is at 1st week of development, special
cells called neurocrest cells start migrating along the
spine.
As they migrate, they differentiate into neurons of the
sympathetic chain on either side of the entire spinal
cord.
In the lumbar region they differentiate into the cells of
the Adrenal medulla
Sympathetic chain and adrenal medulla forms the
sympathetic nervous system.
3. Physiology
When the sympathetic system is stimulated,
the sympathetic nervous system releases
epinephrine and nor epinephrine.
These hormones binds to receptors of
various organs like blood vessels, heart and
lungs ready for the action.
When the hormones are no longer needed,
they are enzymatically converted into the
two metabolites Homovanillic acid (HVA)
and Vanillymandelic acid(VMA).
4. Epidemiology -
Most common extra-cranial solid tumour of childhood
90% of cases are diagnosed by age 5.
Very rare in people over the age of 10 years.
The average age at diagnosis “18 months”→in sporadic cases.
The average age at diagnosis “9 months”→in familial cases.
Neuroblastoma is slightly more common among boys compared to
girls (ratio 1.9 to 1).
Over half of the children present with metastatic disease
Arise from cells of the neural crest that form the adrenal medulla
and sympathetic ganglia
5. Etiology
In Neuroblastoma, some neuro crest cells in sympathetic chain or adrenal medulla
don’t differentiate properly that ultimately going to form a tumor; but mechanism is
unknown.
Nevertheless, it has been linked to have genetic tendency of inheritance
Autosomal dominant pattern of inheritance
Hereditary neuroblastoma predisposition gene chromosome 16p12-13
Associated with mutations-
Oncogene –
N-Myc amplification (seen in roughly 20%)
ALK gene fusion
Tumor suppressor genes -
PHOX2B
Deletion of the short arm of chromosome 1
6. Risk factor-
Genetic factors: The majority of neuroblastomas are sporadic .
• Amplification of the N-MYC.
• Deletion of the short arm of chromosome 1.
• A higher incidence of NB has been suggested in girls with
• Turner syndrome,
• Hirschsprung's disease,
• congenital central hypoventilation, and
• neurofibromatosis type 1
Maternal factors: (COG---Folate deficiency)
• Congenital abnormalities
• Opiate consumption
• Gestational diabetes mellitus
• Folate deficiency
7. Familial Neuroblastoma: in 1 to 2 % of cases.
• These cases appear to be inherited in an autosomal dominant pattern
with incomplete penetrance.
• Inherited cases usually present at an earlier age than sporadic cases
• Familial predisposition may be conferred through disruption of a locus
at 16p12-13.
Others :
• Exposure to chemicals during pregnancy
• Smoking
• Alcohol
• use of hormones and fertility.
8. Sites
Adrenal medulla (30% to 40%)
Para-spinal ganglia lower thoracic and
abdominal (25%)
Posterior mediastinum (19%)
Pelvic ganglia (2%)
Cervical ganglia (1%)
Metastases
Bone, bone marrow, liver, lymph node and
skin
Lung and central nervous system are rare
sites of involvement
9. 70 % HAVE METASTASIS AT TIME OF
PRESENTATION
LYMPH NODE
BONE
BONE MARROW
SKIN
LIVER
10. Clinical presentation
Signs or symptoms caused by the main tumor.
Signs or symptoms caused by cancer spread to other parts of the body.
Signs or symptoms associated with paraneoplastic manifestation.
11. Constitutional symptoms- weight loss, anorexia,
malaise and fever.
In the abdomen-
Pain –
Most common presenting symptoms
Due to local spread &/or metastatic disease.
Respiratory distress: esp. in young infants with massive
hepatomegaly
Abdominal lump.
Severe watery diarrhoea and hypokalemia (due to secretion of
vasoactive intestinal peptide by tumor) (Kerner-Morrison
syndrome)
In the chest-
cough, dyspnea and other breathing problems.
12. In the neck
Cervical sympathetic involvement with Horner’s syndrome (ptosis,
miosis, anhidrosis)
Others due to spread of tumor
Spinal cord compression with paralysis of lower extremities (dumbbell
shaped tumor)
Eye- Tumor infiltration of the per orbital bones, typically unilateral, can
cause the characteristic per orbital ecchymosis ("raccoon eyes"), ptosis,
and proptosis
Skin- bluish tinge of skin (Blueberry muffin sign)
Cytopenia (marrow involvement)
Due to paraneoplastic
Random eye muscle jerks due to anti-neural antibodies (Opsoclonus
myoclonus syndrome)
The characteristic symptoms of OMA are rapid, dancing eye movements,
rhythmic jerking (myoclonus) involving limbs or trunk, and/or ataxia.
13. Diagnosis
Primary disease
• CECT or CEMRI - tumor extent,
lymph node mets, vessel
encasement, intraspinal
extension
• Tissue diagnosis -Biopsy/
FNAC
• MYCN amplification- IHC or
FISH
• Urine catecholamines and
their metabolites
Metastatic evaluation
• I-123 MIBG scan –
differentiate viable tumor
from scar
• Radionuclide bone scan
(If no MIBG uptake)
• CECT abdomen or USG
abdomen – Liver mets
• Bilateral BM aspiration
and biopsy-metastatic
deposit.
14. MRI is more accurate than CT for
detection of stage 4 disease(sn 83%
and 43% respectively)
16. MIBG(Metaiodobenzylguanidine)
Metaiodobenzylguanidine (MIBG) is a guanethidine
derivative and an analogue of norepinephrine.
MIBG is labelled with I131 or I123
Used to image primary and metastatic sites of
neuroblastoma
Thyroid gland must be protected
Simutaneous administration of nonradioactive
iodine (eg.Potassium iodide)
Can be use higher doses for treatment (for high
risk or recurrence disease)
Post-induction response for st.4 – prognostic
marker EFS, survival
17.
18.
19. Pathology
Classic subtypes
Neuroblastoma
Ganglioneuroblastoma increasing differentiation
Ganglioneuroma
Neuroblastoma
It is the most undifferentiated-appearing and aggressive of this family
of tumors.
Because of the lack of Schwannian cells, these tumors are called
"stroma-poor".
Under light microscopy, they appear as a monotonous collection of
“small, round, blue cells”.
“Homer-Wright pseudorosettes”- consist of eosinophilic
neutrophils surrounded by neuroblasts .
20. IHC-
NSE & CG -A(levels correlate with more advanced disease and worse
prognosis)
NB84(highly sensitive; less specific)
CD56(diffuse positivity indicates more blastic component)
S100(diffuse positivity indicates better differentiation)
Negative for:
CD45,CD99,EMA,CK,Desmin,Myogenin
21.
22.
23. Staging
Most commonly used system is the International
Neuroblastoma Staging System (INSS) based on clinical,
radiographic, and surgical findings.
Others staging systems include:
–Evans and D’Angio (1971)
–St. Jude/Pediatric Oncology Group (POG)
24. International Neuroblastoma Staging
System (INSS)
Localized tumour with complete
gross excision with out microscopic
residual disease, LN negative
It’s a post-surgery staging system
25. STAGE 2A
Localized tumour with incomplete gross
excision. Representative ipsilateral non
adherent LN negative
Stage 2B
Localized tumour with or with out complete
gross excision, ipsilateral non adherent LN
positive
26. Unresectable unilateral tumour crossing
the midline , localiszd unilateral tumour
with contralateral LN involvement or
midline tumour with bilateral extention by
infiltration (unresectable ) or by LN
involvement.
27. Any primary tumour with
dissemination to distant lymph
nodes, bone ,bone marrow,
liver , skin or other organs
Localized primary tumour as
defined for stage 1, 2A, 2B with
dissemination limited to skin, liver
and or bone marrow. ( limited to
infants < 1 year of age.
28. Evans and D’Angio
Stage I—tumor confined to organ or structure of origin
Stage II—tumor extending in continuity beyond organ or structure of origin, but
not crossing midline. Regional lymph nodes on ipsilateral side may be
involved.
Stage III—tumor extending in continuity beyond midline. Regional lymph
nodes may be involved bilaterally
Stage IV—remote disease involving skeleton, bone marrow, soft tissue, and
Distant lymph node groups
Stage IV-S—patients who would otherwise be stage I or II, but who have remote
disease confined to liver, skin, or bone marrow (without radiographic evidence of
bone mets on complete skeletal survey)
29. Pediatric Oncology Group
Stage A—complete gross resection of primary tumor, with or without
microscopic residual. Intra cavitary lymph nodes not adhered to and removed
with primary tumor, histologically free of tumor. If primary tumor in abdomen or
pelvis, liver histologically free of tumor
Stage B—grossly unresected primary tumor. Nodes and liver same as stage A
Stage C—complete or incomplete resection of primary tumor. Intracavitary
nodes not adhered to primary tumor histologically positive for tumor. Liver as in
stage A
Stage D—any dissemination of disease beyond intra cavitary notes (i.e., extra
cavitary nodes, liver, skin, bone marrow, bone)
Stage DS—infants <1 yr with stage IVS disease.
30. International neuroblastoma risk
group
L1 Localized tumor, not involving vital structures as defined by the list of image-
defined risk factors (IDRF); confined to one body compartment.
L2 Loco regional tumor with presence of one or more IDRFs
M Distant metastatic disease
Ms Metastatic disease in children younger than 18 months with metastases
confined to skin, liver, and/or bone marrow (bone marrow involvement should be
limited to < 10% of total nucleated cells on smears or biopsy).
31. Pathology
–Shimada system (old)
–International Neuroblastoma Pathology Committee (new, updated Shimada)
Biology
–MYCN gene (most prognostic)
–1p and 11q deletion
–17q gains
–DNA ploidy
Staging
–Multiple older surgical staging systems have fallen out of favor
–Current (1993) Post-op INSS: Stages 1, 2A, 2B, 3, 4, 4S
–Pre-op INRG: Stages L1, L2, M, MS
Age
–<18 mo = favorable
–> 5 years = unfavorable
Prognostic factors
36. Management
Surgery
Chemotherapy
Radiation therapy
High dose chemotherapy/radiotherapy and stem cell
transplant(HDC/SCT rescue)
Retinoid therapy/Immunotherapy
37. Resectable stage 1 or 2:
Surgery alone 5yr os 95 – 99%
Symptomatic OR <50% resection OR progression after surgery:
Chemotherapy x 2 – 4 cycles and surgery, 5yr os 99%
Asymptomatic AND <1 yr AND MYCN non-amplifed:
Observation alone
Favorable biology - no adjuvant therapy
Unfavorable biology - 6- 12 weeks of chemo
Adjuvant chemo and RT has not improved the outcome.
LOW RISK GROUP(INSS Stage 1,2 or 3 with negative nodes.
38. INTERMEDIATE RISK GROUP
Complete surgical
resection
Followed by
adjuvant
chemotherapy
12 – 24 weeks
Unresectable
cases, 5 cycles of
chemo
Second look
surgery
39. In older children with lymph node mets, adjuvant radiation therapy to
primary and regional lymph nodes has improved disease free and overall
survival rates.
After second look surgery-
Radiation therapy was given to gross viable residual tumour on second look
surgery.
Children age 12 – 24 months received 24 Gy in 1.5 Gy per fraction.
Older children received 30 Gy in 1.5 Gy per fraction.
Target volume includes viable microscopic or gross residual tumour
determined by CT , MRI or MIBG scan with 2 cm margins
40. •Favourable histology:
Chemotherapy x 4 cycles and surgery, 5yr os 98%
•Unfavourable histology:
Chemotherapy x 8 cycles and surgery, 5yr os 93%
•Life/organ threatening with slow response to chemo:
Radiation
44. INDUCTION
Dose – intense VAC/ Etoposide+Cisplatinum x 6 – 7 cycles OR
Dose- intense Topotecan + Cyclophosphamide x 2 then VAC/EC x 4 cycles
LOCAL THERAPY
Surgery or Radiation (if indicated)
CONSOLIDATION
Chemo x 1-2 cycles
High Dose Melphalan + Busulfan and Autologous Stem Cell transplant
MAINTENANCE
Dinutuximab + GM-CSF + Interleukin2 x 5 cycles
Isotretinoin x 6 cycles
5yr EFS 66% Maintenance therapy is biological and immunotherapy targeting minimal
residual disease.(Mrd)
13-cis-retinoic acid is given as monthly 14 days cycle for 6 months
Dinutuximab + GM-CSF + interleukin2 x 5 cycles monthly
45. EBRTin large primary entails irradiation of large volume normaltissue. IORT
Treatment of high risk area at time of resection
Critical structures manipulated away from RTfield
High radiation dosedelivered
RTdose – 7-16 Gy
RTmodality – electron or brachytherapy Achieves 85-100% local
control with GTR.
Local failure higher in patients with sub totalresection
IORT
46. Radiotherapy
Neuroblastoma is a radiosensitive tumor.
Uses-
Local control
stage IV or bulky stage III tumors*(Matthayet al, 1989; Castleberry
1991; Evans et al, 1996)
Important role in palliative management of patients with end stage
symptomatic disease.
Dose- 15 and 30 Gy
Intra operative radiation therapy-unresectable disease
47.
48.
49. Palliative RT
Incurable disease
Relief from pain and functional impairment (bonemets) Palliation of
hepatomegaly in Stage4S
Dose fractionation
Daily fraction 2-8.5 Gyand total dose of 4-30Gy
Small fields – 16-20Gy in 4-5# and large fields – 20-30Gy in2-3Gy/# Preterminal case–
6-8Gy in single fraction
50. Iodine-131 MIBG therapy
May be used for stage III or IV neuroblastoma with MIBG-avid lesions at diagnostic
I-123 MIBG or I-131 MIBG scintigraphy.
Generally incorporated after surgery as high dose treatments (12-18 mCi/kg) with
stem cell rescue.
Contraindication
Renal failure
GFR less than 30 mL/min.
51. Complication
Scoliosis: up to 25% according to retrospective study with 58pt
Dose > 17.5Gy are significant
Audiological sequelae due to platinum
Ovarian dysfunction
Hypothyroid: MIBG or neck EBRT
Second malignancy
52. 1) Desmoplastic small-round-cell tumour
2) PNET
3) Ewing's Sarcoma
4) Neuroblastoma
5) Medulloblastoma
6) Rhabdomyosarcoma
7) Synovial sarcoma
8) Carcinoid tumor
9) Mesothelioma
10) Small cell lung cancer
11) Wilms' tumour
12) Retinoblastoma
13) Small-cell lymphoma
14) Hepatoblastoma (anaplastic form)
15) Merkel cell carcinoma
16) Mesenchymal chondrosarcoma
Mnemonic- PM Had
MRND, Was a
MESS done by
MRCS
SMALL, ROUND, BLUE CELLS – Differential Diagnosis