Exploratory thoracotomy on a patient with previous malignancy—“metastasis” or “new primary” or “unrelated lesion”

Surgical resection of a solitary pulmonary metastasis is an established procedure. A medical generation ago when such a shadow appeared on chest roentgenogram of a patient who had known cancer elsewhere in body, it was assumed to be “metastasis” from an extrathoracic site. With increasing advances in knowledge, the occurrence of second primary or new lesion is now no more curiosity in clinical practice. To one's surprise, the lesions that are assumed to be metastatic have often turned out to be “fresh” lesion or even unrelated benign, granulomatous, inflammatory, or parasitic lesion. This paper analyses 66 patients during a period of 20 years who underwent thoracotomy for such solitary pulmonary lesions, and emphasizes the role of diagnostic-cum-therapeutic-thoracotomy in such a clinical situation where in prethoracotomy tissue diagnosis is not forthcoming.     

Colorectal cancer—prognostic signs in “local disease”

This detailed review of the clinical and pathologic signs which effect the prognosis of patients with colorectal cancer. The following are reviewed: (1) the degree of cellular anaplasia, (2) local penetration of the bowel wall, (3) lymph-node spread, (4) venous invasion, (5) perineural invasion, (6) obstruction and perforation, and (7) the number of cm the lesion is located from the anal verge.     

“Early” tongue carcinoma

This is a retrospective study done in 89 patients who were treated for stage I lingual carcinoma, to determine the local control and 5-year salvage rate and the site and frequency of recurrences with salvage rate with a second modality.     

Melanoma metastatic to “lipomata”

Three patients presented with solitary melanoma metastases that mimicked a simple “lipomata.” On further investigation each patient had a discrete fatty tissue tumor mass surrounding a melanoma metastasis. The presence of an enlarging mass in patients with a history of melanoma should be viewed with suspicion and a biopsy should be performed.     

Direct “Metrizamide” Myelocystography in Syringohydromyelia

Metrizamide myelography, followed by CT examination, demonstrated features consistent with syringohydromelia in three patients. One was an adult, male, of 23 years and two were females of 5 and 6 years respectively. Subsequently, metrizamide was introduced into the syrinx by direct needle puncture in each patient. The anatomical details of the syrinx are well demonstrated, continuity of the myelocyst is easily established, and the possibility of communication with the fourth ventricle is readily assessed. The technique is simple and was without complication in these cases. The myelo-graphic and CT findings are also presented. The Arnold-Chiari Type I malformation was present in two patients. The myelocyst did not communicate with the fourth ventricle in two patients. Poor communication was demonstrated in one patient by CT examination immediately after the myelocystogram.     

Does “Black” Brain Mean Doom? Computed Tomography in the Prediction of Outcome in Children with Severe Head Injuries: “Benign” vs “Malignant” Brain Swelling

A retrospective review of initial and subsequent CT scans of 179 children who has suffered severe head injury requiring admission to intensive care was performed. The aim was to define the CT appearance which was always associated with a poor outcome. The children whose brain showed poor definition of basal ganglia and grey-white differentiation overall, together with sufficient swelling to obliterate the ambient cistern and third ventricle always died or remained in a vegetative state. Over half of these had reduced brain density, and several had small focal high densities consistent with contusions or petechial haemorrhages. A typical appearance showed homogeneous scans at the levels of the ambient cistern and thalami with no normal internal brain detail. Conversely obliteration of the ambient cistern associated with a large surface collection was compatible with complete recovery if grey-white definition remained normal and treatment was prompt.     

Resistance to “Castration‐Resistant”

The author challenges the use of the phrase “castration resistance,” which is widely used in the literature and also appears in a recent article by Merseburger et al.In a recent article in The Oncologist, Merseburger et al. [1] outline perspectives arising from current progress in the treatment of advanced prostate cancer (PC). As a nonspecialist in this area, I found their account effectively addresses the challenges posed by this difficult clinical problem. However, I take this opportunity to challenge in turn the widely used phrase “castration resistance.”More than half a century ago, it was established that growth of PC was reduced by bilateral orchiectomy [2], and the rough term “castration” was commonly used. Then it was found that a similar therapeutic effect could be achieved alternatively by the administration of hormone-related agents such as diethylstilbestrol or goserelin [3]: such approaches became known as “chemical castration” (but the adjective was often dropped). Because the growth of PC (just as the development of the normal prostate itself) depends on androgens through androgen-receptor (AR) signaling, there was a sound rationale for these therapeutic procedures of androgen deprivation, frequently called more loosely “hormonal treatments.”Unfortunately, however, all of these beneficial interventions proved time-limited, as PC eventually resumes growth: one might have presumed that it had become independent of AR signaling. However, it transpired that things were not that simple. In an authoritative paper [4] published in 2004, the evidence was reviewed that when PC relapses after hormonal treatment, AR signaling is still on, due to two possible explanations: (a) androgens had not been completely eliminated (they are produced by the adrenal glands and sometimes by the PC itself); (b) even in complete absence of the androgen ligand, AR signaling can still operate through devious means (including AR mutation/amplification, crosstalk-mediated activation of other signaling pathways, and other mechanisms [4, 5]). From then on, the phrase “castration-resistant PC” (CRPC) became popular (n = 1,795 in PubMed).Perhaps the time has come to abrogate this term. First, from the clinical point of view for patients who have CRPC, there are now different remedies available depending on whether the resistance results from (a) or (b) above (e.g., abiraterone versus enzalutamide); thus, the term may cause confusion rather than clarity. Second, we should restore dignity to both patients and terminology. It was a disrespectful mistake in the past to indulge in the phrases “castration” and “chemical castration.” CRPC is worse, and I have even come across the variant “castration-resistant patients,” which some patients perceive as an accusation of refusing to accept something to which unfortunately they have been already subjected. One oncologist told me he used to use the term “castration resistance” freely, but, having PC himself, he has now changed his mind. Instead of CRPC, he suggests, for the two above-mentioned types, respectively, (a) “androgen-deprivation-resistant PC due to persistence of residual androgen” and (b) “androgen-depletion-resistant PC due to androgen-independent persistence of AR signaling.” I admit that these phrases are a bit cumbersome. More simply, androgen deprivation-resistant PC and androgen depletion-resistant PC could both be covered by ADRPC (and they could be called ADPRC-a, ADPRC-b), but the choice of appropriate acronyms is best left to the experts.     

“Hard” and “soft” lesions underlying the HLA class I alterations in cancer cells: Implications for immunotherapy

The ability of cancer cells to escape from the natural or immunotherapy‐induced antitumor immune response is often associated with alterations in the tumor cell surface expression of Major Histocompatibility Complex (MHC) Class I antigens. Considerable knowledge has been gained on the prevalence of various patterns of MHC Class I defects and the underlying molecular mechanisms in different types of cancer. In contrast, few data are available on the changes in MHC Class I expression happening during the course of cancer immunotherapy. We have recently proposed that the progression or regression of a tumor lesion in cancer patients undergoing immunotherapy could be predetermined by the molecular mechanism responsible for the MHC Class I alteration and not by the type of immunotherapy used, i.e., interleukin‐2 (IL‐2), Bacillus Calmette‐Guèrin (BCG), interferon‐alpha (IFN‐α), peptides alone, dendritic cells loaded with peptides, protein‐bound polysaccharide etc. If the molecular alteration responsible for the changes in MHC Class I expression is reversible by cytokines (“soft” lesion), the MHC Class I expression will be upregulated, the specific T cell–mediated response will increase and the lesion will regress. However, if the molecular defect is structural (“hard” lesion), the MHC Class I expression will remain low, the escape mechanism will prevail and the primary tumor or the metastatic lesion will progress. According to this idea, the nature of the preexisting MHC Class I lesion in the cancer cell has a crucial impact determining the final outcome of cancer immunotherapy. In this article, we discuss the importance of these two types of molecular mechanisms of MHC Class I–altered expression.     

“The Displaced Pineal?” A Case Report

A large subdural haematoma caused displacement of the choroid plexus. This was interpreted on the plain skull X-rays as displaced pineal and localised to the wrong side of the head.