The document discusses when to include the foramen ovale in the target volume for parotid cancer. It notes that:
1. The auriculotemporal nerve provides innervation to the parotid gland and passes through the foramen ovale, warranting its coverage if risk of perineural invasion.
2. For tumors with microscopic or gross perineural invasion, especially adenoid cystic carcinoma, coverage should include the mandibular nerve from the auriculotemporal nerve up to the foramen ovale.
3. The facial nerve communicates with the auriculotemporal nerve near the posterior mandible, so tumors invading the facial nerve may also
1. DR KANHU CHARAN PATRO
M.D, D.N.B[RT], MBA, FICRO, FAROI, PDCR,
CEPC
FEBRUARY 2023 ISSUE/83rd VOLUME
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6. When should I include foramen Ovale in parotid target?
18th JAN 2023/H & N
Huaising C. Ko
BS/PRO/2014
1. The auriculotemporal nerve (a branch of CN V3) provides innervation to the glandular tissue, placing CN
V3 at risk for PNI, therefore warranting coverage of the foramen ovale if appropriate.
2. The auriculotemporal nerve communicates with CN VII near the medial posterior portion of the mandible.
3. For tumors of the parotid gland with microscopic PNI, we consider coverage to the facial nerve up to the
stylomastoid foramen and the parapharyngeal space as the nerve tracks up to the skull base at the internal acoustic
meatus.
4. In those tumors that are of ACC histologic subtype, or feature gross PNI, we suggest additional coverage of the
mandibular nerve from the auriculotemporal nerve up to the foramen ovale
7. When should I include internal acoustic canal in hard palate target?
19th JAN 2023/H & N
Huaising C. Ko
BS/PRO/2014
1. We consider covering tumors of the hard palate
with asymptomatic microscopic PNI to the
maxillary nerve up to the foramen rotundum.
2. Cases that involve gross or clinically evident PNI
or are of adenoid cystic carcinoma (ACC)
histologic subtype are additionally covered for the
facial nerve from the vidian and greater
superficial petrosal nerves up to the internal
acoustic meatus
3. The maxillary nerve tracks proximally up into the
foramen rotundum at the base of skull while the
vidian nerve arises from the greater superficial
petrosal nerve (a branch of CN VII).
4. As the hard palate is a midline structure, we
consider bilateral coverage of the CNs in cases
where both sides could be at risk for harboring
tumor.
5. Innervation to the hard palate is largely supplied
by the greater and lesser palatine nerves, which
are branches of the maxillary nerve (CN V2).
6. From the hard palate, the greater and lesser
palatine nerves enter the bone through the
greater and lesser palatine foramina
8. FIELD CANCERIZATION, SLAUGHTER ET AL,1953
20th JAN 2023/GENERAL
SLAUGHTER ET AL/CANCER/1953
Field cancerization or field effect (also termed field change, field change cancerization, field
carcinogenesis, cancer field effect or premalignant field defect) is a biological process in which large areas
of cells at a tissue surface or within an organ are affected by carcinogenic alterations. The process arises from
exposure to an injurious environment, often over a lengthy period
1. The initial step in field cancerization is associated with various
molecular lesions such as acquired genetic
mutations and epigenetic changes, occurring over a widespread, multi-
focal "field".
2. These initial molecular changes may subsequently progress
to cytologically recognizable premalignant foci of dysplasia, and
eventually to carcinoma in situ (CIS) or cancer.
3. The image of a longitudinally opened colon resection on this page
shows an area of a colon resection that likely has a field cancerization
or field defect. It has one cancer and four premalignant polyps.
4. Field cancerization can occur in any tissue.
5. Prominent examples of field cancerization include premalignant field
defects in head and neck cancer, lung cancer, colorectal cancer,
Barrett's esophagus skin, breast ducts and bladder.
6. Field cancerization has implications for cancer surveillance and
treatment.
7. Despite adequate resection and being histologically normal, the
remaining locoregional tissue has an increased risk for developing
multiple independent cancers, either synchronously or metachronously
10. When should I include foramen ovale in cancer lower lip ?
22nd JAN 2023/H & N
Huaising C. Ko
BS/PRO/2014
1. The lower lip (Fig 8A-D) is largely
innervated by the mental nerve,
which arises from the inferior
alveolar nerve as emerges from
the mental foramen of the
mandible.
2. The inferior alveolar nerve is a
branch of the mandibular nerve
(CN V3) that travels inside the
mandible after entering mandibular
foramen (Fig 8B-B″).
3. The mandibular nerve travels
superiorly following the posterior
border of the masticator space at
the division of the lateral and
medial pterygoid muscles (Fig 8C-
C″).
4. The mandibular nerve enters the
skull at the foramen ovale (Fig 8D-
D″).
11. When should I include hypoglossal canal in ca submandibular gland?
23rd JAN 2023/H & N
Huaising C. Ko
BS/PRO/2014
1. In the case of a large T3 lesion of ACC in the
deep portion of the submandibular gland, with
microscopic PNI coverage of CNs V3 and XII
would be considered based on anatomic
proximity to the primary tumor.
2. Axial computed tomographic (CT) slices of
the submandibular gland and related cranial
nerves (CN). The left column (A-D) depicts
axial CT images of the area of interest, the
middle column (A′-D′) depicts the nerves
contoured on CT images, and the right (A″-
D″) depicts these contours with a clinical
target volume (CTV; shown in teal).
3. The mandibular nerve (CN V3) (shown in
orange), and its branch, the lingual nerve
(shown in yellow), provide innervation to the
submandibular gland and are at risk for
harboring cancer in the setting of perineural
invasion.
4. The hypoglossal nerve (CN XII) (shown in
purple) can also be involved in cancers of the
deep lobe of the submandibular gland.
13. VALVULAR HEART DISEASE IN PEDIATRIC CANCER SURVIVORS
Stefania Chounta
/Green/2023
25th JAN 2023/ PAEDIATRIC
1. FRENCH STUDY
2. The occurrence of a valvular heart disease after
treatment for a childhood cancer was statistically
associated with the mean radiation dose to the
heart as well as the administration of chemotherapy.
3. The dose-effect relationship was better explained by
a quadratic model than a linear: the excess of
relative risk (ERR/Gy) increases much faster when
the mean heart-dose is more than 15 Gy.
4. ERR/Gy increased remarkably with attained age.
5. Higher doses (≥ 40 Gy) to any percentage of the
heart volume and doses 20-40 Gy to >50% of the
heart volume are associated with the occurrence of
a VHD.
6. Doses 5-20 Gy to >50% of the heart volume induce a
marginally non-significant risk (HR: 2.75, CI95%:
[0.92-8.24]), that becomes significant when 90% of
the heart volume is affected (HR= 3.94, CI95%:
[1.15-13.49])
14. THYROID DOSE CONSTRAINTS IN HEAD AND NECK RADIATION
James C.H.
Chow/Green/2023
26th JAN 2023/ H/N
1. Validated 22 dose-volume constraints of the
thyroid gland using long-term endocrine
outcomes of 488 HNC patients.
2. Over a median follow-up period of 6.8 years,
42.0 % of patients developed post-radiation
primary hypothyroidism.
3. Thyroid VS60 had the largest area under time-
dependent ROC curve of 0.698 at 5 years after
radiotherapy.
4. Thyroid VS60 at a cutoff value of 10 cc had the
highest F-score of 0.53.
5. The 5-year hypothyroidism risks of patients with
thyroid VS60 ≥ 10 cc and < 10 cc were 14.7 %
and 38.2 %, respectively.
6. VS60 ≥ 10 cc is a robust constraint that limits
the 5-year primary hypothyroidism risk to less
than 15 % and should be routinely employed
during radiotherapy optimization
15. Brain tumor after radiation exposure from CT examinations of children
and young
MICHAEL HAUPTMANN/LANCET ONCOLGY/2023 27th JAN 2023/ PAEDIATRIC
1. The observed significant dose-response
relationship between CT-related radiation
exposure and brain cancer in this large,
multicentre study with individual dose evaluation
emphasises careful justification of paediatric CTs
and use of doses as low as reasonably possible
2. The European EPI-CT study aims to quantify
cancer risks from CT examinations of children
and young adults. Here, we assess the risk of
brain cancer.
3. A significant linear dose-response relationship
was observed for all brain cancers (ERR per 100
mGy 1·27 [95% CI 0·51–2·69]) and for gliomas
separately (ERR per 100 mGy 1·11 [0·36–2·59]).
4. Results were robust when the start of follow-up
was delayed beyond 5 years and when
participants with possibly previously unreported
cancers were excluded
5. We identified 948 174 individuals, of whom
658 752 (69%) were eligible for our study.
368 721 (56%) of 658 752 participants were male
and 290 031 (44%) were female. During a median
follow-up of 5·6 years (IQR 2·4–10·1), 165 brain
cancers occurred, including 121 (73%) gliomas
16. CLINICAL SPECTRUM AND PLEIOTROPIC NATURE OF CDH1 GERMLINE MUTATIONS
JOANA FIGUEIREDO/CANCER GENETICS/2019 28th JAN 2023/ GENETIC
1. CDH1 encodes E-cadherin, a key protein in adherens junctions.
2. Given that E-cadherin is involved in major cellular processes
such as embryogenesis and maintenance of tissue
architecture, it is no surprise that deleterious effects arise
from its loss of function.
3. E-cadherin is recognised as a tumour suppressor gene, and it is
well established that CDH1 genetic alterations cause diffuse
gastric cancer and lobular breast cancer— the foremost
manifestations of the hereditary diffuse gastric cancer
syndrome.
4. However, in the last decade, evidence has emerged
demonstrating that CDH1 mutations can be associated with
lobular breast cancer and/or several congenital abnormalities,
without any personal or family history of diffuse gastric cancer.
To date, no genotype–phenotype correlations have been
observed.
5. Remarkably, there are reports of mutations affecting the same
nucleotide but inducing distinct clinical outcomes. In this
review, we bring together a comprehensive analysis of CDH1-
associated disorders and germline alterations found in each
trait, providing important insights into the biological
mechanisms underlying E-cadherin’s pleiotropic effects.
6. Ultimately, this knowledge will impact genetic counselling and
will be relevant to the assessment of risk of cancer
development or congenital malformations in CDH1 mutation
carriers.
17. HEREDITARY DIFFUSE GASTRIC CANCER INTERNATIONAL GASTRIC CANCER
LINKAGE CONSORTIUM (IGCLC) GUIDELINES
CHRISTOPH TREESE/CURRENT ONCOLOGY/2022 29th JAN 2023/ GENETIC
18. SAFETY OF SBRT IN RCC – RSR1 STUDY
ARIANE LAPIERRE/PRO/2023 30th JAN 2023/ SBRT
19. Vestibular Schwannoma – SRS vs micro SX - Metanalysis
THOMAS JAKUBEIT/SYSTEMATIC REVIEW/2022 31st JAN 2023/SRS
Our systematic review indicates
that sfSRS has greater benefits
than MR in patients with unilateral
vestibular schwannoma
There was an indication of greater
benefit of sfSRS compared with
MR for facial palsy (OR 0.06, 95%
CI 0.02–0.21, p < 0.001, 2 studies),
hearing function (no pooled
estimate available, 2 studies), and
length of hospital stay
Vertigo
Tinnitus
Facial palsy
20.
21. STAGING OF VESTIBULAR SCHWANNOMA
Apoorva T. Ramaswamy/Neuroimag Clin N Am/2018 2nd FEB 2023/SRS
22. EVALUATION OF SYMPTOM IN VESTIBULAR SCHWANNOMA
Apoorva T. Ramaswamy/Neuroimag Clin N Am/2018 3rd FEB 2023/SRS
23. Differential diagnosis of CP angle tumors
Apoorva T. Ramaswamy/Neuroimag Clin N Am/2018 4th FEB 2023/SRS
24. LIKELIHOOD OF HEARING PRESERVATION FOR SMALL TO
MODERATELY SIZED VESTIBULAR SCHWANNOMAS
Apoorva T. Ramaswamy/Neuroimag Clin N Am/2018 5th FEB 2023/SRS
25. COMPARISONS OF ADVERSE EVENTS VARIOUS ANTIEMETICS
Andrew DeLeon/Pharmacology NotesProc(Bayl Univ Med Cent)/2006 6th FEB 2023/GENERAL
26. SEROTONIN ANTAGONISTS ROUTE AND DOSAGE
Rudolph M Navari/Cancer Management and Research/2009 7th FEB 2023/GENERAL
27. Physiology of chemotherapy induced
emesis
RUDOLPH M NAVARI/BIOCHIMICA ET BIOPHYSICA ACTA/2015 8th FEB 2023/GENERAL
28. DECISION TREE FOR EBRT VS SBRT SPINAL
METS
JACOB ECKSTEIN /RADIATION ONCOLOGY/2021 9th FEB 2023/SBRT
34. ICCD- International Childhood Cancer
Day
Googl
e
15th FEB 2023/PUBLIC
INTERNATIONAL CHILDHOOD CANCER DAY IS OBSERVED ON
FEBRUARY 15 EVERY YEAR AND ALL OVER THE WORLD. THE
DAY RAISES AWARENESS OF CHILDHOOD CANCER AND HONORS
ALL THE CHILDREN AND FAMILIES EXPERIENCING THE
EFFECTS OF THE DISEASE. IT ACKNOWLEDGES THEIR PAIN
AND DIFFICULTIES, GIVING THEM SPACE TO PROCESS AND
GRIEVE.