• RECOMMENDATION 51 of the American Thyroid Association
  • RAI remnant ablation is not routinely recommended after thyroidectomy for ATA low-risk DTC patients:
    • Consideration of specific features of the individual patient that could modulate recurrence risk, disease follow-up implications, and patient preferences are relevant to RAI decision-making
  • RAI remnant ablation is not routinely recommended after lobectomy or total thyroidectomy for patients with unifocal papillary microcarcinoma, in the absence of other adverse features.
  • RAI remnant ablation is not routinely recommended after thyroidectomy for patients with multifocal papillary microcarcinoma in absence of other adverse features:
    • Consideration of specific features of the individual patient that could modulate recurrence risk, disease follow-up implications, and patient preferences are relevant to RAI decision-making
  • RAI adjuvant therapy should be considered after total thyroidectomy in ATA intermediate-risk level DTC patients
  • RAI adjuvant therapy is routinely recommended after total thyroidectomy for ATA high risk DTC patients

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The benefit of chemotherapy among women with early-stage, hormone-receptor positive breast cancers has become largely determinant on the use of gene expression profiles, including Oncotype DX, MammaPrint, and PAM50. Oncotype DX score is a 21-gene assay that uses RT-PCR to calculate recurrence risk using a scoring system from 0 to 100, and categorizes women into low, intermediate, and high risk of recurrence based on pre-specified cut points. MammaPrint is a 70-gene assay performed with microarray, and classifies tumors as having good vs poor prognostic signatures. PAM50 tests 50 classifier genes and categorizes women by intrinsic subtypes including luminal A, luminal B, HER2-enriched, basal-like and normal-like. Adjuvant! Online is an online program that uses standard clinicopathologic variables to estimate survival for breast cancer patients treated by local therapy alone and the survival and disease-free survival benefit gained by the addition of systemic adjuvant therapy.

• The 21-gene recurrence score assay (Oncotype DX):
  • Is a reverse-transcriptase-polymerase-chain-reaction assay of:
    • 16 prospectively selected genes and 5 reference genes
  • Analysis is performed in:
    • Paraffin-embedded tumor tissue
  • This assay was developed from:
    • NSABP B-14 and validated with data and specimens from NSABP B-20
  • It estimates the 10-year risk of distant recurrence:
    • By categorizing results into:
      • Low-risk (RS< 18) group
      • Intermediate-risk (RS 18 to 30) group
      • High-risk (RS > 30) groups
  • A low recurrence score (RS < 18):
    • Predicts little benefit of chemotherapy
• The 21-gene recurrence score assay:
  • Is proven to be prognostic for women with:
    • Node-negative
    • ER-positive breast cancer:
      • Treated with tamoxifen
• Retrospective data obtained via optional tumor banking:
  • In accordance with the SWOG 8814 trial:
    • Which demonstrated postmenopausal women:
      • With node-positive, ER-positive tumors:
        • Achieved superior survival when:
          • Cyclophosphamide, doxorubicin, and fluorouracil:
            • Was given before tamoxifen
  • The SWOG 8814 trial:
    • Allowed for retrospective assessment of recurrence score on DFS by treatment group
    • Analysis demonstrated the recurrence score results:
      • To be both prognostic and predictive of benefit:
        • To adjuvant chemotherapy:
          • As there was no added benefit to adjuvant systemic chemotherapy:
            • In women with low recurrence scores and
            • There was an improvement of DFS:
              • In those with high recurrence scores
  • These hypothesis-generating results:
    • Serve as preliminary basis for the RxPonder trial:
      • Which is currently enrolling as a phase III trial
      • Randomizing women with hormone receptor-positive and HER2-negative breast cancer involving 1 to 3 lymph nodes and a 21-gene assay recurrence score of 25 or less to:
        • Endocrine therapy alone versus chemotherapy followed by endocrine therapy
  • The 21-gene recurrence score:
    • Is not used in patients with HER2-positive breast cancer
• In women with hormone receptor positive (HR+), HER2-negative early breast cancer:
  • The 21-gene signature score provides prognostic information:
    • That is independent of clinical and pathological features
  • A high score (on a scale of 0 to 100):
    • Indicates a higher rate of distant recurrence
    • And is predictive of chemotherapy benefit
• The prospective Trial Assigning Individualized Options for Treatment (TAILORx):
  • Showed that endocrine therapy alone was non-inferior to adjuvant chemotherapy plus endocrine (chemoendocrine) therapy:
    • In women with HR+, HER2-negative, axillary node-negative breast cancer and a 21-gene recurrence score of 11 to 25
    • An exploratory analysis indicated some benefit of chemotherapy in women 50 years of age or younger:
      • Who had a recurrence score of 16 to 25:
        • In this analysis there was a:
          • Small (~1.6%) chemotherapy benefit in distant disease-free survival for patients with recurrence score results from 16 to 20
          • Modest (~6.5%) chemotherapy benefit for patients with recurrence score results from 21 to 25
• References:
  • Paik S, Shak S, Tang G, et al. A multigene assay to predict recurrence of tamoxifen-treated, node-negative breast cancer. N Engl J Med. 2004;351(27):2817-2826.
  • Paik S, Tang G, Shak S, et al. Gene expression and benefit of chemotherapy in women with node-negative, estrogen receptor-positive breast cancer. J Clin Oncol. 2006;24(23):3726-3734.
  • Albain KS, Barlow WE, Shak S, et al. Prognostic and predictive value of the 21-gene recurrence score assay in postmenopausal women with node-positive, oestrogen-receptor-positive breast cancer on chemotherapy: a retrospective analysis of a randomised trial. Lancet Oncol. 2010;11(1):55-65.
  • Ramsey SD, Barlow WE, Gonzalez-Angulo AM, et al. Integrating comparative effectiveness design elements and endpoints into a phase III, randomized clinical trial (SWOG S1007) evaluating oncotypeDX-guided management for women with breast cancer involving lymph nodes. Contemp Clin Trials. 2013;34(1):1-9.
  • Sparano JA, Gray RJ, Ravdin PM, Makower DF, Pritchard KI, Albain KS, et al. Clinical and genomic risk to guide the use of adjuvant therapy for breast cancer. New Engl J Med. 2019;380(25):2395-2405.
  • Sparano JA, Gray RJ, Makower DF, Pritchard KI, Albain KS, Hayes DF, et al. Adjuvant chemotherapy guided by a 21-gene expression assay in breast cancer. New Engl J Med. 2018;379(2):111-121.

#Arrangoiz #CancerSurgeon #BreastSurgeon #BreastCancer #SurgicalOncologist #OncotypeDx #CASO #CenterforAdvancedSurgicalOncology

Epidemiology 

• Invasive lobular carcinoma (ILC) is the second most common histologic form of breast cancer:Comprising 5% to 15% of invasive tumors.
• ILC is pathologically distinct from the much more common invasive ductal carcinoma (IDC):With a unique clinical biology and pathogenesis and resultant implications for diagnosis and treatment.  
• The mean age at diagnosis of ILC is 57 years.
• Demonstrated risk factors include:Age at menarche (younger that 12 years)Age at first birth (older than 30 years)
  • Hormone therapy:Emphasizing the role of estrogen exposure in disease pathogenesis, which is also observed in most IDCs but shows a more pronounced association in ILC.
• ILC also displays an increased propensity for multifocal / multicentric presentation.
• The incidence of ILC in the Western world over the past decades has corresponded to trends in the use of hormone replacement therapies:With a sharp increase between 1975 and 2000 and a decline between 2000 and 2004:But now with an increasing incidence since 2005 with an unclear etiology.
• Hereditary ILC is rare but may be seen as a secondary tumor in families with hereditary diffuse gastric cancer syndrome:Caused by a germline mutation in the tumor suppressor CDH1 gene.
• ILC otherwise accounts for a small minority of the breast cancers associated with known breast cancer susceptibility genes:Comprising less than 5% of breast cancers in patients with BRCA1 or TP53 mutations and less than 10% of breast cancers in those with BRCA2 mutations.

Molecular Basics and Pathogenesis

• Classic ILC is characterized by discohesive cells that infiltrate the breast stroma in a distinctive single-file (Indian-file) pattern, with a limited host inflammatory response:

• Several variant (non-classic) forms of ILC have also been described, distinguished by:Morphology:Dispersed
  • • Alveolar
    • Solid
    • Trabecular
    • Mixed
  • Cytology:PleomorphicApocrine
    • Histiocytoid
    • Signet ring
    • Tubulolobular
• Over 90% of ILCs are estrogen receptor (ER) positive, and at the level of the transcriptome, the majority of ILCs are classified as luminal A:This proportion is observed to be slightly lower in more aggressive ILC variants.
• HER-2 overexpression is rare:Seen in 3% to 5% of classic ILCs:Although it is more frequent in up to 10% of ILC variants:Particularly the pleomorphic subgroup, and recurrent ILCs: The more aggressive biology of the pleomorphic subgroup renders it a unique clinical entity, shown to present at a more advanced stage and more frequently metastasize.
• The tumor biology of ILCs, as with all breast cancers, is of focal importance in both surgical and systemic treatment, as well as long-term outcomes.
• Loss of E-cadherin expression is the most consistently reported hallmark feature of ILC:Seen in 80% to 90% of cases, and is believed to play an early and important role in disease pathogenesis.

• E-cadherin dysregulation originates from mutations in the CDH1 gene on chromosome 16q22.1:Reported to occur at a frequency ranging from 30% to 80% in ILC.
• E-cadherin is a calcium-dependent transmembrane protein that forms a crucial component of adherens-type junctions between epithelial cells, the loss of which predisposes to neoplastic proliferation.2 However, E-cadherin positivity does not, by itself, exclude a lobular neoplasm, and not all ILCs harbor CDH1 gene mutations. Several other novel mutations have recently been identified as more frequent in ILC compared with IDC by comprehensive molecular profiling of 817 breast tumors in The Cancer Genome Analysis (TCGA) study, seen both when comparing all ILCs with IDCs and when limiting comparison with luminal A samples. When comparing all cancers, alterations more frequently seen in ILC included CDH1 (63% in ILC versus 2% in IDC), P1K3CA (48% versus 33%), FOXA1 (7% versus 2%), RUNX1 (10% versus 3%), and TBX3 (9% versus 2%), respectively. Conversely, GATA3 mutations were enriched in IDC (5% in ILC versus 13% in IDC). Importantly, when the analysis was limited to luminal A samples only, several alterations remained significantly more common among luminal A ILCs versus luminal A IDCs, as summarized here

• Patients with triple negative breast cancer who only achieve a partial response to neoadjuvant chemotherapy (have residual disease):
  • Failure to achieve pathologic complete response (pCR):
    • Is associated with poorer prognosis, particularly for triple negative breast cancer
• In the CREATE-X trial:
  • 910 patients with HER2-negative residual invasive breast cancer after neoadjuvant chemotherapy:
    • Were randomized to receive standard post surgical treatment with capecitabine or control
  • Adjuvant capecitabine resulted in:
    • Improved disease-free survival and overall survival;
      • With the bulk of the benefit seen only in the patients with triple negative disease
  • Based on this study:
    • Adjuvant capecitabine can be considered for patients with triple negative breast cancer and residual disease after neoadjuvant chemotherapy
• References
  • Cortazar P, Zhang L, Untch M, Mehta K, Costantino JP, Wolmark N, et al. Pathological complete response and long-term clinical benefit in breast cancer: the CTNeoBC pooled analysis. Lancet. 2014;384(9938):164-172.
  • Masuda N, Lee S-J, Ohtani S, Im YH, Lee ES, Yokota I, et al. Adjuvant Capecitabine for breast cancer after preoperative chemotherapy. New Engl J Med. 2017;376(22):2147-2159.

• There are two main groups of diffuse breast cancers:
  • That present as large areas of architectural distortion on the mammogram:
    • Neoductgenesis
    • Diffusely infiltrating carcinoma:
      • Which makes up approximately 5% of all breast cancers
• When the tumor is e-cadherin negative:
  • It is usually called invasive “lobular” carcinoma
• When it is e-cadherin positive:
  • It is called infiltrating “ductal” carcinoma
• The designation based on e-cadherin staining is arbitrary:
  • Because the behavior of diffusely invasive carcinoma:
    • Is the same regardless of the staining
• Lacking calcifications and a central tumor mass:
  • These cancers are notoriously difficult to perceive on mammogram:
    • Even when they are large and palpable or when they occur in fatty involuted breasts:
      • However, the associated connective tissue response:
        • Makes this type of cancer quite visible with ultrasound
• In contrast to diffusely infiltrating cancers:
  • Circular (Image 1) and spiculated (Image 2):
    • Tumors arising in the terminal ductal lobular units (TDLU) have:
      • Bulging, convex contours protruding into the adipose tissue
• The solid variety of infiltrating lobular carcinoma:
  • Most probably arises within the TDLU:
    • Has a circular / oval shape on breast imaging (Images 3)

Image 1: Lobulated spherical tumor mass

Image 2: Multifocal stellate invasive breast cancer

Image 3: Mammographic, MRI and pathologic images of the solid form of invasive lobular

• There are two other variants of invasive lobular carcinoma that arise in the TDLUs:
  • The tubulolobular variant:
    •  Is either a unifocal or multifocal spiculated lesion on the mammogram (Image 5)

Image 4: Mammogram and large format histology of a multifocal tubulolobular breast

• The alveolar type of invasive lobular carcinoma:
  • Is usually mammographically occult;
    • Or it can be seen as a subtle, asymmetric density (Image 5)

Image 5: Mammogram and large format histology alveolar type invasive lobular carcinoma

• The various forms of invasive lobular carcinoma that develop in the TDLUs and present as localized lesions:
  • Have a significantly better prognosis than the diffusely infiltrating type breast cancer
• Complex sclerosing lesions:
  • Present mammographically as non-palpable architectural distortion with no central tumor mass and lucent radiating structures, the so called “black star”:
    • As opposed to cancers originating from the TDLU:
      • Which have a dense central tumor mass surrounded by radiopaque spiculation, giving the impression of looking at a “white star
• Malignant phyllodes tumors:
  • Present as large, high density masses:
    • The borders may be circumscribed or ill defined
• Fat necrosis:
  • Also presents as a hypoechoic, high-density mass

• References
• Tot T. Diffuse invasive breast carcinoma of no special type. Virchows Arch. 2016;468(2):199-206.
• Tabár L, Dean PB. Teaching Atlas of Mammography. New York, NY: Thieme; 2011.
• sity mass.

• Tamoxifen:
  • Is indicated for premenopausal patients with:
    • Node-negative, hormone receptor–positive, HER2-negative breast cancer with low-risk recurrence scores
  • Is a selective estrogen receptor modulator (SERM):
    • With antiestrogenic activity in breast tissue:
      • Reducing epithelial cell proliferation
• Hot flashes are one of the most common and bothersome side effects of tamoxifen:
  • Up to 80% of women prescribed tamoxifen complain of hot flashes:
    • About 30% rate them as severe
  • Premenopausal women have a greater increase in hot flashes after starting tamoxifen compared with perimenopausal or postmenopausal women
  • Hot flashes are believed to be due to a central nervous system antiestrogenic effect:
    • Causing thermoregulatory dysfunction
  • Additionally, some data suggest that polymorphisms in drug metabolizing enzymes (cytochrome P450 enzyme, CYP2D6):
    • Decrease the conversion of tamoxifen to its most active metabolite (endoxifen):
      • They may influence the likelihood of tamoxifen-related hot flashes
    • Co administration of drugs that inhibit the activity of CYP2D6:
      • Such as the selective serotonin reuptake inhibitors (SSRIs):
        • Can reduce tamoxifen-related hot flashes
        • Among SSRIs, there is a gradient of potency for inhibition of CYP2D6:
          • For example, paroxetine and fluoxetine are strong CYP2D6 inhibitors, while sertraline and duloxetine are moderate inhibitors.
          • While the strong CYP2D6 inhibitors have the potential to adversely affect drug efficacy, the data to suggest that this issue decreases tamoxifen effect are very weak
          • Venlafaxine is a weak CYP2D6 inhibitor with proven efficacy against hot flashes without risk of significantly interfering with tamoxifen metabolism
• Black cohosh:
  • Is a substance with purported efficacy treating menopausal symptoms:
    • It is not FDA regulated with reported rare incidence of hepatotoxicity
  • Its use would be contraindicated in a patient on tamoxifen:
    • As it may interfere with CYP2D6 activity
• References:
• Aiello Bowles EJ, Boudreau DM, Chubak J, Yu O, Fujii M, Chestnut J, Buist DS. Patient-reported discontinuation of endocrine therapy and related adverse effects among women with early-stage breast cancer. J Oncol Pract. 2012;8(6):e149-e157.

• Ramaswami R, Villarreal MD, Pitta DM, Carpenter JS, Stebbing J, Kalesan B. Venlafaxine in management of hot flashes in women with breast cancer: a systematic review and meta-analysis. Breast Cancer Res Treat. 2015;152(2):231-237.
• Johns C, Seav SM, Dominick SA, Gorman JR, Li H, Natarajan L, Mao JJ, et al. Informing hot flash treatment decisions for breast cancer survivors: a systematic review of randomized trials comparing active interventions. Breast Cancer Res Treat. 2016;156(3):415-426.

#Arrangoiz #BreastSurgeon #CancerSurgeon #SurgicalOncologist #BreastCancer #Tamoxifen #Hotflashes #EndocrineTherapy #CASO #CenterforAdvancedSurgicalOncology

👉Treatment for thyroid cancer used to be a one size fits all

👉New guidelines have allowed physicians to take a more evidence based / personalized approach and include the patient in the decision-making process

👉That’s the way I like to approach this disease process in my patients

👉Classically, thyroid cancer was treated by removing the entire thyroid gland

👉This has significantly changed from that management option to a very evidenced based / individualized management that not only depends on the type of thyroid cancer but also depends on the size of the thyroid cancer and if it has any other aggressive features

👉One option for treating minimally invasive papillary thyroid cancer is active surveillance in very selected cases

👉Another option is surgery, either a thyroid lobectomy va total thyroidectomy

They also said to make sure you get information about all eventual outcomes.

👉70% to 80% of nodules are benign

👉Also the survival rate of most thyroid cancers is in excess of 90%

#Arrangoiz #ThyroidSurgeon #HeadandNeckSurgeon

• Chromosomal rearrangements:
  • Were the first oncogenic events identified in PTC:
    • Encompassing the rearranged during transfection (RET) proto-oncogene:
      • Which arises from a paracentric inversion of chromosome 10
    • In nearly 20% of PTC the RET fusion proteins (the RET / PTC family) seem to have an oncogenic role:
      • With the RET / PTC 1, RET / PTC 2, and RET / PTC 3 representing the vast majority of cases
  • The NTRK 1 and the MET proto-oncogene may be overexpressed and / or amplified
• Evidence also suggests that some molecules that physiologically regulate the growth of the thyrocytes:
  • Such as interleukin-1 and interleukin-8, or other cytokines (eg, insulin-like growth factor 1, transforming growth factor beta, epidermal growth factor):
    • Could play a role in the pathogenesis of this cancer
• Mutation in the BRAF gene resulting in the BRAF V600E protein is prominent in PTC:
  • Mathur et al, in a single-institution study reported higher rates of BRAF V600E mutations in PTC from 1991 to 2005:
    • Proposing that this may be contributing to the rise in rates of thyroid cancer
  • The BRAF V600E mutation is related with aggressive clinicopathological characteristics of PTC, including:
    • Lymph node metastasis, extrathyroidal invasion, and loss of radioiodine avidity:
      • Which may lead to failure of radioiodine treatment and disease recurrence
• The thyroid gland is very sensitive to the effects of ionizing radiation, both accidental and medical exposure to ionizing radiation has been linked to increased risk for thyroid cancer. Around 7% of individuals exposed to the atomic bombs in Japan developed thyroid cancers. The inhabitants, especially children, who lived in Ukraine during the Chernobyl nuclear accident have higher risk of developing PTC [28-30]. It has been documented that PTC in patients who have been exposed to radiation from the Chernobyl accident could be easily distinguished from sporadic PTC in patients with no history of radiation exposure, on the basis of gene expression profiles involving seven genes (ie, SFRP1, MMP1, ESM1, KRTAP2-1, COL13A1, BAALC, PAGE1).

From 1920 to 1960, therapeutic irradiation was used to treat tumors and benign conditions, including acne; excessive facial hair; tuberculosis in the neck; fungus diseases of the scalp; sore throats; chronic coughs; and enlargement of the thymus, tonsils, and adenoids. Approximately 5% to 10% of individuals who were treated with head and neck irradiation for such disorders developed thyroid cancer after a latency period of 30 to 50 years.

The greater exposure to diagnostic radiation, particularly computed tomography, is a potential culprit for the increased incidence of PTC. Individuals who receive radiotherapy for certain types of head and neck cancer, especially during childhood, may have an increased risk of developing thyroid cancer. Factors that heighten the risk for developing PTC after exposure to radiation include female gender, radiation for childhood cancer, and a family history of thyroid cancer.

There is some small evidence that polybrominated diphenyl ethers (PBDEs), that are flame retardants, that may be found in electrical appliances, plastics, televisions, computers, building supplies, foams, carpets, and upholstery, could possibly contribute to the development of thyroid cancer. PBDEs and their metabolites have a structural similarity to thyroxine and can accumulate in tissues. These compounds have been shown to be endocrine disrupters, with thyroid and estrogen effects being the most common. PBDEs have been shown to have increased oncogenic potential in other tissues which has made them a desirable candidate for additional research in thyroid cancer pathogenesis.

Obesity has repeatedly been cited as a possible etiologic factor in the pathogenesis of thyroid cancer and has been postulated to be a possible origin of the increase incidence of this disease worldwide. Undeniably, being overweight and obesity have been associated with an increased risk of developing numerous malignancies, including thyroid, breast, colorectal, kidney, and endometrial cancers. In the United States from 1995 to 2015, one out of every six PTC and two thirds of PTC greater than 4 cm in size have been linked to being overweight or obesity, based on an analysis of data from three large national US databases. Kitahara et al projected that the total relative risk for PTC was 1.26 for persons who are overweight (body mass index [BMI] 25 to 29 kg/m2) and 1.30 for those who are obese (BMI ≥ 30  kg/m2), compared with persons with normal-weight BMI (18.5 to 24.9 kg/m2). The risk in PTCs greater than 4 cm in size was nearly 3-fold higher (hazard ratio [HR] = 2.93, 95% CI 1.25-6.87) with overweight individuals, and more than 5-fold higher (HR = 5.42, 95% CI 2.24-13.1) in obese individuals compared with normal-weight individuals. A study by Leitzmann et al, found that obese adults had a nearly 40% higher risk for developing thyroid cancer when compared with normal-weight individuals. More research is needed to define the exact role of obesity in the development of thyroid cancer, particularly as the incidence of obesity continues to climb throughout the world. 

Most thyroid cancers are sporadic in nature; nonetheless, roughly 5% of non-medullary thyroid cancers are hereditary. These hereditary cases have been divided into two groups: those tumors associated with a familial cancer syndromes, such as Cowden’s disease, familial adenomatous polyposis (FAP), and its variant Gardner’s syndrome, Carney’s complex type 1, and Werner’s syndrome, and those with thyroid neoplasms as the primary feature such as familial non-medullary thyroid cancer (FNMTC). Particularly FAP is associated with an elevated risk of developing a rare variant of PTC called cribriform morula variant of PTC (CMV-PTC). In a study by Uchino et al, of 129 patients with FAP who underwent screening with cervical ultrasound identified 11 cases of PTC, eight of which were CMV-PTC. All the patients with CMV-PTC were women 35 years of age or younger. 

FNMTC is defined by the presence of three or more first-degree relatives with well-differentiated thyroid cancer. When only two family members are affected only 38% will have FNMTC. When three or more family members are affected there is a 96% likelihood of having FNMTC [47]. The pattern of inheritance is autosomal dominant with incomplete penetrance. Individuals with FNMTC will have a more aggressive biology compared to their sporadic counterparts. 

Numerous articles have shown a connection between iodine deficiency and thyroid cancer [49]. Various other ailments have been linked as predisposing factors to PTC, including oral contraceptive use, benign thyroid nodules, late menarche, and late age at first birth. Smoking appears to be associated with a decreased risk of thyroid cancer.

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Epidemiology

• The American Cancer Society’s most recent estimates for thyroid cancer incidence in the United States for 2021 are 44,280 new cases of thyroid cancer (12,150 in men and 32,130 in women) and approximately 2,200 deaths from thyroid cancer (1,050 men and 1,150 women).
• The highest incidence of thyroid carcinomas in the world is found among female Chinese residents of Hawaii.
• The rate of new cases of thyroid cancer was 15.7 per 100,000 men and women per year. The death rate was 0.5 per 100,000 men and women per year. These rates are age-adjusted and based on 2013 to 2017 cases and 2014 to 2018 death.
• Roughly 1.3% of men and women will be diagnosed with thyroid cancer at some point during their lifetime, based on 2015 to 2017 data.
• In 2017, there were an estimated 859,838 people living with thyroid cancer in the United States.
• Thyroid cancer develops in individuals of all ages but is most often seen in persons aged 45 to 54, with a median age at diagnosis is 51 years.
• In the younger population, PTC tends to occur more often than follicular carcinoma, with a peak in patients aged 30 to 50 years.
• Approximately 67% of thyroid cancers are localized (confined to the primary site), 28% have spread to regional lymph nodes, and 4% had metastasized to distant sites.
• The 5-year relative survival for localized thyroid cancer is 99.9%, for patients with regional metastasis is 98.3% and with distant metastasis is 54.9%.

#Arrangoiz #CancerSurgeon #ThyroidSurgeon #HeadandNeckSurgeon #SurgicalOncologist #ThyroidCancer #PapillaryThyroidCancer #PTC #CASO #CenterforAdvancedSurgicalOncology