Neuroendocrine secretory protein-55 (NESP-55), the latest addition to the chromogranin family, is a product of a genomically imprinted gene transcribed exclusively from the maternal allele. Initial studies have shown it to have a less widespread distribution than that of chromogranin A in normal tissues. It has also been suggested that NESP-55 may be a marker of neuroendocrine tumors differentiating toward the adrenal chromaffin and pancreatic islet cells. Metastatic gastrointestinal and pulmonary carcinoids may occasionally be difficult to distinguish from pancreatic endocrine tumors (PETs) and pheochromocytomas on morphologic grounds alone. We studied neuroendocrine tumors from these sites to see if NESP-55 expression could reliably discriminate pulmonary and gastrointestinal carcinoids from neuroendocrine tumors arising in the pancreas or the adrenal medulla. Sixty-three neuroendocrine tumors positive for one or more immunohistochemical marker of neuroendocrine differentiation (chromogranin A, chromogranin B, synaptophysin, secretogranin II, neuron-specific enolase) were selected for the study and consisted of 34 typical carcinoids (15 pulmonary, 11 ileal, 4 gastric, and 4 rectal), 19 PETs, and 10 pheochromocytomas (4 sporadic, 3 MEN-2, 2 neurofibromatosis type 1, and 1 VHL). All cases were stained for NESP-55 after microwave antigen retrieval using a rabbit polyclonal antibody at a dilution of 1:1000. Sections of normal adrenal medulla were used as positive controls for NESP-55 staining. Negative controls consisted of omission of primary antibody and replacement with normal rabbit serum at an equivalent concentration. NESP-55 immunoreactivity was seen as brown finely granular cytoplasmic staining with prominent perinuclear accentuation. All gastric and ileal carcinoids studied were completely negative for NESP-55. One of four rectal and 1 of 15 pulmonary carcinoids showed focal positivity for it in less than 5% of tumor cells. In contrast, all 10 pheochromocytomas and 14 of 19 PETs showed strong immunohistochemical staining in a variable proportion of tumor cells. Diffuse positivity (>75% of tumor cells) was seen in 6 of 14 PETs and 8 of 10 pheochromocytomas. Our results indicate that, in contrast to the other granins, NESP-55 reactivity is restricted to endocrine tumors of the pancreas and the adrenal medulla. Immunohistochemical expression of NESP-55 may thus be useful in assigning a pancreatic or adrenal origin to metastatic endocrine tumors of unknown origin.

Patient: Female, 67Final Diagnosis: Breast angiosarcomaSymptoms: Skin lesionMedication: —Clinical Procedure: SurgerySpecialty: OncologyObjective:Unusual clinical courseBackground:Radiation-associated breast angiosarcoma is a rare clinical entity that is thought to be increasing in incidence.Case Report:Here we present the case of a 67-year-old female with a history of left breast invasive ductal carcinoma who received breast conserving surgery and radiation therapy eight years ago. She then presented with a painless mild skin discoloration of the left breast that had been present for over one year. Mammograms and ultra-sounds were normal. A punch biopsy and a subsequent excisional biopsy revealed the diagnosis of angiosarcoma. The patient was treated with mastectomy and had no subsequent recurrences.Conclusions:The long-term clinical surveillance for all patients who receive breast conservation surgery is recommended and a high degree of suspicion should be exercised in view of potential atypical presentations of this disease.

Background and Aims Data on adequacy of EUS guided biopsies using different tissue acquisition techniques and fine needle aspiration needle designs have been inconclusive. Data on newer fine needle biopsy (FNB) needles are scarce. This study compared the performance of 3 acquisition techniques and 2 fine needle biopsy designs in solid pancreatic lesions. Methods Single-center, randomized, pilot clinical trial (Trial registration number NCT03264092). Patients undergoing EUS biopsy of pancreatic lesions were randomized to 1 of 3 acquisition techniques (dry suction, wet suction, slow pull) and 1 of 2 22G FNB needle designs. The primary outcome was specimen cellularity. Secondary outcomes included blood contamination and number of passes needed for diagnosis. Results A total of 52 (35.3%), 49 (33.3%) and 46 (31.3%) specimens were obtained with slow pull, dry suction and wet suction, respectively. A total of 56 (38%) and 91 (62%) specimens were obtained with each needle, respectively. No difference in cellularity scores was identified by technique (3.28 vs 3.55 vs 2.94; p = 0.081) or needle type (3.45 vs 3.15; p = 0.19). The same was true for blood contamination and diagnostic pass. A diagnosis was reached after 3 passes in 51 patients (93%). Histological diagnosis was possible in 45 specimens (82%). No severe adverse events occurred. Conclusions Cellularity of pancreatic specimens obtained with FNB needles via EUS was not influenced by technique and needle design. Three passes were enough to obtain a histological diagnosis in most patients. Larger clinical trials are required to validate the results of this study.

Background The Texas/Chihuahua (US/Mexico) border is a medically underserved region with many reported barriers for health care access. Although Hispanic ethnicity is associated with health disparities for many different diseases, the population‐based estimates of incidence and survival for patients with blood cancer along the border are unknown. The authors hypothesized that Hispanic ethnicity and border proximity is associated with poor blood cancer outcomes. Methods Data from the Texas Cancer Registry (1995‐2016) were used to investigate the primary exposures of patient ethnicity (Hispanic vs non‐Hispanic) and geographic location (border vs non‐border). Other confounders and covariates included sex, age, year of diagnosis, rurality, insurance status, poverty indicators, and comorbidities. The Mantel‐Haenszel method and Cox regression analyses were used to determine adjusted effects of ethnicity and border proximity on the relative risk (RR) and survival of patients with different blood cancer types. Results Hispanic patients were diagnosed at a younger age than non‐Hispanic patients and presented with increased comorbidities. Whereas non‐Hispanics had a higher incidence of developing blood cancer compared with Hispanics overall, Hispanics demonstrated a higher incidence of acute lymphoblastic leukemia (RR, 1.92; 95% CI, 1.79‐2.08; P < .001) with worse outcomes. Hispanics from the Texas/Chihuahua border demonstrated a higher incidence of chronic myeloid leukemia (RR, 1.28; 95% CI, 1.07‐1.51; P = .02) and acute myeloid leukemia (RR, 1.17; 95% CI, 1.04‐1.33; P = .0009) compared with Hispanics living elsewhere in Texas. Conclusions Hispanic ethnicity and border proximity were associated with a poor presentation and an adverse prognosis despite the younger age of diagnosis. Future studies should explore differences in disease biology and treatment strategies that could drive these regional disparities.