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The FORDS Manual (pg. 22) states: The first course of treatment includes all methods of treatment recorded in the treatment plan and administered to the patient before disease progression or recurrence. The instructions in the FORDS Manual and clarification from multiple CAnswer Forum posts indicates the planned first course treatment stops following disease progression, even when the first course treatment plan is not altered or changed.

SEER, on the other hand, instructs registrars to do the opposite. The SEER Manual instructs registrars to code all completed treatment given as part of the initial first course treatment plan, even after disease progression, provided the treatment plan is not changed or altered. (See 2016 SEER Manual, Section VII First Course of Therapy, Treatment Timing, Rule 1 and Example 1.)

For consistency in data collection, shouldnt the standard setters use the same guidelines to define first course treatment? Given that the majority of cases are reported to SEER by registrars in CoC facilities, who may not be abstracting treatment modalities that occur after progression, the SEER expectation is likely not able to be performed consistently. Wont this difference in standard setter data collection expectations negatively impact the treatment data reflected on our files?

Bronchial washings were negative. Four lymph nodes were biopsied and found to have metastatic poorly differentiated neuroendocrine carcinoma. The treating oncologist calls it small cell carcinoma, extensive stage, and treats patient with carboplatin and VP-16 (etoposide) The MP/H rule says to take path/cyto from a metastatic site if no pathology/cytology available from the primary site. Is the physician's statement and treatment taken into consideration here?

5/27/02 Transurethral resection of bladder tumor (TURBT)--papillary transitional cell carcinoma, +lamina propria, no muscle invasion. All urine cytologies in 2011 and 2012 (only follow up received) show no malignancy. 3/11/15 Lung fine needle aspirate--poorly differentiated carcinoma consistent with urothelial carcinoma. 4/30/15 Renal pelvis biopsy--low grade papillary urothelial carcinoma, no lamina propria invasion, no muscularis propria invasion.

This terminology is not specifically included in either alternate names list for myelodysplastic syndrome, NOS (9989/3) or refractory anemia with excess blasts (9983/3).

Example: Bone Marrow Biopsy, Final Diagnosis: Consistent with involvement by myelodysplastic syndrome with excess blasts-2 (MDS EB-2).

This specific histology (cribriform-morula variant of papillary thyroid carcinoma) is not found in the ICD-O and is not mentioned in the 2007 MP/H Manual. However, per a web search it appears that this is a distinct type of papillary thyroid carcinoma (http://erc.endocrinology-journals.org/content/24/4/R109.full).

Example: Right lobectomy shows thyroid epithelial neoplasm, pending consultation.

Consultation: Thyroid gland, right lobe: papillary thyroid carcinoma, favor cribriform-morula variant.

Consultation Comment: IHC stains argue against medullary carcinoma. The histologic features of growth patterns and cytologic atypia (with rare grooves and pseudoinclusions) and the immunohistochemical profile support a diagnosis of papillary thyroid carcinoma, favoring the cribriform-morula variant. It is important to note that a significant number of patients with this variant of papillary thyroid carcinoma have been associated with familial adenomatous polyposis syndrome.

Patient had radical resection of pelvic giant cell tumor of bone in August 2012. Final diagnosis clarified that no features to suggest a frankly malignant giant cell tumor were identified.

July 2013 left upper lobe nodules were removed and found to be consistent with multifocal metastatic lung involvement with a previous pelvic giant cell tumor of bone. However, the pathology report comment specifies there are no histological high-grade features to suggest a malignancy:

While SINQ 20091087 may apply, these metastases clearly arrived in the lung by hematogenous spread. The previous SINQ note refers to a case where the implants/metastases can seed the surrounding pelvic and abdominal structures by rupture of the tumor or intraoperative tumor spillage. That type of spread is not quite the same as the current case showing tumor cells leaving the primary tumor/site and travelling through the blood to implant in the lungs.

Discussion: Example: Shave biopsy with superficial spreading melanoma, Breslow 0.25 mm, Clark level II. Excision with no residual melanoma and gross description of specimen size is 4.0 x 1.6 cm skin ellipse excised to a depth of 1.8 cm.

We have differing opinions in our registry.

Opinion 1: We can assume margins are greater than 1 cm based on the excision specimen size when there is no residual tumor on excision and all dimensions of the excision specimen are more than 1 cm. Surgery would be coded in 40s range.

Opinion 2: We should assume the melanoma defect was in the middle of the excision specimen, so for a skin ellipse that is 4.0 x 1.6 cm, there would be a 2 cm and 0.8 cm margin (respectively) from the middle of the specimen, thus margins are not > 1 cm. Surgery would be coded in 30s range.

Patient has only a LUL tumor on imaging. The tumor board initially states, possibly a mixed tumor, likely IIIA SCC and/or IIIA or B small cell. Later, the physician refers to it as "Stage III lung cancer, mixed histology with small cell in the lymph node and squamous cell in the LUL mass." Patient has no further workup and has declined therapy.

Pathology report diagnosis: Urethral lesion: Intraductal carcinoma of the prostate, see microscopic. Clinical Information: Urethral Lesion/Hematura. Microscopic Description: The biopsy shows dilated ductal structures filled with anaplastic epithelium showing areas of comedo-type necrosis. The tumor cells have enlarged nuclei prominent nucleoli and mitoses are identified. Surrounding benign prostatic tissue is also present. Immunostains show that the tumor cells stain for PSA, PSAP, P504s but are negative for GATA-3. The other components of the PIN 4 stain CK5/14 and P63 stain the basal cells surrounding the tumor confirming the intraductal nature of the process. Intraductal carcinoma should not be confused with high grade PIN as the former is usually associated with high grade invasive tumor. Is this C619 and 8500/2?

The patient has a history of CLL/SLL dating back to 2007, but has had progressive disease with development of a new left frontal brain tumor. The brain tumor resection proved CLL/SLL with large cell transformation, but neither the pathologist nor the managing physician called this a Richter transformation, Richter syndrome or provided a diagnosis of DLBCL. However, a large cell transformation of CLL/SLL is a Richter transformation. Can this be accessioned as a new acute neoplasm per Rule M10?