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Aim It is often safe to treat pT1 tumours with local resection due to the low risk of lymph node metastasis. The risk of lymph node metastasis in pT2 colon cancer is less well investigated. The recommendation for patients diagnosed with T2 colon cancer is a segmental resection including regional lymph nodes. The aim of this work was to determine the risk of lymph node metastasis in pT2 colon cancer and identify the possible associated clinical and pathological risk factors for lymph node metastasis. Method PubMed and Embase were systematically searched for studies describing patients with T2 colon cancer and lymph node status after histopathological assessment. Lymph node metastasis and the effect of histological and clinical factors were included. Results Overall, 5489 studies were screened, and 10 studies consisting of a total of 91 460 patients were included in the review. The overall risk of lymph node metastasis was 19.3% (95% confidence interval 19.0%–19.5%). A meta-analysis was not possible as very few studies described the clinical and pathological risk factors for lymph node metastasis. Conclusion The risk of lymph node metastasis in patients with pT2 colon cancers is higher than for pT1. The studies included patients operated on from 1985 to 2015 with variations in surgical procedure, pathological handling, and definition of lymph node metastasis. Further studies reporting risk factors for lymph node metastasis in pT2 colon cancer are warranted as more data are needed to determine if local resection for a subgroup of patients could be an alternative treatment modality., Aim: It is often safe to treat pT1 tumours with local resection due to the low risk of lymph node metastasis. The risk of lymph node metastasis in pT2 colon cancer is less well investigated. The recommendation for patients diagnosed with T2 colon cancer is a segmental resection including regional lymph nodes. The aim of this work was to determine the risk of lymph node metastasis in pT2 colon cancer and identify the possible associated clinical and pathological risk factors for lymph node metastasis. Method: PubMed and Embase were systematically searched for studies describing patients with T2 colon cancer and lymph node status after histopathological assessment. Lymph node metastasis and the effect of histological and clinical factors were included. Results: Overall, 5489 studies were screened, and 10 studies consisting of a total of 91 460 patients were included in the review. The overall risk of lymph node metastasis was 19.3% (95% confidence interval 19.0%–19.5%). A meta-analysis was not possible as very few studies described the clinical and pathological risk factors for lymph node metastasis. Conclusion: The risk of lymph node metastasis in patients with pT2 colon cancers is higher than for pT1. The studies included patients operated on from 1985 to 2015 with variations in surgical procedure, pathological handling, and definition of lymph node metastasis. Further studies reporting risk factors for lymph node metastasis in pT2 colon cancer are warranted as more data are needed to determine if local resection for a subgroup of patients could be an alternative treatment modality.

Aim It is often safe to treat pT1 tumours with local resection due to the low risk of lymph node metastasis. The risk of lymph node metastasis in pT2 colon cancer is less well investigated. The recommendation for patients diagnosed with T2 colon cancer is a segmental resection including regional lymph nodes. The aim of this work was to determine the risk of lymph node metastasis in pT2 colon cancer and identify the possible associated clinical and pathological risk factors for lymph node metastasis. Method PubMed and Embase were systematically searched for studies describing patients with T2 colon cancer and lymph node status after histopathological assessment. Lymph node metastasis and the effect of histological and clinical factors were included. Results Overall, 5489 studies were screened, and 10 studies consisting of a total of 91 460 patients were included in the review. The overall risk of lymph node metastasis was 19.3% (95% confidence interval 19.0%–19.5%). A meta-analysis was not possible as very few studies described the clinical and pathological risk factors for lymph node metastasis. Conclusion The risk of lymph node metastasis in patients with pT2 colon cancers is higher than for pT1. The studies included patients operated on from 1985 to 2015 with variations in surgical procedure, pathological handling, and definition of lymph node metastasis. Further studies reporting risk factors for lymph node metastasis in pT2 colon cancer are warranted as more data are needed to determine if local resection for a subgroup of patients could be an alternative treatment modality., Aim: It is often safe to treat pT1 tumours with local resection due to the low risk of lymph node metastasis. The risk of lymph node metastasis in pT2 colon cancer is less well investigated. The recommendation for patients diagnosed with T2 colon cancer is a segmental resection including regional lymph nodes. The aim of this work was to determine the risk of lymph node metastasis in pT2 colon cancer and identify the possible associated clinical and pathological risk factors for lymph node metastasis. Method: PubMed and Embase were systematically searched for studies describing patients with T2 colon cancer and lymph node status after histopathological assessment. Lymph node metastasis and the effect of histological and clinical factors were included. Results: Overall, 5489 studies were screened, and 10 studies consisting of a total of 91 460 patients were included in the review. The overall risk of lymph node metastasis was 19.3% (95% confidence interval 19.0%–19.5%). A meta-analysis was not possible as very few studies described the clinical and pathological risk factors for lymph node metastasis. Conclusion: The risk of lymph node metastasis in patients with pT2 colon cancers is higher than for pT1. The studies included patients operated on from 1985 to 2015 with variations in surgical procedure, pathological handling, and definition of lymph node metastasis. Further studies reporting risk factors for lymph node metastasis in pT2 colon cancer are warranted as more data are needed to determine if local resection for a subgroup of patients could be an alternative treatment modality.

Central neuropathic pain is a core clinical sign of syringomyelia in humans and Cavalier King Charles Spaniel (CKCS) dogs. This histopathological study used spinal cords from CKCS dogs with syringomyelia to investigate the following conditions: (1) whether specific structural cervical spinal cord entities involved in nociception were affected by loss of neuroparenchyma or other pathological changes in CKCS dogs with pain-related behaviour and phantom scratching, (2) whether pain-related behaviour or phantom scratching correlated with loss of a specific anatomical entity or upregulation of glia cells, and (3) whether syringomyelia-related lesions affected specific functional spinal cord units of nociception. Spinal cord segments C1-C8 from CKCS dogs with magnetic resonance imaging-confirmed syringomyelia and clinical signs of pain and phantom scratching (n = 8) were compared with those from CKCS dogs without syringomyelia (n = 4). Dogs with unilateral scratching (n = 7) had a volume loss (P = 0.043) of the dorsal horn laminae I-III in the ipsilateral side compared with the contralateral dorsal horn. A clear pattern of ipsilateral changes in the dorsal root entry zone characterised by deafferentation and reorganization of first-order axons into deeper laminae was found in cases with lateralised scratching. Significant changes in cell number density were not found for astrocytes or microglia, suggesting that the dogs represented cases of end-stage syringomyelia and thus could not reveal astrogliosis and microgliosis, which may be involved in the early phases of syrinx development and phantom scratching. The present relationship between clinical findings and dorsal horn and pain pathway pathology in CKCS dogs suggests that these dogs may be of interest as a supplement to experimental model pain research.

Guidelines and requirements for diagnosing pathological complete response (pCR) in rectal adenocarcinoma following neoadjuvant treatment vary, and there is currently no consensus on the appropriate number of sections to examine per formalin-fixed, paraffin-embedded (FFPE) tissue block. The consequences of systematic use of deeper sections on the diagnostic accuracy and prognosis for patients classified as ypT0 rectal cancer were investigated. In this retrospective study, 23 out of 155 patients who underwent neoadjuvant therapy and surgical resection between 2015 and 2020 were diagnosed with ypT0 rectal cancer. Three additional deeper sections were cut from each FFPE block from the primary tumor site and reviewed for presence of residual tumor cells. Additional sections revealed residual viable tumor cells in seven patients (30.4%), reducing the rate of pCR in the cohort from 14.8 to 10.3%. Of the seven patients, three patients later had local recurrence or distant metastasis during the follow-up period, compared with one patient with no residual tumor cells in deeper sections (p = 0.07). A nonsignificant reduction in disease-free survival (p = 0.08) was observed in the patients with residual tumor. Systematic use of deeper sections in evaluation of tumor regression in rectal cancer reveals the presence of residual tumor cells in a subset of patients originally diagnosed with pCR based on a single section per FFPE block. Although the results are not statistically significant, it cannot be excluded that accurately distinguishing complete from near-complete response may be clinically relevant for prognostic prediction.

Human MCF-7 breast cancer cells were exposed to a Random Positioning Machine (RPM). After 24 hours (h) the cells grew either adherently within a monolayer (AD) or within multicellular spheroids (MCS). AD and MCS populations were separately harvested, their cellular differences were determined performing qPCR on genes, which were differently expressed in AD and MCS cells. Gene array technology was applied to detect RPM-sensitive genes in MCF-7 cells after 24 h. Furthermore, the capability to form multicellular spheroids in vitro was compared with the intracellular distribution of NF-kappaB (NF kappa B) p65. NF kappa B was equally distributed in static control cells, but predominantly localized in the cytoplasm in AD cells and nucleus in MCS cells exposed to the RPM. Gene array analyses revealed a more than 2-fold change of only 23 genes including some whose products are affected by oxygen levels or regulate glycolysis. Significant upregulations of the mRNAs of enzymes degrading heme, of ANXA1, ANXA2, CTGF, CAV2 and ICAM1, as well as of FAS, Casp8, BAX, p53, CYC1 and PARP1 were observed in MCS cells as compared with 1g-control and AD cells. An interaction analysis of 47 investigated genes suggested that HMOX-1 and NF kappa B variants are activated, when multicellular spheroids are formed.