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Code sodium iodine (I 131) therapy in Radiation Treatment Modality as code 13 (Radioisotopes, NOS). Code Radiation External Beam Planning Technique as code 88 (not applicable). Do not code if used in diagnostic procedures.

Radioactive I 131 should be coded when given in therapeutic doses (usually 30-50mCi but could be higher in high risk patients). The same agent is used for diagnostic imaging, but the dose is very small (1-3mCi).

We will update SEER*Rx.

Code ATG/Cyclosporine as biological response modifier (BRM)/Immunotherapy as first course of treatment using the current Heme Manual. Based on changes to the 2026 Heme rules for coding treatment, heme and lymphoid neoplasms are now treated differently than Solid Tumors when it comes to treatment failure.

It can be used for treatment of selected MDS cases particularly those with low-risk disease, HLA-DR15 histocompatibility type, bone marrow hypoplasia. Prednisone should not be coded as it is not disease modifying agent in MDS. It is usually given to reduce/treat infusion reactions/serum sickness associated with ATG infusion.

We will update SEER*Rx.

Assign a second primary as Acute Myeloid Leukemia, NOS (9861/3), per Rule M10, the first being polycythemia vera (9950/3). The physician states “consistent with transformation of the patient's known polycythemia vera to acute myeloid leukemia.” This is not the same thing as “Acute myeloid leukemia with myelodysplasia-related changes.”

The Heme DB states:

Do not automatically assign this histology (Acute myeloid leukemia with myelodysplasia-related changes (9895/3) if patient has a history of a myeloproliferative neoplasm (Myelodysplastic Syndrome [MDS], or Myeloproliferative Neoplasm [MPN]). Note: Polycythemia Vera is a Myeloproliferative Neoplasm (MPN). The pathologist must make the diagnosis of being myelodysplasia-related.

Assign 9522/3 (olfactory neuroblastoma) as a single histology to this case based on the initial pathology and managing physician’s diagnosis. World Health Organization Classification Head and Neck Tumors, 5th edition defines olfactory neuroblastoma as a malignant neuroectodermal neoplasm derived from the specialized sensory olfactory neuroepithelium.

Report this ovarian tumor as histology 8442/3. Our subject matter expert, a specialized pathologist who deems this case reportable, advises if a rupture occurs, the presence of borderline tumor cells in peritoneal fluid is considered true tumor spread and malignant. Both ICD-O-3.2 and ICD-O-4 classify this as behavior /1 (Serous borderline tumor, NOS); however, based on the matrix rule, you should be able to update the behavior to /3. If you cannot override or enter it into your software, please contact your vendor.

Cancer PathCHART guidance for 8442/3 in the ovary recommends using 8460/3 (Low-grade serous carcinoma) or 8461/3 (High-grade serous carcinoma). Code 8442/3 should be used only when the grade cannot be determined.

Armour thyroid is listed under "Thyroid" in SEER*Rx and in Appendix C Thyroid Coding Guidelines of the 2026 SEER Program Coding and Staging Manual. Code natural thyroid products as hormonal therapy in papillary, follicular, or oncocytic thyroid carcinoma. Thyroid histology must be known as coding depends on histology. Do not code if it is medullary or anaplastic thyroid carcinoma. If histology is unknown, assign Hormone Therapy as code 99.

In papillary, follicular, and oncocytic carcinoma, natural or synthetic thyroid hormone products have a dual role:

1. Suppression of thyroid stimulating hormone (TSH): This is cancer directed therapy since the tumor cells of the above mentioned morphologies express TSH receptor. TSH is a trophic hormone that can promote tumor growth.

2. Hormonal replacement therapy to treat post-surgical or post-radiation hypothyroidism. C-cells in medullary carcinoma do not express TSH receptor, thus, TSH suppression would not be indicated. However, replacement hormonal therapy with synthetic or natural thyroid hormones post surgery is given to treat the post-surgical hypothyroidism. In operable thyroid anaplastic carcinoma, the goal of levothyroxine therapy is hormone replacement.

The Thyroid Coding Guidelines are being updated to include oncocytic thyroid cancer in the 2027 release of the SEER Manual.

Assign primary site as colon, NOS (C18.9) when the only information about the diagnosis you have is "colorectal cancer."

We consulted with a subject matter expert who believes that colon, NOS is closest to being correct and that rectosigmoid is not appropriate.

If further information becomes available through further workup and/or treatment, update the primary site as appropriate.

We will add clarification to the 2027 SEER Manual, Appendix C, Colon Coding Guidelines.

Do not code Thyrogen as hormone therapy when given as a stimulating agent in I-131 therapy. The therapeutic agent is I-131.

The Thyrogen/thyroid stimulating hormone (TSH) is sensitizing the gland to absorb more I-131. Thyrogen/TSH is a trophic hormone so it can cause growth of cancer cells. Thyroid hormones are given in follicular and papillary thyroid cancers to suppress TSH. Although Thyrogen can promote cancer growth its use in Thyrogen stimulated I-131 radioactive therapy is justified (benefits exceed the risk), since the use is short (2 days) and the high amount of I-131 would kill cancer cells in addition to majority of thyroid tissue.

We will update the Thyrogen entry in SEER*Rx and clarify in the next release of the SEER manual, Appendix C Coding Guidelines for Thyroid.

Do not report a case of atypical lobular hyperplasia of the breast until/unless it is definitively diagnosed as LCIS or another reportable neoplasm. WHO defines this as a non-invasive lobular neoplasia. Atypical lobular hyperplasia does not have an ICD-O code and is not equivalent to in situ.

Report this case of spindle cell neoplasm with CLCN6::BRAF fusion based on the physician diagnosis of spindle cell sarcoma (8801/3).

CLCN6::BRAF is described as rare kinase fusion identified in a subset of spindle cell sarcomas. It is part of an expanding group of BRAF fusions in spindle cell neoplasms though it not extensively detailed in the literature. Along with other BRAF fusions, CLCN6::BRAF represents a potential oncogenic driver for targeted therapy.