Thyroid cancer reportThyroid cancer report

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

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

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

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

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

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

Ttreatment principle of anaplastic cancer

eradication by complete surgical resection

Followed by concurrent doxorubicin-based

Chemotherapy and RT

Follicular variant of PTC

the clinical behavior is similar to pure

PTC,and completely different from FTC

Bone metastasis of differentiated thyroid cancer

localized one : surgery + 131I or RT

multiple ones : 131I

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

INDICATION for total thyroidectomy:

1.cancer involving two lobes

2.distal metastasis and need 131I therapy

3.LNM in two sides

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

Follow –up:

differentiated thyroid cancer ：

thyroglobulin + 131I,

thyroglobulin + 131I （ - ） In-octreotide ，

FDG-PET （ Tsh )

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

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

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

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

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

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

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

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

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,

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

6.AdhTERTtk:

hTERT: human telomerase reverse transcriptase

To obtain restricted expression of a suicide gene

Only in tumor GCV

gene therapy for anaplastin cancer

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

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

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

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.