Thyroid cancer report. Operation extent: primary site To differentiated thyroid cancer 1.one lobe...
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Transcript of Thyroid cancer report. Operation extent: primary site To differentiated thyroid cancer 1.one lobe...
![Page 1: Thyroid cancer report. Operation extent: primary site To differentiated thyroid cancer 1.one lobe invovled: lobectomy + isthmusectomy 2.two lobes invovled:preserve.](https://reader035.fdocuments.net/reader035/viewer/2022062715/56649db55503460f94aa6d8a/html5/thumbnails/1.jpg)
Thyroid cancer reportThyroid cancer report
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Operation extent: primary site
To differentiated thyroid cancer
1.one lobe invovled: lobectomy + isthmusectomy
2.two lobes invovled:preserve small part of inferior or superior part
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Postoperative management of differentiated thyroid cancer:
1.131I ablation and thyroid hormone suppretion
2.external radiation for residual disease
3.Detecting thyroglobulin and 131I for followup
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Prophylactic thyroidectomy in multile endocrine neoplasia:
Ret proto-oncogene ,located on chromosome 10q11.2,
Mutation at exon 10.11,codon634 mutation for MEN2A FMTC, Prophylactic thyroidectomy at the age of 4-6 years
Mutation at exon 16,codon 918 mutation for
MEN2B, Prophylactic thyroidectomy by the age of one year
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Treatment principle of MTC:
1.clinicallly evident MTC:total thyroidectomy
primary tumor >1CM and central nodes positive,ipsilateral neck dissection
2. Prophylactic contralateral neck dissection
When primary tumor is bilateral and there is
extensive lymphadenopathy and MEN2B
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3.postoperative radiation for residual disease
4. Prophylactic thyroidectomy for heredital MTC
5.elevated basal or stimulated plasma calcitonin
Level and intrathyroidal nodule on ultrasound
a total thyroidectomy and central neck dissection should be done
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6.persistent or recurrent MTC should have a complete thyroidectomy and bilateral central
and nek dissection
7.bone metastasis should be resected if possible,RT for unresected one
8.localized pulmonary metastasis should be resected
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Ttreatment principle of anaplastic cancer
eradication by complete surgical resection
Followed by concurrent doxorubicin-based
Chemotherapy and RT
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Follicular variant of PTC
the clinical behavior is similar to pure
PTC,and completely different from FTC
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Bone metastasis of differentiated thyroid cancer
localized one : surgery + 131I or RT
multiple ones : 131I
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Treatment of brain matastases from thyroid cancer
1.solitary one :surgery,radiosurgery when high risk for surgery
2.multiple lesions: whole brain radiation
3.radioactive iodine therapy when the lesions can take iodine , cerebral edema
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INDICATION for total thyroidectomy:
1.cancer involving two lobes
2.distal metastasis and need 131I therapy
3.LNM in two sides
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Treatment of laryngotracheal invasion by well differentiated thyroid cancer:
Local shaving-off, partial laryngotracheal resection with SCM myoperiosteal flap, sleeve
tracheal resection,complete laryngectomy
Naked clearance can have good result,RT for
residual one
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Follow –up:
differentiated thyroid cancer :
thyroglobulin + 131I,
thyroglobulin + 131I ( - ) In-octreotide ,
FDG-PET ( Tsh )
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Either basal Tg level is high or TgAb increases, 131I is needed
Tg mesurement should be after thyroxine
Withdrawl or rhTsh stimulation
rhTsh is suggested for patients who do not respond to hormone withdrawl or cannot tolerate hypothyroidism
Tg>2mg/L is sufficient sensitive
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Tg mRNA in blood is more sensitive
maker for metastatic disease than Tg
And is unaffected by anti-Tg antibodies
No need for thyroid withdrawl and Tsh
stimulation
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Sentinel LN in thyroid cancer:
More sensitivity and spectivity
LNM are of debatable prognostic value
SLN appears less than promissing
Residual LNM is associated with local recurrence whereas distant metastasis is correlared with poorer survival rates
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Thyroid neoplasm after radiation during childhood or adolecence
Incidence :33%,1/3 of these lesions are malignent
Dose-response relation was linear until the highest dose (>1000cGY)
Interval : 6-30 years
The majority in a nonaggressive fashion
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Dedifferentiation of differentiated cancer
Those with metastasis ,1/3 arede differentiaed
Some makers:
1.P53:promte patients into lower grade of Dedifferentiation
2.p16INK4A : hypermethylation of promotor region is a frequent and an early event during thyroid carcinogenesis and is associated with tumor progression and dedifferetiation
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3.Cyclin G2: a cyclin negatively dregulating cell cycle progession
lack of Cyclin G2 malignant transformation of PTC
4.KAL1 :a metastasis suppressor gene ,ralated to the progression of PTC
5.COX2 : up-regulation may contribute predominantly in the early phase of PTC progression
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6.IL-4 ,IL-10: increase Bcl-2 Bcl-xl levels
promote progression and resistance to
chemotherapy ,new theraputic targets for the
treatment of thyroid cancer
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Other markers:
1.CD44v6:inherence molecular
Participate in infiltration and metastasis
poor prognosis
2.VEGF-C: promote proliferation of
Lymphatic ,high expression indicates high LNM, gene therapy
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3.CD10:a membrane-bound zinc metalloproteinase
CD10 was not detected in normal thyroid tissue ,benign lesions and pure PTC
High expression in FTC and Follicular variant
of PTC
4.Id-1:member of Id helix-loop-helix proteins
Key regulators of cell growth and differentiation
Overexpressed in PTC,
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5.Gadd45: Gadd45 fammily proteins have been implicated in a variety of growth-regulatory mechanism .
significantly lower lever in anaplastin cancer
adenovirus-mediated reexpression of Gadd45gamma
significantly inhibited prolification of anaplastin cancercells-------gene therapy
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6.AdhTERTtk:
hTERT: human telomerase reverse transcriptase
To obtain restricted expression of a suicide gene
Only in tumor GCV
gene therapy for anaplastin cancer
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7.Ras-Raf-MEK-MAPK pathway:
the pathway transmits a mitogenic signal to
the nucleus, and activation of the pathway
is thought to Promote uncontrolled cell
division
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8. HS90 (heat shock protein):
plays a critical role in tumor cell growth and survival
Geldanamycin: a specific inhibitor,
9.p70S6K and Akt:
are kinases downstream of PI3K,
activted in the majority of PTC promote
progression by stimulating cell proliferation and
preventing apoptosis
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10.r-PTPeta(rat tyrosine phosphatase):
Ad-r-PTP
overexpression of r-PTPeta significantly inhibit
The growth thyroid cancer lines
11.NIS and TPO:
combination of NIS and TPO gene are transfected into thyroid cancer cells ,to increase
131I absorbtion
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12.RA:
inhibit tumor cell proliferation and induce
differetiation
13.TRAIL:
TNF-related apoptosis –inducing ligand
significant anticancer activity and acceptable
toxity to be used as a novel therapy for thyroid
Cancer.